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1
Owen, Penelope Jane. "Bradykinin stimulation of bovine adrenal chromaffin cells." Thesis, University of Leicester, 1991. http://hdl.handle.net/2381/33600.
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Cultured bovine adrenal chromaffin cells provide a useful model of stimulus secretion coupling and respond to cholinergic agonists by secreting catecholamines. Work in this thesis concentrates on the responses to a non-cholinergic agonist, bradykinin. Bradykinin as shown to stimulate a two phase, dose dependent increase in catecholamine release which is mediated by a receptor of the B2 subtype. Calcium entry is shown to be required for release to occur but studies with various calcium channel blockers suggest that, in contrast to the response to potassium, a non-voltage sensitive calcium channel is involved. Other possible alternatives are discussed. As bradykinin stimulated an increase in inositol phosphate production, I attempted to measure the production of the other product of phospholipase C action on inositol phospholipids, diacylglycerol, in order to evaluate its possible role in the release response. This was attempted using both mass measurement, by the diacylglycerol kinase assay, and lipid labelling techniques. No increases in diacylglycerol in response to bradykinin were observed, even in the presence of inhibitors of diacylglycerol breakdown, which were able to increase basal diacylglycerol levels when added alone. These inhibitors, along with TPA, were used to evaluate the possible mechanism of action of protein kinase C in chromaffin cells, eg. feedback regulation or stimulation of release mechanisms. Failure to detect rises in diacylglycerol in response to bradykinin led to the final section of this work which looks at the production of one of the metabolic products of diacylglycerol breakdown, phosphatidic acid. Bradykinin is shown to stimulate a rapid, dose dependent increase in phosphatidic acid in chromaffin cells, which is, partially independent of extracellular calcium, independent of protein kinase C activation, and may be G-protein mediated. Studies of the route of formation of the phosphatidic acid show that phospholipase D is not involved and that inositol phospholipids or phosphatidylcholine are unlikely to be the main substrates for a phospholipase C mediated route, leaving the possibility of phospholipase C action on an alternative phospholipid. Finally the possible role of this production of phosphatidic acid in the chromaffin cell is discussed.
2
Pappas, Vassilios Konstantinos. "Ca2+ signalling in bovine adrenal chromaffin cells." Thesis, University of Leicester, 1995. http://hdl.handle.net/2381/33634.
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Cells possess two mechanisms, the inositol 1,4,5-trisphosphate (Ins(l,4,5)P3) and ryanodine receptors, by which Ca2+ in intracellular stores can be mobilised. There are also a number of pathways which can mediate Ca2+ entry across the cell plasma membrane. In this study bovine adrenal chromaffin cells were used to investigate the role of intracellular Ca2+ stores in Ca2+ signalling and the relationship between Ca2+ entry and store release. The major part of the exocytotic process in chromaffin cells is due to Ca2+ entry across the plasma membrane. Bradykinin (an Ins(l,4,5)P3 generating agonist) and nicotine (a depolarising stimulus) were found to evoke catecholamine secretion in the presence of extracellular Ca2+. Nicotinic responses were abolished in the absence of extracellular Ca2+, whereas bradykinin resulted in reduced catecholamine secretion, indicating that Ca2+ release from intracellular stores may activate secretion. Studies in permeabilised chromaffin cells showed that both Ins(l,4,5)P3 and caffeine induced Ca2+ mobilisation from intracellular Ca2+ stores. Challenge of the chromaffin cells with inositol 4,5-bisphosphorothioate resulted in depletion of the Ins(l,4,5)P3-sensitive Ca2+ stores. However, subsequent addition of caffeine stimulated Ca2+ mobilisation, indicating that the caffeine releasable stores had not been emptied. Ins(l,4,5)P3 and caffeine, when added simultaneously, resulted in a larger response than each of these agonists alone. Ryanodine pretreatment inhibited subsequent caffeine responses. Ins(l,4,5)P3 was able to stimulate Ca2+ release after prior depletion of the ryanodine-sensitive Ca2+ stores, providing a pharmacological differentiation of these stores, suggesting that the Ins(l,4,5)P3 receptor-expressing stores may be physically different from the ryanodine receptor-expressing Ca2+ stores in chromaffin cells. Experiments using epifluorescence microscopy were carried out to investigate the relationship between Ins(l,4,5)P3- and caffeine-sensitive Ca2+ stores in fura-2 loaded intact chromaffin cells. Bradykinin evoked Ca2+ responses appeared to involve activation of ryanodine receptors, probably occuring secondary to Ca2+ release via Ins(l,4,5)P3 receptors. Depletion of the Ins(l,4,5)P3- and caffeine-sensitive Ca2+ stores resulted in activation of Ca2+ entry indicating that the Ins(l,4,5)P3- and ryanodine-sensitive Ca2+ stores are both linked to the promotion of Ca2+ entry. Several aspects of Ca2+ signalling have been elucidated in this study, notably the possible expression of at least two different Ca2+ stores and the degree of physical or functional overlap between the Ins(l,4,5)P3 receptor-expressing and ryanodine-receptor expressing Ca2+ stores. Ca2+ release from the ryanodine-sensitive Ca2+ stores was found to activate Ca2+ entry across the chromaffin cells plasma membrane. These findings may have important implications for our understanding of how Ca2+ signalling occurs in adrenal chromaffin and other excitable cells in vivo.
3
Hagan, Todd. "Finite-difference time-domain modeling of a waveguide-based radiofrequency exposure system for studying non-thermal effects on catecholamine release from chromaffin cells : characterization and optimization /." abstract and full text PDF (free order & download UNR users only), 2005. http://0-wwwlib.umi.com.innopac.library.unr.edu/dissertations/fullcit/1433103.
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Thesis (M.S.)--University of Nevada, Reno, 2005.<br>"May, 2005." Includes bibliographical references. Library also has microfilm. Ann Arbor, Mich. : ProQuest Information and Learning Company, [2005]. 1 microfilm reel ; 35 mm. Online version available on the World Wide Web.
4
gov, Clearys@ninds nih, and Susannah Cleary. "From chromaffin cells to Phaeochromocytoma : insight into the sympathoadrenal cell lineage." Murdoch University, 2007. http://wwwlib.murdoch.edu.au/adt/browse/view/adt-MU20080526.105525.
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Chromaffin cells are a modified post-ganglionic sympathetic neuron, which synthesise and secrete catecholamines. The neoplastic transformation of chromaffin cells is demonstrated by the tumour phaeochromocytoma, a functional tumour that recapitulates the normal role of chromaffin cells by synthesising, storing and releasing excess catecholamines. Within this thesis we have explored several aspects of chromaffin cell and phaeochromocytoma tumour biology, including the specific expression of key sympathoadrenal markers such as the noradrenaline transporter (NAT), neuropeptide Y (NPY) and chromogranin A (CGA) in normal human and mouse chromaffin cells versus phaeochromocytomas of human and mouse origin.
Catecholamine-mediated signalling in chromaffin cells is terminated by the sequestration of extracellular catecholamines back into the cell via the noradrenaline transporter (NAT). Following observations that within the rat adrenal medulla, NAT is expressed in PNMT-positive chromaffin cells we explored whether this pattern of expression is also present in the human adrenal medulla. While we successfully established that NAT and PNMT are co localised, we also found that all human adrenal chromaffin cells are PNMT-positive. In the rat, NAT is also observed within the cytoplasm and has been suggested to be associated with secretory vesicles, thus using the secretory vesicle marker, CGA, we demonstrate that NAT is associated with secretory vesicles. However, in contrast to our findings within the normal chromaffin cells, in situ NAT expression in human phaeochromocytoma tumour samples was distorted, with observed changes including the level and type of staining observed, and disruptions to the strict NAT-CGA association observed in the normal adrenal.
Continuing our theme of NAT, we investigated if pre treating the phaeochromocytoma PC12 cell line with the chemotherapy drug cisplatin had an effect on the expression of NAT, to give an indication of the efficacy of this compound in the treatment of metastatic phaeochromocytoma with radiolabelled 131Iodometabenzylguanidine (131I-MIBG), a noradrenaline analogue which can be incorporated into phaeochromocytoma tumour cells though uptake through NAT. The premise of this study is derived from previous work in which neuroblastoma cells pre-treated with cisplatin were more responsive to (131I-MIBG) accumulation due to increased activity and expression of the transporter. Thus we treated PC12 cells for 24-hours in a range of cisplatin concentrations and measured the effect on NAT expression. However, unlike the findings in neuroblastoma cells, in our study, we did not observe an effect of cisplatin pretreatment on NAT activity or expression in PC12 cells.
Upto 30% of phaeochromocytoma arise as apart of a hereditary syndrome. The von Hippel-Lindau (VHL) syndrome, due to germline mutations to the VHL gene, and Multiple Endocrine Neoplasia type 2 (MEN 2), due to germline mutations to the RET gene represent two examples of hereditable endocrine disorders where phaeochromocytoma is a presenting feature. Notable differences in clinical presentation and tumour biology have been identified in phaeochromocytomas from patients with VHL and MEN 2. These differences prompted us to explore whether these observations extend to the chromaffin granule constituents, NPY and CGA.
Patients with MEN 2 disease have a greater incidence of hypertension than patients with VHL disease, MEN 2 are characterised by an adrenergic phenotype (produce predominantly-adrenaline), whereas VHL phaeochromocytomas are noradrenergic (produce predominantly-noradrenaline). Neuropeptide Y, which has powerful vasoactive properties capable of significantly elevating blood pressure, is stored and released with catecholamines and is thought to be associated with PNMT-positive chromaffin cells. Thus, we questioned whether the differences in the symptomatology between VHL and MEN 2 patients may be related to differences in NPY expression between the two groups, and whether any differences in NPY relate to adrenaline and/or PNMT content, or are linked to hereditary factors. Thus we compared tumour samples from four cohorts of patients: (i) adrenergic versus noradrenergic phenotype, (ii) hereditary versus no hereditary syndrome. Results demonstrated that although tumour NPY levels (mRNA and peptide) correlate with PNMT expression and/or adrenaline content, when NPY expression was compared between groups of patients (adrenergic vs noradrenergic; hereditary versus nonhereditary) difference in NPY levels were only significant between VHL and MEN 2 tumour and not between sporadic adrenergic and noradrenergic Immunohistochemistry also supported the above observations. Hence, we concluded that NPY expression in all groups of phaeochromocytoma examined in this study, this effect is not related to tumour biochemical phenotype but rather appears to be a specific unique trait of VHL phaeochromocytomas.
Continuing our theme of the possible differential expression of chromaffin granule constituents between VHL and MEN 2 patients, we also investigated CGA levels in plasma and tumour samples. Given, VHL tumours possess less chromaffin granules than MEN 2 tumours, and CGA has been implicated as a key director of secretory vesicle biogenesis we investigated whether CGA was differentially expressed between VHL and MEN 2 tumours. We found CGA expression was significantly greater in MEN 2 tumours (mRNA; 3-fold, and protein; 20-fold), with western blot confirming this trend. We also found that plasma CGA was greater in MEN 2 patients but not significantly, consequently, we explored the co-variables tumour size and tumour secretory activity (measured by plasma catecholamine concentrations), which influence plasma CGA and found that tumour size and plasma CGA are related but there was no influence of genotype on this relationship. In contrast, plasma CGA was significantly related to tumour secretory activity and the effect of genotype on this relationship narrowly missed significance, but when we expressed plasma CGA as a ratio of plasma catecholamines, plasma CGA was 2-fold greater in MEN 2 patients than VHL patients. Thus despite the tendency of phaeochromocytomas from VHL disease to readily and continuously release their catecholamine stores, plasma CGA levels still appeared to be higher in MEN 2 patients.
Finally, we examined whether the expression of NPY, Leu- enkephalin (Leu-Enk), NAT and the vesicular monoamine transporters type 1 and 2 (VMAT1 and VMAT2,), in normal mouse adrenal glands, and in histologically-confirmed adrenal phaeochromocytomas generated by injected nude mice with a phaeochromocytoma (MPC) cells line. The results of this study established that similar to the rat and human NAT expression is preferentially localised with PNMT within mouse chromaffin cells, while VMAT1 and NPY are found in both PNMT-negative and PNMT-positive cell populations, although expression of NPY was reduced in PNMT-negative cells. In contrast, both VMAT2 and Leu-Enk were found in PNMT-negative noradrenergic cells, and VMAT2 was present in all noradrenergic chromaffin cells while Leu-Enk was observed in a subpopulation of noradrenergic chromaffin cells. In contrast to the normal adrenal but similar to our findings in human phaeochromocytoma, the pattern of marker expression within adrenal phaeochromocytoma lesions of MPC-injected mice are severely disrupted related to both the level of expression of the respective markers, and association with PNMT within the tissue. Thus, the experimentally generated phaeochromocytoma mouse model provides a valuable tool in studying human phaeochromocytoma.
The data presented in this thesis further validate the heterogeneity observed in many aspects of phaeochromocytoma tumour biology, including the expression several chromaffin cell markers such as NAT, NPY and CGA. The altered expression of these markers may contribute to the clinical picture of these tumours, particularly relating to hereditary phaeochromocytoma from VHL and MEN 2 disease.
5
Cleary, Susannah. "From chromaffin cells to Phaeochromocytoma: insight into the sympathoadrenal cell lineage." Thesis, Cleary, Susannah (2007) From chromaffin cells to Phaeochromocytoma: insight into the sympathoadrenal cell lineage. PhD thesis, Murdoch University, 2007. https://researchrepository.murdoch.edu.au/id/eprint/659/.
Der volle Inhalt der QuelleAnnotation:
Chromaffin cells are a modified post-ganglionic sympathetic neuron, which synthesise and secrete catecholamines. The neoplastic transformation of chromaffin cells is demonstrated by the tumour phaeochromocytoma, a functional tumour that recapitulates the normal role of chromaffin cells by synthesising, storing and releasing excess catecholamines. Within this thesis we have explored several aspects of chromaffin cell and phaeochromocytoma tumour biology, including the specific expression of key sympathoadrenal markers such as the noradrenaline transporter (NAT), neuropeptide Y (NPY) and chromogranin A (CGA) in normal human and mouse chromaffin cells versus phaeochromocytomas of human and mouse origin.
Catecholamine-mediated signalling in chromaffin cells is terminated by the sequestration of extracellular catecholamines back into the cell via the noradrenaline transporter (NAT). Following observations that within the rat adrenal medulla, NAT is expressed in PNMT-positive chromaffin cells we explored whether this pattern of expression is also present in the human adrenal medulla. While we successfully established that NAT and PNMT are co localised, we also found that all human adrenal chromaffin cells are PNMT-positive. In the rat, NAT is also observed within the cytoplasm and has been suggested to be associated with secretory vesicles, thus using the secretory vesicle marker, CGA, we demonstrate that NAT is associated with secretory vesicles. However, in contrast to our findings within the normal chromaffin cells, in situ NAT expression in human phaeochromocytoma tumour samples was distorted, with observed changes including the level and type of staining observed, and disruptions to the strict NAT-CGA association observed in the normal adrenal.
Continuing our theme of NAT, we investigated if pre treating the phaeochromocytoma PC12 cell line with the chemotherapy drug cisplatin had an effect on the expression of NAT, to give an indication of the efficacy of this compound in the treatment of metastatic phaeochromocytoma with radiolabelled 131Iodometabenzylguanidine (131I-MIBG), a noradrenaline analogue which can be incorporated into phaeochromocytoma tumour cells though uptake through NAT. The premise of this study is derived from previous work in which neuroblastoma cells pre-treated with cisplatin were more responsive to (131I-MIBG) accumulation due to increased activity and expression of the transporter. Thus we treated PC12 cells for 24-hours in a range of cisplatin concentrations and measured the effect on NAT expression. However, unlike the findings in neuroblastoma cells, in our study, we did not observe an effect of cisplatin pretreatment on NAT activity or expression in PC12 cells.
Upto 30% of phaeochromocytoma arise as apart of a hereditary syndrome. The von Hippel-Lindau (VHL) syndrome, due to germline mutations to the VHL gene, and Multiple Endocrine Neoplasia type 2 (MEN 2), due to germline mutations to the RET gene represent two examples of hereditable endocrine disorders where phaeochromocytoma is a presenting feature. Notable differences in clinical presentation and tumour biology have been identified in phaeochromocytomas from patients with VHL and MEN 2. These differences prompted us to explore whether these observations extend to the chromaffin granule constituents, NPY and CGA.
Patients with MEN 2 disease have a greater incidence of hypertension than patients with VHL disease, MEN 2 are characterised by an adrenergic phenotype (produce predominantly-adrenaline), whereas VHL phaeochromocytomas are noradrenergic (produce predominantly-noradrenaline). Neuropeptide Y, which has powerful vasoactive properties capable of significantly elevating blood pressure, is stored and released with catecholamines and is thought to be associated with PNMT-positive chromaffin cells. Thus, we questioned whether the differences in the symptomatology between VHL and MEN 2 patients may be related to differences in NPY expression between the two groups, and whether any differences in NPY relate to adrenaline and/or PNMT content, or are linked to hereditary factors. Thus we compared tumour samples from four cohorts of patients: (i) adrenergic versus noradrenergic phenotype, (ii) hereditary versus no hereditary syndrome. Results demonstrated that although tumour NPY levels (mRNA and peptide) correlate with PNMT expression and/or adrenaline content, when NPY expression was compared between groups of patients (adrenergic vs noradrenergic; hereditary versus nonhereditary) difference in NPY levels were only significant between VHL and MEN 2 tumour and not between sporadic adrenergic and noradrenergic Immunohistochemistry also supported the above observations. Hence, we concluded that NPY expression in all groups of phaeochromocytoma examined in this study, this effect is not related to tumour biochemical phenotype but rather appears to be a specific unique trait of VHL phaeochromocytomas.
Continuing our theme of the possible differential expression of chromaffin granule constituents between VHL and MEN 2 patients, we also investigated CGA levels in plasma and tumour samples. Given, VHL tumours possess less chromaffin granules than MEN 2 tumours, and CGA has been implicated as a key director of secretory vesicle biogenesis we investigated whether CGA was differentially expressed between VHL and MEN 2 tumours. We found CGA expression was significantly greater in MEN 2 tumours (mRNA; 3-fold, and protein; 20-fold), with western blot confirming this trend. We also found that plasma CGA was greater in MEN 2 patients but not significantly, consequently, we explored the co-variables tumour size and tumour secretory activity (measured by plasma catecholamine concentrations), which influence plasma CGA and found that tumour size and plasma CGA are related but there was no influence of genotype on this relationship. In contrast, plasma CGA was significantly related to tumour secretory activity and the effect of genotype on this relationship narrowly missed significance, but when we expressed plasma CGA as a ratio of plasma catecholamines, plasma CGA was 2-fold greater in MEN 2 patients than VHL patients. Thus despite the tendency of phaeochromocytomas from VHL disease to readily and continuously release their catecholamine stores, plasma CGA levels still appeared to be higher in MEN 2 patients.
Finally, we examined whether the expression of NPY, Leu- enkephalin (Leu-Enk), NAT and the vesicular monoamine transporters type 1 and 2 (VMAT1 and VMAT2,), in normal mouse adrenal glands, and in histologically-confirmed adrenal phaeochromocytomas generated by injected nude mice with a phaeochromocytoma (MPC) cells line. The results of this study established that similar to the rat and human NAT expression is preferentially localised with PNMT within mouse chromaffin cells, while VMAT1 and NPY are found in both PNMT-negative and PNMT-positive cell populations, although expression of NPY was reduced in PNMT-negative cells. In contrast, both VMAT2 and Leu-Enk were found in PNMT-negative noradrenergic cells, and VMAT2 was present in all noradrenergic chromaffin cells while Leu-Enk was observed in a subpopulation of noradrenergic chromaffin cells. In contrast to the normal adrenal but similar to our findings in human phaeochromocytoma, the pattern of marker expression within adrenal phaeochromocytoma lesions of MPC-injected mice are severely disrupted related to both the level of expression of the respective markers, and association with PNMT within the tissue. Thus, the experimentally generated phaeochromocytoma mouse model provides a valuable tool in studying human phaeochromocytoma.
The data presented in this thesis further validate the heterogeneity observed in many aspects of phaeochromocytoma tumour biology, including the expression several chromaffin cell markers such as NAT, NPY and CGA. The altered expression of these markers may contribute to the clinical picture of these tumours, particularly relating to hereditary phaeochromocytoma from VHL and MEN 2 disease.
6
Cleary, Susannah. "From chromaffin cells to Phaeochromocytoma: insight into the sympathoadrenal cell lineage." Cleary, Susannah (2007) From chromaffin cells to Phaeochromocytoma: insight into the sympathoadrenal cell lineage. PhD thesis, Murdoch University, 2007. http://researchrepository.murdoch.edu.au/659/.
Der volle Inhalt der QuelleAnnotation:
Chromaffin cells are a modified post-ganglionic sympathetic neuron, which synthesise and secrete catecholamines. The neoplastic transformation of chromaffin cells is demonstrated by the tumour phaeochromocytoma, a functional tumour that recapitulates the normal role of chromaffin cells by synthesising, storing and releasing excess catecholamines. Within this thesis we have explored several aspects of chromaffin cell and phaeochromocytoma tumour biology, including the specific expression of key sympathoadrenal markers such as the noradrenaline transporter (NAT), neuropeptide Y (NPY) and chromogranin A (CGA) in normal human and mouse chromaffin cells versus phaeochromocytomas of human and mouse origin.
Catecholamine-mediated signalling in chromaffin cells is terminated by the sequestration of extracellular catecholamines back into the cell via the noradrenaline transporter (NAT). Following observations that within the rat adrenal medulla, NAT is expressed in PNMT-positive chromaffin cells we explored whether this pattern of expression is also present in the human adrenal medulla. While we successfully established that NAT and PNMT are co localised, we also found that all human adrenal chromaffin cells are PNMT-positive. In the rat, NAT is also observed within the cytoplasm and has been suggested to be associated with secretory vesicles, thus using the secretory vesicle marker, CGA, we demonstrate that NAT is associated with secretory vesicles. However, in contrast to our findings within the normal chromaffin cells, in situ NAT expression in human phaeochromocytoma tumour samples was distorted, with observed changes including the level and type of staining observed, and disruptions to the strict NAT-CGA association observed in the normal adrenal.
Continuing our theme of NAT, we investigated if pre treating the phaeochromocytoma PC12 cell line with the chemotherapy drug cisplatin had an effect on the expression of NAT, to give an indication of the efficacy of this compound in the treatment of metastatic phaeochromocytoma with radiolabelled 131Iodometabenzylguanidine (131I-MIBG), a noradrenaline analogue which can be incorporated into phaeochromocytoma tumour cells though uptake through NAT. The premise of this study is derived from previous work in which neuroblastoma cells pre-treated with cisplatin were more responsive to (131I-MIBG) accumulation due to increased activity and expression of the transporter. Thus we treated PC12 cells for 24-hours in a range of cisplatin concentrations and measured the effect on NAT expression. However, unlike the findings in neuroblastoma cells, in our study, we did not observe an effect of cisplatin pretreatment on NAT activity or expression in PC12 cells.
Upto 30% of phaeochromocytoma arise as apart of a hereditary syndrome. The von Hippel-Lindau (VHL) syndrome, due to germline mutations to the VHL gene, and Multiple Endocrine Neoplasia type 2 (MEN 2), due to germline mutations to the RET gene represent two examples of hereditable endocrine disorders where phaeochromocytoma is a presenting feature. Notable differences in clinical presentation and tumour biology have been identified in phaeochromocytomas from patients with VHL and MEN 2. These differences prompted us to explore whether these observations extend to the chromaffin granule constituents, NPY and CGA.
Patients with MEN 2 disease have a greater incidence of hypertension than patients with VHL disease, MEN 2 are characterised by an adrenergic phenotype (produce predominantly-adrenaline), whereas VHL phaeochromocytomas are noradrenergic (produce predominantly-noradrenaline). Neuropeptide Y, which has powerful vasoactive properties capable of significantly elevating blood pressure, is stored and released with catecholamines and is thought to be associated with PNMT-positive chromaffin cells. Thus, we questioned whether the differences in the symptomatology between VHL and MEN 2 patients may be related to differences in NPY expression between the two groups, and whether any differences in NPY relate to adrenaline and/or PNMT content, or are linked to hereditary factors. Thus we compared tumour samples from four cohorts of patients: (i) adrenergic versus noradrenergic phenotype, (ii) hereditary versus no hereditary syndrome. Results demonstrated that although tumour NPY levels (mRNA and peptide) correlate with PNMT expression and/or adrenaline content, when NPY expression was compared between groups of patients (adrenergic vs noradrenergic; hereditary versus nonhereditary) difference in NPY levels were only significant between VHL and MEN 2 tumour and not between sporadic adrenergic and noradrenergic Immunohistochemistry also supported the above observations. Hence, we concluded that NPY expression in all groups of phaeochromocytoma examined in this study, this effect is not related to tumour biochemical phenotype but rather appears to be a specific unique trait of VHL phaeochromocytomas.
Continuing our theme of the possible differential expression of chromaffin granule constituents between VHL and MEN 2 patients, we also investigated CGA levels in plasma and tumour samples. Given, VHL tumours possess less chromaffin granules than MEN 2 tumours, and CGA has been implicated as a key director of secretory vesicle biogenesis we investigated whether CGA was differentially expressed between VHL and MEN 2 tumours. We found CGA expression was significantly greater in MEN 2 tumours (mRNA; 3-fold, and protein; 20-fold), with western blot confirming this trend. We also found that plasma CGA was greater in MEN 2 patients but not significantly, consequently, we explored the co-variables tumour size and tumour secretory activity (measured by plasma catecholamine concentrations), which influence plasma CGA and found that tumour size and plasma CGA are related but there was no influence of genotype on this relationship. In contrast, plasma CGA was significantly related to tumour secretory activity and the effect of genotype on this relationship narrowly missed significance, but when we expressed plasma CGA as a ratio of plasma catecholamines, plasma CGA was 2-fold greater in MEN 2 patients than VHL patients. Thus despite the tendency of phaeochromocytomas from VHL disease to readily and continuously release their catecholamine stores, plasma CGA levels still appeared to be higher in MEN 2 patients.
Finally, we examined whether the expression of NPY, Leu- enkephalin (Leu-Enk), NAT and the vesicular monoamine transporters type 1 and 2 (VMAT1 and VMAT2,), in normal mouse adrenal glands, and in histologically-confirmed adrenal phaeochromocytomas generated by injected nude mice with a phaeochromocytoma (MPC) cells line. The results of this study established that similar to the rat and human NAT expression is preferentially localised with PNMT within mouse chromaffin cells, while VMAT1 and NPY are found in both PNMT-negative and PNMT-positive cell populations, although expression of NPY was reduced in PNMT-negative cells. In contrast, both VMAT2 and Leu-Enk were found in PNMT-negative noradrenergic cells, and VMAT2 was present in all noradrenergic chromaffin cells while Leu-Enk was observed in a subpopulation of noradrenergic chromaffin cells. In contrast to the normal adrenal but similar to our findings in human phaeochromocytoma, the pattern of marker expression within adrenal phaeochromocytoma lesions of MPC-injected mice are severely disrupted related to both the level of expression of the respective markers, and association with PNMT within the tissue. Thus, the experimentally generated phaeochromocytoma mouse model provides a valuable tool in studying human phaeochromocytoma.
The data presented in this thesis further validate the heterogeneity observed in many aspects of phaeochromocytoma tumour biology, including the expression several chromaffin cell markers such as NAT, NPY and CGA. The altered expression of these markers may contribute to the clinical picture of these tumours, particularly relating to hereditary phaeochromocytoma from VHL and MEN 2 disease.
7
Zhu, Jinghua. "The transformation of chromaffin cells into sympathetic neurons." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386926.
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8
Robinson, Iain Martin. "Ca'2'+ signalling in bovine adrenal chromaffin cells." Thesis, University of Liverpool, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.317281.
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9
Fisher, Richard James. "Amperometric analysis of exocytosis in adrenal chromaffin cells." Thesis, University of Liverpool, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367144.
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10
Powell, Andrew Dennis. "Modulation of neurotransmitter release from adrenal chromaffin cells." Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310685.
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11
Fournier, Sue. "Calmodulin binding proteins in chromaffin and other neurosecretory cells." Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=75881.
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The Ca$ sp{2+}$ binding protein, calmodulin, has been implicated in several Ca$ sp{2+}$ dependent processes during secretion in many different secretory systems. One area where calmodulin is suggested to play a role is the fusion of the secretory granule with the plasma membrane during exocytosis. Calmodulin may mediate the interaction or fusion through specific calmodulin-binding proteins (CMBPs) present in these two membranes.<br>CMBPs present in bovine chromaffin cell granule membranes were characterized using the techniques of calmodulin affinity chromatography and $ sp{125}$I calmodulin overlay. Several CMBPs were detected in these membranes. One of these proteins, of molecular mass 65 kilodaltons (65-CMBP), was found to be immunologically identical to a protein previously identified in rat brain synaptic vesicles termed "p65".<br>Recent studies have debated the subcellular localization of 65-CMBP (p65) as well as another synaptic vesicle protein, synaptophysin (p38). A controversial question surrounding these proteins is whether or not they are present in large dense core secretory granules of neurons and endocrine cells, or exclusively localized on small synaptic or synaptic-like vesicles present in these tissues. Subcellular fractionation studies of adrenal medulla showed that both 65-CMBP and p38 were present in fractions corresponding to granule membranes and intact granules. However, an additional membrane fraction equilibrating near the upper portion of the sucrose gradient, also showed strong immunoreactivity with an antibody to p38.<br>CMBPs were also isolated from bovine posterior pituitary neurosecretory granules and rat brain synaptic vesicles. These membranes were also found to contain the 65-CMBP (63 kDa in rat brain synaptic vesicles).<br>Chromaffin cell membranes were isolated using positively charged microcarriers. The 65-CMBP (p65) was also identified in this structure. In addition, immunoblots of plasma and granule membranes showed that the 65-CMBP was a component of both membranes, whereas p38 was only present in granule membranes. Thus, there appears to be a different subcellular localization between the 65-CMBP and p38 in chromaffin cells.<br>These findings on the 65-CMBP are discussed in relation to its possible role as a mediator of the fusion step of the exocytotic process.
12
Walker, Angela. "Electrochemical study of vesicular release in bovine chromaffin cells." Thesis, McGill University, 1995. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=23431.
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The time course of the spontaneous current spikes produced by the release of the catecholamines from individual vesicles was examined in bovine chromaffin cells by using the carbon filament technique in the amperometric mode.<br>Frequency histograms of the rise and decay times of the current spikes showed a paucity of very short duration events. Scatterograms of the rise and decay times consistently showed a positive relation, and the best fitted lines intercepted the ordinate (the axis of the decay time) at: 16.06 $ pm$ 6.45 msec (n = 11).<br>The effect of temperature changes upon the time course of release of content of individual vesicles in chromaffin cells was also examined. The amplitudes of the current spikes did not change significantly, whereas the rise times and the decay times diminished from (23.2 $ pm$ 11.6 to 11.9 $ pm$ 2.7 msec, and from 76.6 $ pm$ 25.4 to 47.3 $ pm$ 9.3 msec respectively) as the temperature was raised from 15$ sp circ$C to 35$ sp circ$C (n = 5). Nevertheless, the Q$ sb{10}$ values of the rise and decay times were surprisingly low.<br>The experimental findings suggest that in bovine chromaffin cells the duration of the release of content of single vesicles is much longer than in synapses. The results also suggest that this mechanism does not involve processes that are strongly temperature sensitive.
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O'Sullivan, Antony John. "The control of secretion from bovine adrenal chromaffin cells." Thesis, University of Liverpool, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333504.
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Cheek, T. R. "Molecular mechanisms of secretion from bovine adrenal chromaffin cells." Thesis, University of Liverpool, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382015.
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15
Morgan, Alan. "Molecular mechanisms of exocytosis from bovine adrenal chromaffin cells." Thesis, University of Liverpool, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385297.
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Colville, Caroline Anne. "The interaction of tetanus toxin with adrenal chromaffin cells." Thesis, University of Edinburgh, 1992. http://hdl.handle.net/1842/19641.
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Tetanus toxin exerts its primary biological effect by impairing the release of inhibitory neurotransmitters in the central nervous system; the mechanism of this blockade, however, remains unknown. Studies using adrenal medullary chromaffin cells, which are closely related to the toxin's target neurones but much more accessible to biochemical investigation, have the potential to provide information on various aspects of the intoxication process of tetanus. Nicotine-evoked (but not basal) secretion of catecholamines from intact chromaffin cells was inhibited by tetanus toxin in a dose-dependent fashion up to a maximum of 75%, half-maximal inhibition being achieved at 0.7 nM toxin (in single- or double-chain form). The time course of this inhibition was long, approximately 16 hours. Catecholamine release evoked by Ba<SUP>2+</SUP> ions was not affected by the toxin, while its effect on K<SUP>+</SUP> -evokedsecretion was never greater than 30%. Pre-incubation ofcells with ganglioside GT1, a specific ligand of the toxin, in the absence of toxin itself inhibited nicotine-evoked release of catecholamines (50&37 inhibition with 24 uM GT1), making it impossible to evaluate the role of GT1 in mediating the action of the toxin. Tetanus toxin (radiolabelled) was also shown to bind in a specific fashion to chromaffin cells. Toxin binding under less physiological conditions of pH and ionic strength was a higher capacity (B<SUB>max</SUB> 0.7-1.2 pmol/mg protein) than that found under more physiological conditions (B<SUB>max</SUB> 0.2-0.3 pmol/mg protein); this is also characteristic of toxin binding to synaptic membrances. In both cases there appeared to be at least two components to toxin binding, a higher affinity component with a K<SUB>d</SUB> value of approximately 1nM (which did not account for more than 20% of total binding capacity), and a lower affinity binding with a K<SUB>d</SUB> value of 10-25 nM. As expected, pre-incubationof chromaffin cells with ganglioside GT1 enhanced their toxin-binding capacity, but did not noticeably affect K<SUB>d</SUB> value, perhaps indicating that gangliosides mediate binding of tetanus toxin to untreated chromaffin cells. This was further suggested by the finding that neuraminidase treatment of cells markedly reduced toxin-binding capacity (by 50% at pH 7.4, 90% at pH 6.0) and also by the observation that pre-incubation of <SUP>125</SUP>I-labelled tetanus toxin with GT1 led to a reduction in its binding to chromaffin cells. Mild trypsinisation of chromaffin cells completely abolished toxin-binding under both sets of conditions, suggesting the involvement of a protein component in toxin binding also.
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Lawrence, Gary William. "Dissecting exocytosis from chromaffin cells with botulinum and tetanus toxins." Thesis, Imperial College London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321807.
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Doreian, Bryan William. "Molecular Regulation of the Exocytic Mode in Adrenal Chromaffin Cells." Cleveland, Ohio : Case Western Reserve University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1245785721.
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Thesis (Ph.D.)--Case Western Reserve University, 2009<br>Title from PDF (viewed on 19 August 2009) Department of Physiology and Biophysics Includes abstract Includes bibliographical references Available online via the OhioLINK ETD Center
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El-Hajj, Raed Ahmad. "Pharmacological and immunological identification of native [alpha]7 nicotinic receptors: evidence for homomeric and heteromeric [alpha]7 receptors /." Columbus, Ohio : Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1198155366.
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Geertsen, Susanne. "The regulation of nicotinic alpha-bungarotoxin receptors in adrenal chromaffin cells." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=39391.
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The present studies investigate the molecular mechanisms involved in the nicotinic antagonist-induced up-regulation of $ alpha$-bungarotoxin ($ alpha$-BGT) binding sites in bovine adrenal chromaffin cells in culture. To assess the possibility that cellular depolarization and/or the activation of protein kinase C might be involved in the nicotinic antagonist-induced up-regulation, experiments were carried out in which nicotinic antagonists, K$ sp+$ and/or phorbol esters were added to the cells in various combinations. These latter two treatments resulted in increases in the number of toxin binding sites in these cells. The results of the additivity experiments suggested that at least two distinct mechanisms seem to be involved in the up-regulation of $ alpha$-BGT binding sites. One of these appears to be uniquely induced by nicotinic antagonists such as d-tubocurarine while a second may be mediated via the activation of protein kinase C. The effects of K$ sp+$ seem to be primarily mediated via protein kinase C although its action may also be exerted in part in a manner similar to that of d-tubocurarine.<br>The increase in receptors induced by nicotinic antagonists, K$ sp+$ or phorbol esters was attenuated by an activator of adenylate cyclase, as well as an analog of cAMP, suggesting that the cAMP dependent protein kinase may play a role in regulating the number of toxin receptors. The effects of various Ca$ sp{2+}$ channel agonists and antagonists were also determined; however, these agents had no effect on toxin binding under any condition indicating that the regulation of Ca$ sp{2+}$ influx into the cells is not required for receptor up-regulation.<br>Recent studies had demonstrated that a thymic polypeptide, thymopoietin (Tpo), potently and specifically inhibited $ alpha$-BGT binding. Studies in chromaffin cells in culture showed that Tpo resulted in an up-regulation of toxin binding sites in a manner similar to that of d-tubocurarine. The effect of Tpo was specific for $ alpha$-BGT sites as nicotinic acetylcholine receptor mediated events were not altered by Tpo.<br>In conclusion, neuronal nicotinic $ alpha$-BGT receptors in chromaffin cells in culture are regulated by a variety of agents, an observation which suggests that these sites may play a role in this tissue. The results of the studies with Tpo indicate that this polypeptide may represent an endogenous ligand for the nicotinic $ alpha$-BGT receptor.
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Samasilp, Prattana. "MOLECULAR CONTROL OF FUSION PORE EXPANSION IN MOUSE ADRENAL CHROMAFFIN CELLS." Case Western Reserve University School of Graduate Studies / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=case1396426579.
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Wenger, Bryan W. "Expression of multiple populations of nicotinic acetylcholine receptors in bovine adrenal chromaffin cells." Connect to this title online, 2003. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1070496780.
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Thesis (Ph. D.)--Ohio State University, 2003.<br>Title from first page of PDF file. Document formatted into pages; contains xii, 120 p.; also includes graphics. Includes bibliographical references (p. 110-120).
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Dumpala, Bindya. "Design, construction, optimization, and characterization of a temperature control system for studying the effects of a rapid and reversible changes in temperature on neurosecretion." abstract and full text PDF (free order & download UNR users only), 2006. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:1438916.
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Villanueva, Melissa Wightman R. Mark. "Electrochemical detection of modulation of exocytosis from chromaffin cells monitored with amperometry." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2006. http://dc.lib.unc.edu/u?/etd,378.
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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2006.<br>Title from electronic title page (viewed Oct. 10, 2007). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Chemistry." Discipline: Chemistry; Department/School: Chemistry.
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Drake, Julie. "Effect of Choline on Ca2+ -activated K+ channels in bovine chromaffin cells." Thesis, McGill University, 1990. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=60447.
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The actions of internal choline on single "maxi" Ca$ sp{2+}$-activated K$ sp{+}$ channels were studied in excised patches of chromaffin cell membrane. The channels had a unit conductance of approximately 200 pS in a physiological K$ sp{+}$ gradient.<br>Choline (20-70 mM) applied to the intracellular membrane surface dose dependently reduced outward current flow through the channel. The reduction in single channel current amplitude increased with depolarization.<br>These data suggest that choline is a fast blocker that binds within the channel pore. The K$ sb{ rm d}$(0) for the reaction is 90 mM while $ delta$ is 0.27, suggesting that the choline binding site senses 27% of the transmembrane electric field.<br>The average open state probability appeared not to be affected by choline at any of the membrane potentials that were studied.
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Roth, Dagmar. "The role of proteins in regulated exocytosis from bovine adrenal chromaffin cells." Thesis, University of Liverpool, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284252.
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Jonsson, Anna. "Reference interval for urinary catecholamines and methylated catecholamines analysed using HPLC." Thesis, Uppsala universitet, Institutionen för medicinsk biokemi och mikrobiologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-180252.
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Catecholamines are stress hormones that are produced and released by a rare tumor called pheochromocytoma. This tumor can cause hypertension which if undiagnosed and untreated leads to death. Since good therapy is available, it is important to find the tumor in time. The most common way to diagnose the tumor is measurement of the biochemical markers; catecholamines and their metabolites, methylated catecholamines. After observation that almost all normetanephrine results for women were higher than the upper reference limit and therefore pathological, the accuracy of the present reference intervals was questioned. Therefore new reference intervals for both urinary catecholamines and methylated catecholamines were developed by analysis of 46 samples using HPLC. Creatinine was analysed in acidified urine in order to see if the results became the same as when analysed in non-acidified urine. Urinary catecholamines and methylated catecholamines were analysed using HPLC. Comparison between measurement of creatinine in acidified urine and non-acidified urine with an enzymatic method was performed using Architect ci 8200, Abbott. As suspected, there was a difference between the present and new intervals. Therefore the new intervals will be used for future diagnosis. There was no difference between the two treatments of creatinine samples wherefore it can be measured in both.In conclusion reference intervals determind in this study will be used and it was shown that creatinine can be measured in acidified urine.
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Yoon, Jihwan. "Non-thermal effects of pulsed-microwave fields on catecholamine release from chromaffin cells exposure system design and characterization and experimental data /." abstract, 2008. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3339154.
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Al-Rasheed, Nouf. "Receptor-mediated catecholamine release from chromaffin cells : the role of protein kinase C." Thesis, University of Leicester, 2006. http://hdl.handle.net/2381/29950.
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This study reveals that bovine chromaffin cells express PKC-alpha, -beta, -epsilon and -iota and that they were differentially activated by nicotine receptors and a range of Gaq/11-coupled GPCRs. Thus, nicotinic receptor stimulation recruited PKC-alpha, -beta and -epsilon from the cytoplasm to the plasma membrane, indicative of activation. In contrast, activation of Gaq/11-coupled receptors with histamine activated all the expressed PKC isoforms and angiotensin II only activated PKC-alpha and -epsilon.;Inhibition of PKC using general or isoform-selective inhibitors potentiated catecholamine release in response to activation of Gaq/11-coupled receptors, most likely as consequence of potentiated phospholipase C-mediated signalling. However, inhibition of PKC, particularly PKCalpha, markedly inhibited nicotinic receptor-mediated catecholamine release. PKCalpha is a classical isoform of PKC, activated by Ca2+ and diacylglycerol (DAG).;The current study suggests that Ca2+ influx across the plasma membrane in response to nicotinic receptor activation is largely through the nicotinic receptors themselves. Furthermore, this Ca2+ entry activates PLC, generating both Ins(1,4,5)P3 and DAG. This activation of PLC contributes significantly to the activation of PKC. The mechanism through which PKC facilitates the release of catecholamines requires the PKC-dependent phosphorylation of myristoylated alanine-rich C protein kinase substrate (MARCKS), the subsequent disassembly of the cortical F-actin cytoskeleton and probably therefore, increased access of a reserve exocytotic vesicle pool to release sites at the plasma membrane. Moreover, this study also suggests that PLC-dependent generation of DAG recruits Munc13-1, a known vesicle priming agent. Thus, activation of Munc13-1 may also contribute to nicotinic receptor-mediated catecholamine release in a manner dependent on the activation of PLC.
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Wykes, Robert C. E. "Calmodulin regulation of calcium channels and neurotransmitter release in bovine adrenal chromaffin cells." Thesis, University of Leicester, 2004. http://hdl.handle.net/2381/29943.
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Calmodulin is a molecule implicated in regulating voltage-gated calcium channels (VGCCs) and the exocytotic machinery to fine tune neurotransmitter release. I have investigated the role this molecule plays in stimulus-secretion coupling in bovine adrenal chromaffin cells by over-expressing either wild-type (CaMwt), or a mutated calmodulin (CaM1234), rendered incapable of binding calcium by adenoviral infection. Stimulus-evoked secretion was monitored by combined measurements of membrane capacitance (DeltaC m) and voltage-clamp recording of calcium currents in single cells. Cells were clamped in either the perforated patch or whole-cell configuration and calcium-dependent exocytosis evoked by single depolarising voltage steps or trains of depolarisations. I show that the exocytotic efficiency, derived by dividing DeltaCm by the intergral of the calcium current, is reduced for N-type channels compared to P/Q-type channels. Cation substitution experiments revealed that pharmacologically isolated N-type channels displayed the most profound sensitivity to calcium-dependent inactivation. Studies aimed at eluding the molecular mechanisms underlying calcium-dependent inactivation show that inhibiting calcinuerin by 20 mins preincubation with 1muM cyclosporine A or by introducing 30muM calmodulin inhibitory peptides through the patch pipette did not significantly reduce the level of whole cell calcium-dependent inactivation. In contrast, adenoviral mediated expression of a mutant calmodulin deficient in calcium binding resulted in a highly significant reduction in N-type, but not P/Q-type channel inactivation. This is the first time that calmodulin has been shown to regulate endogenously expressed N-type calcium channels. These results are consistent with calmodulin acting directly to control N-type channel inactivation and therefore limit this channel's ability to couple to exocytosis during prolonged stimulation. Ca2+/calmodulin was also found to interact with the secretory machinery. Expression of CaM 1234 significantly reduced the exocytotic efficiency of brief depolarisations (≤ 100ms), however, the exocytotic efficiency to longer depolarisations (≥ 200ms) was not significantly different between cells expressing CaM 1234 and CaMwt. This suggests that Ca2+ -Calmodulin is required for filling and/or release from a rapidly releasable pool of vesicles which is easily depleted, but not from the slowly releasable pool which dominates exocytotic responses measured with prolonged responses.
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Dry, Katherine L. "Catecholamine release from isolated chromaffin cells under conditions of anoxia or metabolic inhibition." Thesis, University of Edinburgh, 1990. http://hdl.handle.net/1842/18845.
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A significant release of catecholamines within the heart has been observed during myocardial ischaemia. Ischaemia-induced catecholamine release can be markedly inhibited by desipramine and other amine uptake blocking agents, allowing investigation of the importance of such release for arrhythmia production. The mechanism of this release appears to occur by a carrier-mediated efflux from neurones, which is not operative under normal conditions. The aim of the project has been to study this release process in chromaffin cells isolated from the bovine adrenal medulla, which are recognised as a model system for studying the sympathetic nervous system. Understanding this process of catecholamine release may lead to new methods of protecting the heart against ischaemia-induced arrhythmias. Isolated chromaffin cells could be maintained in primary culture for up to 7 days and retained all their normal secretory responses. Conditions designed to mimic ischaemia, that is, anoxia or metabolic inhibition, resulted in a significant release of catecholamines. This release was shown to be independent of extracellular calcium but, in contrast to the release observed in ischaemic hearts, it was not inhibited by uptake<SUB>1</SUB> blockers. One of the main criteria for exocytosis is the co-release of other secretory granule components. Polyacrylamide gel electrophoresis and Western blotting techniques were utilised to examine this following metabolic inhbition. Significant levels of the granule proteins chromogranin A, neuropeptide Y and ATP were measured following metabolic inhibition, indicative of an exocytotic mechanism. Furthermore, there was no release of the cytosolic protein lactate dehydrogenase, indicating that there was no breakdown of the cell membrane during metabolic inhibition. Over the first 10 minutes of metabolic inhibition there was a marked uptake of <SUP>22</SUP>Na<SUP>+</SUP> by the cells. It is suggested that this Na<SUP>+</SUP> influx triggers the catecholamine release by affecting the cytosolic Ca<SUP>2+</SUP> concentration through a direct effect on intracellular stores. Intracellular Ca<SUP>2+</SUP> mobilisation was measured using the calcium-sensitive fluorescent probe Fura-2. It was found that cytosolic free calcium levels were increased in response to metabolic inhibition. The conditions requird to evoke carrier-mediated efflux were also examined. Cytosolic levels of catecholarmines could be artificially raised following treatment with reserpine. Cytoplasmic catecholamine levels were measured following permeabilisation with the detergent digitonin which renders the plasma membrane leaky. Conditions designed to reverse the uptake carrier and cause carier-mediated efflux in the presence of raised cytoplasmic catecholamines such as removal of extracellular sodium, did not evoke any catecholamine overflow. These studies suggest the chromaffin cell uptake<SUB>1</SUB> carrier is not reversible and may be gated in some way. This work has, therefore, raised questions concerning the suitability of chromaffin cells as a conventional model for sympathetic nerve terminals.
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Wenger, Bryan William. "Expression of multiple populations of nicotinic acetylcholine receptors in bovine adrenal chromaffin cells." The Ohio State University, 2003. http://rave.ohiolink.edu/etdc/view?acc_num=osu1070496780.
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Förander, Petter. "On the actions of neurotrophic factors on the chromaffin cells of the adrenal medulla /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4145-9/.
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Joshi, Atul. "A possible link between calmodulin and calcium-activated potassium channels in bovine chromaffin cells /." Thesis, McGill University, 1989. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=55663.
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Milman, Alexandre. "Contribution à l'étude du rôle physiologique du canal de fuite sodique NALCN dans les cellules excitables : approche sur cellules chromaffines de souris." Thesis, Montpellier, 2018. http://www.theses.fr/2018MONTT060.
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Les cellules chromaffines des glandes surrénales sont des cellules neuroendocrines excitables impliquées dans la sécrétion de catécholamines. En réponse à un stress, ces hormones, parmi les premières à être libérées exercent de multiples actions sur leurs organes-cibles, contribuant à la réponse adaptive de l'organisme. Ainsi, élucider la physiopathologie du stress est un enjeu de santé publique et mieux connaître les mécanismes permettant au tissu médullosurrénalien d'optimiser la sécrétion de catécholamines aux besoins de l'organisme est un défi à relever.La sécrétion des catécholamines est liée à l'activité électrique des cellules chromaffines et élucider les mécanismes cellulaires qui en contrôlent l'excitabilité est d'intérêt. L'activité électrique de ces cellules est régulée par le nerf splanchnique ainsi que par des conductances ioniques intrinsèques. Dans ce contexte, les conductances opérant autour du potentiel de repos jouent un rôle majeur dans le déclenchement des potentiels d'action. C'est en particulier le cas du canal NALCN (sodium leak channel), récemment décrit comme régulant le potentiel de repos des neurones. C'est pourquoi nous avons orienté nos travaux vers la caractérisation du rôle de NALCN dans l'excitabilité des cellules chromaffines, dans des tranches de glandes surrénales de souris. L'enregistrement du potentiel de membrane révèle qu'environ 62% des cellules chromaffines présentent des potentiels d'action spontanés et que le profil de décharge suit un mode régulier ou un mode en bouffées. Des enregistrements plus longs révèlent qu'une même cellule présente alternativement ces 2 modes de décharge. Un changement de potentiel de quelques mV autour du potentiel de repos favorise un mode, indiquant que les courants ioniques actifs autour du potentiel de repos sont des composantes cruciales de l'excitabilité cellulaire. NALCN est-il un de ces courants?Pour commencer, nous avons observé, par hybridation in situ, la présence du transcrit codant NALCN dans les cellules chromaffines chez la souris (coll Dr. Ventéo, INM, Montpellier). Nous avons alors cherché à déterminer si NALCN est impliqué dans l'activité électrique des cellules chromaffines. Nous avons utilisé un protocole de diminution de la concentration extracellulaire de Na+, classiquement utilisé pour l'étude électrophysiologique de NALCN. La diminution du Na+ extracellulaire induit une hyperpolarisation et un arrêt des potentiels d'action. Cet effet n'est pas bloqué par la TTX. En potentiel imposé, la diminution du Na+ réduit le courant de maintien, elle n'est ni bloquée par la TTX ni par le Cs+. La courbe courant/potentiel du courant sensible à la réduction du Na+ révèle un courant linéaire entre -130 et -50 mV et un potentiel d'inversion en accord avec la contribution de plusieurs espèces ioniques. Ce courant présente une perméabilité majeure au Na+ vs K+. Ainsi, ces résultats décrivent une conductance ionique partageant des propriétés biophysiques et pharmacologiques similaires à celles de NALCN.Afin de poursuivre dans cette direction, nous avons initié des travaux ambitieux visant à éteindre l'expression du gène codant NALCN dans les cellules chromaffines, au travers d'une stratégie d'injection de virus in vivo. Une construction codant pour un shRNA dirigé contre NALCN, a été injectée dans la glande surrénale gauche. Les résultats sont très encourageants, montrant i) la présence, dans les glandes injectées, de cellules chromaffines transduites et ii) une diminution significative de l'expression de NALCN dans les glandes injectées avec le ShRNA-anti NALCN. Cette approche de transduction virale mérite d'être poursuivie.En conclusion, et même si les résultats actuels ne permettent pas d'affirmer avec certitude que NALCN contribue à l'excitabilité des cellules chromaffines, ce travail de thèse apporte néanmoins une contribution majeure à l'étude de l'excitabilité de ces cellules et ouvre des perspectives attractives quant au rôle de NALCN<br>Adrenal chromaffin cells are excitable neuroendocrine cells involved in the secretion of catecholamines. Once delivered into the blood circulation, these hormones exert multiple actions, leading to physiological adjustments enabling the organism to cope with stress. Deciphering the physiology/pathology of stress is a major public health issue, especially in the field of the mechanisms that lead to optimal catecholamine secretion.The electrical activity of chromaffin cells critically shapes the catecholamine secretory pattern. Elucidating the mechanisms regulating the firing discharge is therefore of interest. In situ, chromaffin cell excitability is regulated by both the splanchnic nerve inputs and the intrinsic ion conductances expressed in cells. Regarding this, the conductances operating near the resting membrane potential are crucial in the cell competence to spontaneously fire. In particular, the background current flowing through the sodium leak channel NALCN has been recently reported to tune the resting potential of neuronal cells. This finding prompted us to investigate the possible contribution of NALCN to chromaffin cell excitability in mouse acute adrenal slices. The first part of my thesis was aimed at investigating chromaffin cell electrical firing pattern. Whole-cell recordings indicate that about 62% of mouse chromaffin cell spontaneously fire and exhibit two discharge patterns, a regular firing mode and a bursting mode. Long-lasting recordings of spontaneous electrical activity reveal that the two firing modes can occur in the same cells. When the membrane potential is challenged around the resting value, the firing pattern alternate between the two modes, indicating that currents operating around the resting membrane potential are key components in regulating cell excitability. Is NALN one of these currents?To answer this question, we first unveiled, by in situ hybridization, the presence of the transcript encoding NALCN in mouse chromaffin cells (coll with Dr. Ventéo, INM, Montpellier). Second, we performed electrophysiological experiments using protocols and pharmacological agents commonly used to study NALCN currents. Decreasing external NaCl leads to a robust membrane hyperpolarization, abrogating action potentials. This effect is not blocked by TTX. In voltage-clamp conditions, external Na+ reduction leads to a decrease in the holding current. This effect is not blocked by Cs+. Depolarizing voltage ramps unveil that the current blocked by lowering external Na+ blocks is linear between -130 and -50 mV, and displays a reversal potential arguing for a non-selective conductance. The ionic permeability is dominant for Na+ over K+. Collectively, our results describe a voltage-independent and non-selective cationic conductance operating near the resting potential of mouse chromaffin cells. Its electrophysiological and pharmacological properties recapitulate two NALCN attributes.In the third part, we developed an ambitious approach aiming at silencing NALCN expression specifically in chromaffin cells in vivo. Viral vectors encoding anti-NALCN shRNA under the control of the tyrosine hydroxylase promoter, as well as appropriate positive and negative viral constructs, were injected in the left gland. As promising results, transduced cells were detected in the injected glands only and a significant decrease in NALCN expression was observed in glands injected with the anti-NALCN shRNA. As such, the data collected from in vivo manipulation of NALCN expression are encouraging and this approach deserves to be pursued.This thesis describes a Na+-sensitive current operating near the resting membrane potential of mouse chromaffin cells, sharing biophysical and pharmacological properties with NALCN. Even though further experiments are needed to ascertain that NALCN supports this conductance, our work contributes to a better knowledge of chromaffin cell excitability
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Karaplis, Andy C. "The role of prostaglandin E2 and other eicosanoids in catecholamine secretion from adrenal chromaffin cells /." Thesis, McGill University, 1987. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=75418.
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Prostaglandins E$ sb1$ and E$ sb1$ are bound with high affinity and specificity to particulate fractions from bovine, ovine and human adrenal medulla. An identical fraction from fetal bovine and ovine adrenals binds PGEs with similar kinetic properties and specificities. The ${ rm lbrack sp3H rbrack}$PGE$ sb2$-binding site complex dissociates in a biphasic manner, suggesting the presence of both a low and high affinity form of the complex. Gpp(NH)p, a stable GTP analogue, inhibits PGE$ sb2$ binding by promoting the conversion of the high affinity form of the complex to the lower affinity state. In subcellular fractionation studies, PGE$ sb2$ binding sites co-purity with acetylcholinesterase and Ca$ sp{2+}$-ATPase activities (marker enzymes for the chromaffin cell plasma membrane). Bovine adrenal medullary cells in culture, prelabeled with ${ rm lbrack sp3H rbrack}$arachidonic acid, metabolize the precursor fatty acid to PGE$ sb2,$ 6-oxoPGF$ sb{1 alpha}$ and other unidentified products, when stimulated with the calcium-ionophore A23187. PGE$ sb2$ (10$ sp{-9}$ M) inhibits both nicotine and high K$ sp+$-induced catecholamine secretion from chromaffin cells by a mechanism unrelated to alterations in intracellular levels of cyclic nucleotides. LTC$ sb4$ and LTB$ sb4$ stimulate spontaneous catecholamine release but this effect is not always reproducible. NDGA attenuates nicotine-induced secretion, while indomethacin has no effect. These data suggest that the inhibitory effect of PGE$ sp2$ on chromaffin cell secretion is initiated by the release of the prostaglandin during cellular activation, followed by the binding of PGE$ sb2$ to its receptor and the subsequent interaction of this complex with a guanine nucleotide-binding protein.
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Estay, Ahumada Catherine. "Mécanismes moléculaires du couplage exocytose-endocytose dans les cellules neuroendocrines : rôle des protéines Scramblase-1 et Oligophrénine-1." Thesis, Strasbourg, 2016. http://www.theses.fr/2016STRAJ088/document.
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De récentes études ont montré dans les cellules chromaffines que la libération des granules de sécrétion est temporellement et spatialement couplée au processus d’endocytose. Nous avons proposé l’hypothèse que la membrane du granule préserve son intégrité au sein de la membrane plasmique durant l’exocytose avant d’être internalisée ainsi avec ses composants. Cependant, les mécanismes moléculaires de ce processus d’endocytose compensatrice sont encore inconnus. Ainsi, mon projet de thèse vise a répondre à la question suivante : Quels sont les différents mécanismes déclenchant et régulant l’exocytose et l’endocytose compensatrice? Les propriétés physiques des lipides jouent des rôles fondamentaux dans le trafic membranaire. Ils servent de système d’échafaudage pour maintenir la machinerie spécifique à des endroits précis de la membrane plasmique. Par exemple, la formation de microdomaines de gangliosides et de PIP2 au niveau des sites d’exocytose ou encore le mélange de lipides au sein de la bicouche lipidique représentent des processus attractifs pour permettre cette fonction au cours des événements d’exo-endocytose dans les cellules neuroendocrines. De plus, en raison de leur implication importante dans les processus d’exo-endocytose ou dans le remodelage des lipides, l’annexine A2, la synaptotagmine 1, l’oligophrénine1 et la scramblase 1 doivent être considérées comme des signaux potentiels pour le déclenchement de l’endocytose de la membrane granulaire. Au cours de mon doctorat, je me suis intéressée à étudier comment l’exocytose et l’endocytose compensatrice sont régulées par la scramblase1 et l’oligophrénine1 dans les cellules chromaffines de la glande surrénale<br>Recent studies in neuroendocrine chromaffin cells have suggested that the secretory granule release is temporally and spatially coupled to a compensatory endocytic process. Hence, we hypothesized that the secretory granule membrane would preserve its integrity within the plasma membrane after exocytosis before being retrieved as such along with its components. However, the underlying molecular mechanisms of this compensatory endocytic process are largely unknown today. Therefore my thesis project is aiming to address the following specific question: What are the different mechanisms triggering and regulating exocytosis and the compensatory endocytosis? Physical properties of lipids play fundamental roles in membrane trafficking. They act as a scaffolding system to maintain specific machinery at restricted site of the plasma membrane. For example, the formation of ganglioside- and PIP2-enriched microdomains at the exocytic sites or the phospholipid scrambling across the bilayer plasma membrane, represent attractive processes to fulfill this function during exo- endocytosis events in neuroendocrine cells. Moreover, in view to their important implication in exo-endocytotic processes or lipid remodeling, annexin-A2, synaptotagmin- 1, oligophrenin-1 and phospholipid scramblase-1 have to be considered as potential signal-triggers of the granule endocytosis. During my PhD, I focused in investigating how exocytosis and compensatory endocytosis are regulated by PLSCR-1 and OPHN1 in adrenal chrommaffin cells
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Tapechum, Sompol. "Role of Doc2β in regulated exocytosis of large dense-core vesicles in bovine adrenal chromaffin cells". Thesis, University of Edinburgh, 2003. http://hdl.handle.net/1842/27506.
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Bonifas-Arredondo, Imelda. "Amperometric determination of the flux of neurotransmitters released by chromaffin cells : a biological application of microelectrodes." Paris 7, 2004. http://www.theses.fr/2004PA077207.
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Hockman, Dorit. "The development and evolution of vertebrate oxygen-sensing cells." Thesis, University of Cambridge, 2014. https://www.repository.cam.ac.uk/handle/1810/276679.
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Oxygen-sensing cells release neurotransmitters, including serotonin, in response to hypoxia in the blood or surrounding air/water. This stimulates the glossopharyngeal and/or vagal nerves, triggering increased ventilation via the respiratory reflex. In the adult, they are located in the carotid body (glomus cells) and lung epithelia (pulmonary neuroendocrine cells) of amniotes, and in the epithelia of the gills and orobranchial cavity (‘neuroepithelial cells’) of anamniotes. Despite their physiological importance, little is known about the molecular mechanisms of their development, while the evolutionary relationships between the various oxygen-sensing cell types are unknown. The chromaffin cells of the mammalian adrenal medulla are hypoxia-sensitive transiently during neonatal life. Both carotid body glomus cells and adrenal chromaffin cells arise from the neural crest and require the transcription factors Phox2b and Ascl1 for their development. Given these similarities, I aimed to test the hypothesis that the same molecular mechanisms underlie their development. Expression analysis of 13 sympathoadrenal pathway genes throughout chicken carotid body development revealed striking similarities with adrenal chromaffin cell development. Analysis of mouse mutants showed that the transcription factors Hand2, Sox4 and Sox11 are required for carotid body development. In addition, loss of the receptor tyrosine kinase Ret or the transcription factor AP-2β, which significantly affects sympathetic ganglion but not adrenal chromaffin cell development, has no effect on the carotid body. Adrenal chromaffin cells differentiate from neurons that migrate into the adrenal gland from ‘primary’ sympathetic ganglia at the dorsal aorta. Carotid body glomus cells were previously proposed to arise from neuronal “émigrés” from neighbouring ganglia: the superior cervical ganglion in mammals and the nodose ganglion in the chick. However, nodose neurons are considered to be nodose placode-derived. Using electroporation and grafting in the chick, I confirmed that the nodose placode does not contribute to the carotid body, identified a small population of autonomic neural crest-derived neurons in the nodose ganglion, and confirmed the existence of “bridges” of neurons between the nodose ganglion and the carotid body. My data suggest that, like adrenal chromaffin cells, carotid body glomus cells differentiate from autonomic neural crest-derived neurons in nearby ganglia, which migrate into the carotid body primordium and down-regulate neuronal markers. The proposed evolutionary relationship between the carotid body glomus cells and the serotonin-positive neuroepithelial cells of anamniote gills has never been tested. Using vital dye labelling, neural fold grafts, genetic lineage-tracing in zebrafish and analysis of zebrafish mutants lacking all neural crest cells, I found that serotonin-positive cells in the gills and orobranchial epithelia of lamprey (jawless fish), zebrafish (ray-finned bony fish) and frog (anamniote tetrapod) are not neural crest-derived, and hence are not homologous to carotid body glomus cells. Genetic lineage-tracing in mouse and neural fold grafts in chick also confirmed that serotonin-positive neuroendocrine cells in the lung are not neural crest- derived, hence must have an endodermal origin (since the lungs are out-pocketings of the gut). My results suggest that the neuroepithelial cells of anamniotes are not related to carotid body glomus cells, but rather are homologous to the oxygen-sensing cells of the lung. Consistent with this hypothesis, I found that many genes expressed during carotid body development are not expressed by the epithelia of either chick lungs or lamprey gills. Taken together, my data suggest that as air-breathing evolved, gut endoderm- derived cells that originally responded to hypoxia in water were maintained in the lungs to monitor oxygen levels in air, while a population of neural crest-derived chromaffin cells near the pharyngeal arch arteries was recruited to monitor oxygen levels in blood.
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Lopez, Isabel. "Effects of antimitotic agents on cultured adrenal chromaffin cells : implications for microtubule involvement with adrenal nicotinic receptors /." The Ohio State University, 1992. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487776801318513.
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Antypas, Elias Joseph. "The Characterization of Menkes Copper Transporter and Dopamine ß-monooxygenase Carboxy-Terminus in Neuroendocrine Cells." University of Toledo Health Science Campus / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=mco1213789670.
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Jarukanont, Daungruthai [Verfasser]. "Theory of Vesicle Motion and Interpretation of Electrophysiological Experiments in Chromaffin Cells, Hippocampal Neurons and Neuromuscular Junctions / Daungruthai Jarukanont." Kassel : Universitätsbibliothek Kassel, 2018. http://d-nb.info/1163735515/34.
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Mason, Helen Sarah. "The effect of fatty acids on calcium-activated and inwardly-rectifying potassium channel activity in bovine chromaffin and endothelial cells." Thesis, University of Aberdeen, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.245247.
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The effect of a variety of fatty acids was examined on two types of potassium channels in bovine chromaffin (BCC) and bovine aortic endothelial cells (BAEC). Large-conductance calcium-activated potassium channels were recorded from inside-out patches excised from cultured BCC. Fatty acids were applied to the intracellular surface of the patch at a concentration of 10μM. All the fatty acids examined (arachidonic acid (C20:4 <I>n-6</I>), eicosapentaenoic acid (C20:5 <I>n-3</I>), docosahexaenoic acid (C22:6 <I>n-3</I>) and myristic acid (C14:0)) increased the patch open probability at a potential of +40mV. The effect was immediate and reversible. The <I>n-3</I> fatty acids were more effective than either the <I>n-6</I> or saturated fatty acids. Fatty acids shifted the voltage required to half-activate the channel in a hyperpolarising direction. The current-voltage relationship was unaffected. The effect was independent of the intracellular calcium concentration as the same response was observed in a "calcium-free" solution (no added CaCl<sub>2</sub>, 5mM EGTA). The fatty acid-mediated increase in BK channel activity is proposed to provide a negative feedback on exocytosis from bovine chromaffin cells. The effect of fatty acids on the whole-cell current of cultured BAEC was examined. Acute exposure of BAEC to 10μM fatty acids in the presence of 10<sup>-8</sup>M intracellular calcium did not affect the predominant whole-cell current, characterised as an inwardly rectifying potassium current. Arachidonic acid did not affect the whole-cell current whether it was applied to the extra- or intracellular surface of the membrane. Increasing the intracellular calcium concentration to 10<sup>-6</sup>M revealed the presence of an outward calcium-sensitive potassium current. Application of arachidonic acid (10μM) significantly increased the magnitude of this current. The effect was immediate and reversible. The activation of this calcium-sensitive potassium current hyperpolarises the cell, sustaining the influx of calcium and nitric oxide/prostacyclin production.
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Dutta, Soumyajit [Verfasser], and Dieter [Akademischer Betreuer] Bruns. "A pHluorin-based method to monitor exocytosis by release of peptidergic cargo molecules from chromaffin cells / Soumyajit Dutta. Betreuer: Dieter Bruns." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2016. http://d-nb.info/1099282098/34.
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Chen, Xiaohui. "Optical stimulation of quantal exocytosis on transparent microchips." Diss., Columbia, Mo. : University of Missouri-Columbia, 2007. http://hdl.handle.net/10355/4890.
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Thesis (Ph. D.)--University of Missouri-Columbia, 2007.<br>The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on January 30, 2008) Vita. Includes bibliographical references.
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Ramirez-Lavergne, Carmen. "The effect of the second messenger cyclic AMP on scinderin redistribution, F-actin disassembly and catecholamine secretion in bovine adrenal chromaffin cells." Thesis, University of Ottawa (Canada), 1994. http://hdl.handle.net/10393/10241.
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Work in our laboratory has demonstrated that stimulation of bovine chromaffin cells with nicotine elicits as a prelude to exocytosis, (a) redistribution of scinderin (Sc), a novel 80 kD Ca$\sp{2+}$-dependent actin filament severing protein and (b) cortical F-actin disassembly. The work presented in this thesis shows that the second messenger, cyclic AMP (cAMP) modulates Sc redistribution, F-actin disassembly and catecholamine (CA) secretion. Here we show that forskolin (F) produces a concentration-related (10 $\mu$M-50$\mu$M) inhibition of Sc redistribution, F-actin disassembly and CA release in response to 10 $\mu$M nicotine. F also induces a concentration-dependent (10 $\mu$M-50 $\mu$M) increase in cAMP levels. Increasing intracellular cAMP with 50 $\mu$M F or incubation with the F analogs 6-acetyl-7-deacetylforskolin or deacetylforskolin (100 $\mu$M) as well as the cAMP membrane permeant analog, 8-Bromo cAMP (2.5mM) for 40 s also inhibits Sc redistribution, F-actin disassembly and CA secretion. The inhibitory effect of F on nicotine-induced Sc redistribution and F-actin disassembly is observed even upon 5 s of incubation while inhibition of CA secretion cannot be detected until 20 s of incubation with F. These effects are accompanied by an increase in cAMP. The discrepancy in timing between inhibition of both Sc redistribution and F-actin disassembly in relation to CA secretion may be explained by the fact that Sc redistribution and F-actin disassembly seem to occur simultaneously and to precede secretion. Although work on cAMP by others has yielded conflicting results, our findings suggest that cAMP may play a role in modulating cytoskeleton dynamics during secretion. This also implies that this second messenger can attenuate the secretory response either by preventing disassembly of F-actin or activation of Sc thus, denying the secretory vesicles access to exocytotic sites. Alternatively, the observed effects may represent a modulation of nicotinic receptor activity by cAMP.
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Maurer, Jennifer A. "Effects of protein kinase inhibitors on cultured bovine adrenal chromaffin cells: evidence for the role of protein phosphorylation reactions in calcium homeostasis /." The Ohio State University, 1994. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487853913101481.
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Dembla, Ekta Mayur [Verfasser], and Ute [Akademischer Betreuer] Becherer. "Biogenesis of large dense core vesicles and molecular mechanisms of dead-end docking in mouse chromaffin cells / Ekta Mayur Dembla ; Betreuer: Ute Becherer." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2017. http://d-nb.info/1182312969/34.
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Gu, Hyangja. "The effects of antimitotic drugs and mAb35 on ?-tubulin mRNA, microtubules and nicotinic receptor-mediated catecholamine secretion in adrenal chromaffin cells in culture /." The Ohio State University, 1992. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487759914759158.
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