Добірка наукової літератури з теми "Tachykinins"

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Статті в журналах з теми "Tachykinins":

1
Maggio, J. E. "Tachykinins." Annual Review of Neuroscience 11, no. 1 (March 1988): 13–28. http://dx.doi.org/10.1146/annurev.ne.11.030188.000305.
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2
Hanley, Michael R. "Mixed tachykinins." Nature 320, no. 6057 (March 1986): 26. http://dx.doi.org/10.1038/320026a0.
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3
CULMAN, JURAJ, KEIICHI ITOI, and THOMAS UNGER. "Hypothalamic Tachykinins." Annals of the New York Academy of Sciences 771, 1 Stress (December 1995): 204–18. http://dx.doi.org/10.1111/j.1749-6632.1995.tb44682.x.
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4
Liu, Katherine, Marianne D. Castillo, Raghav G. Murthy, Nitixa Patel, and Pranela Rameshwar. "Tachykinins and Hematopoiesis." Clinica Chimica Acta 385, no. 1-2 (October 2007): 28–34. http://dx.doi.org/10.1016/j.cca.2007.07.008.
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5
Bunnett, N. "Tachykinins 2005 Meeting." Vascular Pharmacology 45, no. 4 (October 2006): 199. http://dx.doi.org/10.1016/j.vph.2006.06.013.
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6
Lagente, V., and C. Advenier. "Tachykinins and Airway Function." Pulmonary Pharmacology & Therapeutics 11, no. 5-6 (October 1998): 331–40. http://dx.doi.org/10.1006/pupt.1999.0162.
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7
Holzer, P., S. Löffler, H. Kilbinger, and C. A. Maggi. "Tachykinins and intestinal motility." Neuropeptides 26 (April 1994): 55. http://dx.doi.org/10.1016/0143-4179(94)90275-5.
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8
Lavielle, S., G. Chassaing, D. Loeuillet, P. Robilliard, A. Marquet, J. Viret, J.-C. Beaujouan, et al. "Selective agonists of tachykinins." Regulatory Peptides 22, no. 1-2 (July 1988): 108. http://dx.doi.org/10.1016/0167-0115(88)90328-x.
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9
Khawaja, Aamir M., and Duncan F. Rogers. "Tachykinins: receptor to effector." International Journal of Biochemistry & Cell Biology 28, no. 7 (July 1996): 721–38. http://dx.doi.org/10.1016/1357-2725(96)00017-9.
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10
Hauser, K. L. "Tachykinins and neurological diseases." Acta Neurologica Scandinavica 79, no. 3 (March 1989): 268. http://dx.doi.org/10.1111/j.1600-0404.1989.tb03780.x.
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Дисертації з теми "Tachykinins":

1
Chambers, J. K. "Molecular forms of tachykinins." Electronic Thesis or Dissertation, University of Cambridge, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334079.
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2
Bell, Nicola Jane. "Peripheral tachykinins and tachykinin receptors." Electronic Thesis or Dissertation, University of Reading, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.428305.
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3
Patak, Eva Nicole. "Modulation of mammalian uterine contractility by tachykinins." Monash University, Dept. of Pharmacology, 2003. http://arrow.monash.edu.au/hdl/1959.1/9501.
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4
Kaiser, William Joseph. "Peripheral tachykinins in platelets, plasma & endocrine tissues." Electronic Thesis or Dissertation, University of Reading, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.542266.
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5
Makeham, John Murray. "Functional neuroanatomy of tachykinins in brainstem autonomic regulation." University of Sydney, 1997. http://hdl.handle.net/2123/1960.
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Анотація:
Doctor of Philosophy (PhD)
Little is known about the role that tachykinins, such as substance P and its receptor, the neurokinin-1 receptor, play in the generation of sympathetic nerve activity and the integration within the ventrolateral medulla (VLM) of many vital autonomic reflexes such as the baroreflex, chemoreflex, somato-sympathetic reflex, and the regulation of cerebral blood flow. The studies described in this thesis investigate these autonomic functions and the role of tachykinins through physiological (response to hypercapnoea, chapter 3), anatomical (neurokinin-1 receptor immunohistochemistry, chapter 4) and microinjection (neurokinin-1 receptor activation and blockade, chapters 5 and 6) experiments. In the first series of experiments (chapter 3) the effects of chemoreceptor activation with hyperoxic hypercapnoea (5%, 10% or 15% CO2 in O2) on splanchnic sympathetic nerve activity and sympathetic reflexes such as the baroreflex and somato-sympathetic reflex were examined in anaesthetized rats. Hypercapnoea resulted in sympatho-excitation in all groups and a small increase in arterial blood pressure in the 10 % CO2 group. Phrenic nerve amplitude and phrenic frequency were also increased, with the frequency adapting back to baseline during the CO2 exposure. Hypercapnoea selectively attenuated (5% CO2) or abolished (10% and 15% CO2) the somato-sympathetic reflex while leaving the baroreflex unaffected. This selective inhibition of the somato-sympathetic reflex while leaving the baroreflex unaffected was also seen following neurokinin-1 receptor activation in the rostral ventrolateral medulla (RVLM) (see below). Microinjection of substance P analogues into the RVLM results in a pressor response, however the anatomical basis for this response is unknown. In the second series of experiments (chapter 4), the distribution of the neurokinin-1 receptor in the RVLM was investigated in relation to catecholaminergic (putative sympatho-excitatory “C1”) and bulbospinal neurons. The neurokinin-1 receptor was demonstrated on a small percentage (5.3%) of C1 neurons, and a small percentage (4.7%) of RVLM C1 neurons also receive close appositions from neurokinin-1 receptor immunoreactive terminals. This provides a mechanism for the pressor response seen with RVLM microinjection of substance P analogues. Neurokinin-1 receptor immunoreactivity was also seen a region overlapping the preBötzinger complex (the putative respiratory rhythm generation region), however at this level a large percentage of these neurons are bulbospinal, contradicting previous work suggesting that the neurokinin-1 receptor is an exclusive anatomical marker for the propriobulbar rhythm generating neurons of the preBötzinger complex. The third series of experiments (chapter 5) investigated the effects of neurokinin-1 receptor activation and blockade in the RVLM on splanchnic sympathetic nerve activity, arterial blood pressure, and autonomic reflexes such as the baroreflex, somato-sympathetic reflex, and sympathetic chemoreflex. Activation of RVLM neurokinin-1 receptors resulted in sympatho-excitation, a pressor response, and abolition of phrenic nerve activity, all of which were blocked by RVLM pre-treatment with a neurokinin-1 receptor antagonist. As seen with hypercapnoea, RVLM neurokinin-1 receptor activation significantly attenuated the somato-sympathetic reflex but did not affect the sympathetic baroreflex. Further, blockade of RVLM neurokinin-1 receptors significantly attenuated the sympathetic chemoreflex, suggesting a role for RVLM substance P release in this pathway. The fourth series of experiments (chapter 6) investigated the role of neurokinin-1 receptors in the RVLM, caudal ventrolateral medulla (CVLM), and nucleus tractus solitarius (NTS) on regional cerebral blood flow (rCBF) and tail blood flow (TBF). Activation of RVLM neurokinin-1 receptors increased rCBF associated with a decrease in cerebral vascular resistance (CVR). Activation of CVLM neurokinin-1 receptors decreased rCBF, however no change in CVR was seen. In the NTS, activation of neurokinin-1 receptors resulted in a biphasic response in both arterial blood pressure and rCBF, but no significant change in CVR. These findings suggest that in the RVLM substance P and the neurokinin-1 receptor play a role in the regulation of cerebral blood flow, and that changes in rCBF evoked in the CVLM and NTS are most likely secondary to changes in arterial blood pressure. Substance P and neurokinin-1 receptors in the RVLM, CVLM and NTS do not appear to play a role in the brainstem regulation of tail blood flow. In the final chapter (chapter 7), a model is proposed for the role of tachykinins in the brainstem integration of the sympathetic baroreflex, sympathetic chemoreflex, cerebral vascular tone, and the sympatho-excitation seen following hypercapnoea. A further model for the somato-sympathetic reflex is proposed, providing a mechanism for the selective inhibition of this reflex seen with hypercapnoea (chapter 3) and RVLM neurokinin-1 receptor activation (chapter 5). In summary, the ventral medulla is essential for the generation of basal sympathetic tone and the integration of many vital autonomic reflexes such as the baroreflex, chemoreflex, somato-sympathetic reflex, and the regulation of cerebral blood flow. The tachykinin substance P, and its receptor, the neurokinin-1 receptor, have a role to play in many of these vital autonomic functions. This role is predominantly neuromodulatory.
6
Makeham, John Murray. "Functional neuroanatomy of tachykinins in brainstem autonomic regulation." University of Sydney, 1997. http://hdl.handle.net/2123/1960.
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Анотація:
Doctor of Philosophy (PhD)
Little is known about the role that tachykinins, such as substance P and its receptor, the neurokinin-1 receptor, play in the generation of sympathetic nerve activity and the integration within the ventrolateral medulla (VLM) of many vital autonomic reflexes such as the baroreflex, chemoreflex, somato-sympathetic reflex, and the regulation of cerebral blood flow. The studies described in this thesis investigate these autonomic functions and the role of tachykinins through physiological (response to hypercapnoea, chapter 3), anatomical (neurokinin-1 receptor immunohistochemistry, chapter 4) and microinjection (neurokinin-1 receptor activation and blockade, chapters 5 and 6) experiments. In the first series of experiments (chapter 3) the effects of chemoreceptor activation with hyperoxic hypercapnoea (5%, 10% or 15% CO2 in O2) on splanchnic sympathetic nerve activity and sympathetic reflexes such as the baroreflex and somato-sympathetic reflex were examined in anaesthetized rats. Hypercapnoea resulted in sympatho-excitation in all groups and a small increase in arterial blood pressure in the 10 % CO2 group. Phrenic nerve amplitude and phrenic frequency were also increased, with the frequency adapting back to baseline during the CO2 exposure. Hypercapnoea selectively attenuated (5% CO2) or abolished (10% and 15% CO2) the somato-sympathetic reflex while leaving the baroreflex unaffected. This selective inhibition of the somato-sympathetic reflex while leaving the baroreflex unaffected was also seen following neurokinin-1 receptor activation in the rostral ventrolateral medulla (RVLM) (see below). Microinjection of substance P analogues into the RVLM results in a pressor response, however the anatomical basis for this response is unknown. In the second series of experiments (chapter 4), the distribution of the neurokinin-1 receptor in the RVLM was investigated in relation to catecholaminergic (putative sympatho-excitatory “C1”) and bulbospinal neurons. The neurokinin-1 receptor was demonstrated on a small percentage (5.3%) of C1 neurons, and a small percentage (4.7%) of RVLM C1 neurons also receive close appositions from neurokinin-1 receptor immunoreactive terminals. This provides a mechanism for the pressor response seen with RVLM microinjection of substance P analogues. Neurokinin-1 receptor immunoreactivity was also seen a region overlapping the preBötzinger complex (the putative respiratory rhythm generation region), however at this level a large percentage of these neurons are bulbospinal, contradicting previous work suggesting that the neurokinin-1 receptor is an exclusive anatomical marker for the propriobulbar rhythm generating neurons of the preBötzinger complex. The third series of experiments (chapter 5) investigated the effects of neurokinin-1 receptor activation and blockade in the RVLM on splanchnic sympathetic nerve activity, arterial blood pressure, and autonomic reflexes such as the baroreflex, somato-sympathetic reflex, and sympathetic chemoreflex. Activation of RVLM neurokinin-1 receptors resulted in sympatho-excitation, a pressor response, and abolition of phrenic nerve activity, all of which were blocked by RVLM pre-treatment with a neurokinin-1 receptor antagonist. As seen with hypercapnoea, RVLM neurokinin-1 receptor activation significantly attenuated the somato-sympathetic reflex but did not affect the sympathetic baroreflex. Further, blockade of RVLM neurokinin-1 receptors significantly attenuated the sympathetic chemoreflex, suggesting a role for RVLM substance P release in this pathway. The fourth series of experiments (chapter 6) investigated the role of neurokinin-1 receptors in the RVLM, caudal ventrolateral medulla (CVLM), and nucleus tractus solitarius (NTS) on regional cerebral blood flow (rCBF) and tail blood flow (TBF). Activation of RVLM neurokinin-1 receptors increased rCBF associated with a decrease in cerebral vascular resistance (CVR). Activation of CVLM neurokinin-1 receptors decreased rCBF, however no change in CVR was seen. In the NTS, activation of neurokinin-1 receptors resulted in a biphasic response in both arterial blood pressure and rCBF, but no significant change in CVR. These findings suggest that in the RVLM substance P and the neurokinin-1 receptor play a role in the regulation of cerebral blood flow, and that changes in rCBF evoked in the CVLM and NTS are most likely secondary to changes in arterial blood pressure. Substance P and neurokinin-1 receptors in the RVLM, CVLM and NTS do not appear to play a role in the brainstem regulation of tail blood flow. In the final chapter (chapter 7), a model is proposed for the role of tachykinins in the brainstem integration of the sympathetic baroreflex, sympathetic chemoreflex, cerebral vascular tone, and the sympatho-excitation seen following hypercapnoea. A further model for the somato-sympathetic reflex is proposed, providing a mechanism for the selective inhibition of this reflex seen with hypercapnoea (chapter 3) and RVLM neurokinin-1 receptor activation (chapter 5). In summary, the ventral medulla is essential for the generation of basal sympathetic tone and the integration of many vital autonomic reflexes such as the baroreflex, chemoreflex, somato-sympathetic reflex, and the regulation of cerebral blood flow. The tachykinin substance P, and its receptor, the neurokinin-1 receptor, have a role to play in many of these vital autonomic functions. This role is predominantly neuromodulatory.
7
Jones, Sarah. "Peripheral tachykinins and the NK1 receptor regulate platelet function." Electronic Thesis or Dissertation, University of Reading, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493813.
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Tachykinins are a family of neuropeptides characterised by the conserved C-terminal motif FXGLM-NH2, where X represents a hydrophobic amino acid. Substance P (SP) a member of the tachykinin family has recently been shown to stimulate platelet aggregation and a SP-like immunoreactivity has been demonstrated in platelets and shown to be released upon platelet activation, suggesting that SP may act as a secondary platelet agonist. In recent years a gene encoding new members of the tachykinin family has been identified named TTAC4, which unlike the classical tachykinins is predominantly expressed in the periphery, with high expression in the megakaryocytic cell line HEL. The predicted products of the human TAC4 gene, endokinins A and B share high homology with SP and display similar binding characteristics as SP for the neurokinin-1 (NKl) receptor, which is present on the platelet surface. The high sequence homology between endokinins A and B and SP renders them indistinguishable using SP-imunoassays raising the possibility that platelets may be a source of endokinins. The purpose of this study was to assess the roles of peripheral tachykinins in regulating platelet function.
8
Norris, Sarah K. "Electrophysiological studies of tachykinins in the rat medial habenula nucleus." Electronic Thesis or Dissertation, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.319545.
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9
Graham, Gwenda Joanne. "The role of tachykinins in the regulation of platelet function." Electronic Thesis or Dissertation, University of Reading, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408330.
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10
McLaughlin, Lynn. "The role of tachykinins in depression, mood disorders and epilepsy." Electronic Thesis or Dissertation, University of Liverpool, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.632136.
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Transgenic and knockout mouse models of disease and gene function have revolutionised the field of biomedical research and the targeted mutations of genes expressed in the brain are revealing the mechanisms underlying normal behaviour and behavioural abnormalities which has led to the development of behavioural neuroscience. However, it is also clear that the phenomena know as "redundancy" can limit the effectiveness of traditional knockout models by the effects of compensatory mechanisms. This thesis utilises transgenic and knockout mouse models to explore the role of the tachykinins in the pathogenesis of anxiety, depression and epilepsy focusing on the TACl gene products and their functionality via the TACRl (NKl) receptor. The generation of a novel double knockout line via the cross breeding of single knockout models relevant for the tachykinin signalling pathways circumnavigates the problems associated with redundancy and also reveals that this phenomena is contributing to the data generated using the single knockouts. The use of these animals in a variety of experimental models to compare their function with the original "parental" knockouts and their corresponding wildtype controls reveals novel models for the action of the tachykinins in epilepsy and suggests a correlation with serotonin levels with an ultimate effect on the behavioural responses observed.

Книги з теми "Tachykinins":

1
Holzer, Peter, ed. Tachykinins. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18891-6.
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2
Eric, K. Fernström Symposium (8th 1985 Örenäs Castle Glumslöv Sweden). Tachykinin antagonists: Proceedings of the 8th Eric K. Fernström Symposium, held in Örenäs Castle, Glumslöv, Sweden on 10-11 June, 1985. Amsterdam: Elsevier, 1985.
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3
Holzer, Peter. Tachykinins. Springer, 2004.
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4
Tachykinins. Berlin: Springer, 2004.
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5
The Tachykinin receptors. Totowa, N.J: Humana Press, 1994.
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6
Gunnell, Andrea. Regulation of mucin secretion from airway epithelia by proteases and tachykinins. 2004.
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7
Substance P and neurokinins: Proceedings of "substance P and neurokinins--Montreal '86" : a satellite symposium of the XXX International Congress of the International Union of Physiological Sciences. New York: Springer-Verlag, 1987.
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8
Henry, J. L. Substance P and Neurokinins: Proceedings of Substance P and Neurokinins-Montreal '86 a Satellite Symposium of the Xxx International Congress of the I. Springer, 1987.
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9
Substance P and related peptides: Cellular and molecular physiology. New York, N.Y: New York Academy of Sciences, 1991.
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10
Krause, James Edward, and Susan E. Leeman. Substance P and Related Peptides: Cellular and Molecular Physiology (Annals of the New York Academy of Sciences). New York Academy of Sciences, 1991.
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Частини книг з теми "Tachykinins":

1
Tuluc, Florin. "Tachykinins." In Encyclopedia of Cancer, 1–8. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_7200-3.
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2
Tuluc, Florin. "Tachykinins." In Encyclopedia of Cancer, 4437–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_7200.
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3
Turiault, Marc, Caroline Cohen, Guy Griebel, David E. Nichols, Britta Hahn, Gary Remington, Ronald F. Mucha, et al. "Tachykinins." In Encyclopedia of Psychopharmacology, 1301–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_210.
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4
Turiault, Marc, Caroline Cohen, and Guy Griebel. "Tachykinins." In Encyclopedia of Psychopharmacology, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27772-6_210-2.
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5
Turiault, Marc, Caroline Cohen, and Guy Griebel. "Tachykinins." In Encyclopedia of Psychopharmacology, 1695–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-36172-2_210.
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6
Holzer, Peter. "Tachykinins." In Drug Development, 113–46. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-202-9_5.
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7
Conlon, J. M., C. F. Deacon, M. Thorndyke, L. Thim, and S. Falkmer. "Phylogeny of the Tachykinins." In Substance P and Neurokinins, 15–17. New York, NY: Springer New York, 1987. http://dx.doi.org/10.1007/978-1-4612-4672-5_6.
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8
Manzini, Stefano, Cristina Goso, and Arpad Szallasi. "Sensory Nerves and Tachykinins." In Neuropeptides in Respiratory Medicine, 173–96. Taylor & Francis Group, 6000 Broken Sound Parkway NW, Suite 300, Boca Raton, FL 33487-2742: CRC Press, 2017. http://dx.doi.org/10.4324/9780203745915-9.
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9
Howard, M. R., K. Haddley, T. Thippeswamy, S. Vasiliou, and J. P. Quinn. "Substance P and the Tachykinins." In Handbook of Neurochemistry and Molecular Neurobiology, 427–61. Boston, MA: Springer US, 2006. http://dx.doi.org/10.1007/978-0-387-30381-9_20.
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10
Birch, P. J. "Tachykinins: Central and Peripheral Effects." In Handbook of Experimental Pharmacology, 117–33. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60777-6_6.
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