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Journal articles on the topic 'Ventrale tegmentale Area'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

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1

Jones, D. L. "Central integration of cardiovascular and drinking responses elicited by central administration of angiotensin II: divergence of regulation by the ventral tegmental area and nucleus accumbens." Canadian Journal of Physiology and Pharmacology 64, no. 7 (July 1, 1986): 1011–16. http://dx.doi.org/10.1139/y86-172.

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Previous studies had implicated the involvement of the ventral tegmental area and its dopamine projections to the nucleus accumbens in goal-directed behavior. This study investigated whether or not the GABAergic inputs to the ventral tegmental area and, in turn, dopaminergic input to the nucleus accumbens from the ventral tegmental area modify drinking and cardiovascular responses elicited by central administration of angiotensin II. Injections of 25 ng of angiotensin II into a lateral cerebral ventricle of the rat elicited water intakes averaging 7–8 mL in 15 min with latencies usually less than 3 min. Pretreatment of the nucleus accumbens with spiperone, a dopamine antagonist, or the ventral tegmental area with γ-amino butyric acid (GABA) produced dose-dependent reductions in water intake and number of laps taken while increasing the latency to drink. The spiperone injection did not alter the pressor response. On the other hand, the GABA injections attenuated the pressor responses to central angiotensin II administration. These findings suggest that GABA input to the ventral tegmental area modifies both the cardiovascular and drinking responses elicited following central administration of angiotensin II. However, the dopamine projections to the nucleus accumbens appear to be involved only in the drinking responses elicited by central injections of angiotensin II. Divergence for the coordination of the skeletal motor behavioral component and the cardiovascular component elicited by central administration of angiotensin II must occur before the involvement of these dopamine pathways.

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Zhang, Song, Xiao-Na Yang, Ting Zang, Jun Luo, Zhiqiang Pan, Lei Wang, He Liu, et al. "Astroglial MicroRNA-219-5p in the Ventral Tegmental Area Regulates Nociception in Rats." Anesthesiology 127, no. 3 (September 1, 2017): 548–64. http://dx.doi.org/10.1097/aln.0000000000001720.

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Abstract Background The authors previously reported that noncoding microRNA miR-219-5p is down-regulated in the spinal cord in a nociceptive state. The ventral tegmental area also plays critical roles in modulating nociception, although the underlying mechanism remains unknown. The authors hypothesized that miR-219-5p in the ventral tegmental area also may modulate nociception. Methods The authors studied the bidirectional regulatory role of ventral tegmental area miR-219-5p in a rat complete Freund’s adjuvant model of inflammatory nociception by measuring paw withdrawal latencies. Using molecular biology technologies, the authors measured the effects of astroglial coiled-coil and C2 domain containing 1A/nuclear factor κB cascade and dopamine neuron activity on the down-regulation of ventral tegmental area miR-219-5p–induced nociceptive responses. Results MiR-219-5p expression in the ventral tegmental area was reduced in rats with thermal hyperalgesia. Viral overexpression of ventral tegmental area miR-219-5p attenuated complete Freund’s adjuvant–induced nociception from 7 days after complete Freund’s adjuvant injection (paw withdrawal latencies: 6.09 ± 0.83 s vs. 3.96 ± 0.76 s; n = 6/group). Down-regulation of ventral tegmental area miR-219-5p in naïve rats was sufficient to induce thermal hyperalgesia from 7 days after lentivirus injection (paw withdrawal latencies: 7.09 ± 1.54 s vs. 11.75 ± 2.15 s; n = 8/group), which was accompanied by increased glial fibrillary acidic protein (fold change: 2.81 ± 0.38; n = 3/group) and reversed by intraventral tegmental area injection of the astroglial inhibitor fluorocitrate. The nociceptive responses induced by astroglial miR-219-5p down-regulation were inhibited by interfering with astroglial coiled-coil and C2 domain containing 1A/nuclear factor-κB signaling. Finally, pharmacologic inhibition of ventral tegmental area dopamine neurons alleviated this hyperalgesia. Conclusions Down-regulation of astroglial miR-219-5p in ventral tegmental area induced nociceptive responses are mediated by astroglial coiled-coil and C2 domain containing 1A/nuclear factor-κB signaling and elevated dopamine neuron activity.

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3

Good, Cameron H., and Carl R. Lupica. "Properties of distinct ventral tegmental area synapses activated via pedunculopontine or ventral tegmental area stimulationin vitro." Journal of Physiology 587, no. 6 (March 13, 2009): 1233–47. http://dx.doi.org/10.1113/jphysiol.2008.164194.

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Ferreira, J. G. P., F. Del-Fava, R. H. Hasue, and S. J. Shammah-Lagnado. "Organization of ventral tegmental area projections to the ventral tegmental area–nigral complex in the rat." Neuroscience 153, no. 1 (April 2008): 196–213. http://dx.doi.org/10.1016/j.neuroscience.2008.02.003.

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5

Qiu, Gaolin, Ying Wu, Zeyong Yang, Long Li, Xiaona Zhu, Yiqiao Wang, Wenzhi Sun, Hailong Dong, Yuanhai Li, and Ji Hu. "Dexmedetomidine Activation of Dopamine Neurons in the Ventral Tegmental Area Attenuates the Depth of Sedation in Mice." Anesthesiology 133, no. 2 (May 12, 2020): 377–92. http://dx.doi.org/10.1097/aln.0000000000003347.

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Background Dexmedetomidine induces a sedative response that is associated with rapid arousal. To elucidate the underlying mechanisms, the authors hypothesized that dexmedetomidine increases the activity of dopaminergic neurons in the ventral tegmental area, and that this action contributes to the unique sedative properties of dexmedetomidine. Methods Only male mice were used. The activity of ventral tegmental area dopamine neurons was measured by a genetically encoded Ca2+ indicator and patch-clamp recording. Dopamine neurotransmitter dynamics in the medial prefrontal cortex and nucleus accumbens were measured by a genetically encoded dopamine sensor. Ventral tegmental area dopamine neurons were inhibited or activated by a chemogenetic approach, and the depth of sedation was estimated by electroencephalography. Results Ca2+ signals in dopamine neurons in the ventral tegmental area increased after intraperitoneal injection of dexmedetomidine (40 μg/kg; dexmedetomidine, 16.917 [14.882; 21.748], median [25%; 75%], vs. saline, –0.745 [–1.547; 0.359], normalized data, P = 0.001; n = 6 mice). Dopamine transmission increased in the medial prefrontal cortex after intraperitoneal injection of dexmedetomidine (40 μg/kg; dexmedetomidine, 10.812 [9.713; 15.104], median [25%; 75%], vs. saline, –0.498 [–0.664; –0.355], normalized data, P = 0.001; n = 6 mice) and in the nucleus accumbens (dexmedetomidine, 8.543 [7.135; 11.828], median [25%; 75%], vs. saline, –0.329 [–1.220; –0.047], normalized data, P = 0.001; n = 6 mice). Chemogenetic inhibition or activation of ventral tegmental area dopamine neurons increased or decreased slow waves, respectively, after intraperitoneal injection of dexmedetomidine (40 μg/kg; delta wave: two-way repeated measures ANOVA, F[2, 33] = 8.016, P = 0.002; n = 12 mice; theta wave: two-way repeated measures ANOVA, F[2, 33] = 22.800, P < 0.0001; n = 12 mice). Conclusions Dexmedetomidine activates dopamine neurons in the ventral tegmental area and increases dopamine concentrations in the related forebrain projection areas. This mechanism may explain rapid arousability upon dexmedetomidine sedation. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New

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6

Geugies, Hanneke, Roel J. T. Mocking, Caroline A. Figueroa, Paul F. C. Groot, Jan-Bernard C. Marsman, Michelle N. Servaas, J. Douglas Steele, Aart H. Schene, and Henricus G. Ruhé. "Impaired reward-related learning signals in remitted unmedicated patients with recurrent depression." Brain 142, no. 8 (July 5, 2019): 2510–22. http://dx.doi.org/10.1093/brain/awz167.

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Abstract One of the core symptoms of major depressive disorder is anhedonia, an inability to experience pleasure. In patients with major depressive disorder, a dysfunctional reward-system may exist, with blunted temporal difference reward-related learning signals in the ventral striatum and increased temporal difference-related (dopaminergic) activation in the ventral tegmental area. Anhedonia often remains as residual symptom during remission; however, it remains largely unknown whether the abovementioned reward systems are still dysfunctional when patients are in remission. We used a Pavlovian classical conditioning functional MRI task to explore the relationship between anhedonia and the temporal difference-related response of the ventral tegmental area and ventral striatum in medication-free remitted recurrent depression patients (n = 36) versus healthy control subjects (n = 27). Computational modelling was used to obtain the expected temporal difference errors during this task. Patients, compared to healthy controls, showed significantly increased temporal difference reward learning activation in the ventral tegmental area (PFWE,SVC = 0.028). No differences were observed between groups for ventral striatum activity. A group × anhedonia interaction [t(57) = −2.29, P = 0.026] indicated that in patients, higher anhedonia was associated with lower temporal difference activation in the ventral tegmental area, while in healthy controls higher anhedonia was associated with higher ventral tegmental area activation. These findings suggest impaired reward-related learning signals in the ventral tegmental area during remission in patients with depression. This merits further investigation to identify impaired reward-related learning as an endophenotype for recurrent depression. Moreover, the inverse association between reinforcement learning and anhedonia in patients implies an additional disturbing influence of anhedonia on reward-related learning or vice versa, suggesting that the level of anhedonia should be considered in behavioural treatments.

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Yamaguchi, Ken'ichi, Hitoshi Hama, and Kazuo watanabe. "Possible contribution of dopaminergic receptors in the anteroventral third ventricular region to hyperosmolality-induced vasopressin secretion in conscious rats." European Journal of Endocrinology 134, no. 2 (February 1996): 243–50. http://dx.doi.org/10.1530/eje.0.1340243.

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Yamaguchi K, Hama H, Watanabe K. Possible contribution of dopaminergic receptors in the anteroventral third ventricular region to hyperosmolality-induced vasopressin secretion in conscious rats. Eur J Endocrinol 1996;134:243–50. ISSN 0804–4643 We have reported previously that regions encompassing the cerebral ventricle may contain dopamine receptors responsible for facilitatory roles in the osmotic release of vasopressin in conscious rats. In order to explore the location of these receptors, we injected (0.5 μl) the dopamine antagonist haloperidol (13.3 nmol) or dopamine (26.4 nmol) topically into the anteroventral third ventricular region or the paraventricular nucleus of rats, and their effects on the levels of plasma vasopressin and its controlling factors were examined in the presence or absence of an osmotic stimulus. The effects of haloperidol injections into the ventral tegmental area were also tested to study whether information associated with drinking behavior may affect the osmotic vasopressin secretion. Intravenous infusion (0.1 ml kg−1 body wt min−1) of hypertonic saline (2.5 mol/l) enhanced plasma vasopressin 15 and 30 min later, and this was accompanied by an augmentation of plasma osmolality, sodium and chloride, and by elevated or unaltered arterial pressure. The vasopressin response was abolished by haloperidol injection into the anteroventral third ventricular region 10 min before the beginning of the hypertonic saline infusion. The injection sites were confirmed histologically to have been in or near the organum vasculosum of the laminae terminalis and a ventral part of the median preoptic nucleus. Similarly, a partial but significant reduction of the vasopressin response was noted after bilateral injections of haloperidol into the ventral tegmental area, whereas bilateral haloperidol injections into the paraventricular nucleus had no appreciable effect. The responses of plasma osmolality, electrolytes and arterial pressure to the osmotic load were not affected significantly by haloperidol injections into the anteroventral third ventricular region, ventral tegmental area or the paraventricular nucleus. The iv infusion of isotonic saline (0.15 mol/l) did not change plasma vasopressin and the other variables significantly, and this was also the case when preceded by application of haloperidol into the anteroventral third ventricular region, ventral tegmental area or the paraventricular nucleus. Dopamine injection into the anteroventral third ventricular region increased plasma vasopressin 5 min later, without affecting plasma osmolality, electrolytes or arterial pressure. On the basis of these results, we concluded that dopamine receptors responsible for facilitatory roles in osmotically stimulated vasopressin secretion may exist in the anteroventral third ventricular region and ventral tegmental area. ken'ichi Yamaguchi, Department of Physiology, Niigata University School of Medicine, Asahimachi-Dori 1, Niigata City, Niigata 951, Japan

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8

Borgkvist, Anders, Ana Mrejeru, and David Sulzer. "Multiple Personalities in the Ventral Tegmental Area." Neuron 70, no. 5 (June 2011): 803–5. http://dx.doi.org/10.1016/j.neuron.2011.05.024.

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9

Bozzali, Marco, Marcello D’Amelio, and Laura Serra. "Ventral tegmental area disruption in Alzheimer’s disease." Aging 11, no. 5 (March 9, 2019): 1325–26. http://dx.doi.org/10.18632/aging.101852.

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10

Kirouac, G. J., and J. Ciriello. "Cardiovascular afferent inputs to ventral tegmental area." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 272, no. 6 (June 1, 1997): R1998—R2003. http://dx.doi.org/10.1152/ajpregu.1997.272.6.r1998.

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Extracellular single-unit recording experiments were done in alpha-chloralose-anesthetized, paralyzed, and artificially ventilated rats to investigate the effect of selective activation of arterial baroreceptors and stimulation of cardiovascular depressor sites in the nucleus of the solitary tract (NTS) on the discharge rate of neurons in the ventral tegmental area (VTA). Electrical stimulation of the aortic depressor nerve (ADN), which is known to carry aortic baroreceptor afferent fibers only, excited 12 of 21 (mean onset latency 42.4 +/- 8.8 ms) and inhibited 2 of 21 (mean onset latency 42.5 +/- 6.5 ms) single units in the VTA. The discharge rate of VTA units was also altered during the reflex activation of arterial baroreceptors by the acute rise in arterial pressure (AP) to systemic injections of phenylephrine (10 micrograms/kg i.v.): 12 of 44 units were excited and 15 of 44 were inhibited. Units that responded to either ADN stimulation or the reflex activation of the baroreflex also responded to stimulation of depressor sites in the NTS. An additional 12 units that were found in barodenervated controls to be responsive to NTS stimulation were nonresponsive to selective activation of arterial baroreceptors. These data indicate that cardiovascular afferent inputs modulate the activity of neurons in the VTA and suggest that changes in systemic AP may exert an effect on the activity of neurons involved in mesolimbic and mesocortical function.

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11

Trojniar, Weronika, and Małgorzata Staszewska. "Unilateral damage to the ventral tegmental area facilitates feeding induced by stimulation of the contralateral ventral tegmental area." Brain Research 641, no. 2 (April 1994): 333–40. http://dx.doi.org/10.1016/0006-8993(94)90163-5.

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12

Santana, Yanira, Angel Montejo, Javier Martín, Ginés LLorca, Gloria Bueno, and Juan Blázquez. "Understanding the Mechanism of Antidepressant-Related Sexual Dysfunction: Inhibition of Tyrosine Hydroxylase in Dopaminergic Neurons after Treatment with Paroxetine but Not with Agomelatine in Male Rats." Journal of Clinical Medicine 8, no. 2 (January 23, 2019): 133. http://dx.doi.org/10.3390/jcm8020133.

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Antidepressant-related sexual dysfunction is a frequent adverse event caused by serotonergic activation that intensely affects quality of life and adherence in depressed patients. The dopamine system has multiple effects promoting sexual behavior, but no studies have been carried out to confirm dopaminergic changes involved in animal models after antidepressant use. Methods: The sexual behavior-related dopaminergic system in the rat was studied by comparing two different antidepressants and placebo for 28 days. The antidepressants used were paroxetine (a serotonergic antidepressant that causes highly frequent sexual dysfunction in humans) and agomelatine (a non-serotonergic antidepressant without associated sexual dysfunction). The tyrosine hydroxylase immunoreactivity (THI) in the substantia nigra pars compacta, the ventral tegmental area, the zona incerta, and the hypothalamic arcuate nucleus, as well as the dopaminergic projections to the striatum, hippocampus, cortex, and median eminence were analyzed. Results: The THI decreased significantly in the substantia nigra and ventral tegmental area after treatment with paroxetine, and the labeling was reduced drastically in the zona incerta and mediobasal hypothalamus. The immunoreactive axons in the target regions (striatum, cortex, hippocampus, and median eminence) almost disappeared only in the paroxetine-treated rats. Conversely, after treatment with agomelatine, a moderate reduction in immunoreactivity in the substantia nigra was found without appreciable modifications in the ventral tegmental area, zona incerta, and mediobasal hypothalamus. Nevertheless, no sexual or copulatory behavior was observed in any of the experimental or control groups. Conclusion: Paroxetine but not agomelatine was associated with important decreased activity in dopaminergic areas such as the substantia nigra and ventral tegmental areas that could be associated with sexual performance impairment in humans after antidepressant treatment.

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Huang, Mengbing, Ming Bai, Zhimin Zhang, Lu Ge, Kang Lu, Xiang Li, Ye Li, et al. "Downregulation of thioredoxin-1 in the ventral tegmental area delays extinction of methamphetamine-induced conditioned place preference." Journal of Psychopharmacology 32, no. 9 (August 23, 2018): 1037–46. http://dx.doi.org/10.1177/0269881118791523.

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Background: Drug addiction is characterized by compulsive drug use and relapse. Thioredoxin-1 is emerging as an important modulator involved in the cellular protective response against a variety of toxic stressors. Previous study has reported that thioredoxin-1 overexpression prevents the acquisition of methamphetamine-conditioned place preference. Here, we aimed to investigate the effect of thioredoxin-1 on methamphetamine-conditioned place preference extinction and the possible mechanism. Methods: (a) An extinction procedure in mice was employed to investigate the effect of thioredoxin-1 on the extinction of methamphetamine-conditioned place preference. After the acquisition of methamphetamine-conditioned place preference, mice underwent the following procedures: the injection of thioredoxin-1 small interfering RNA in the ventral tegmental area followed by the post-conditioned place preference test, four days of extinction training followed by four days of recovery after surgery. (b) The levels of thioredoxin-1, dopamine D1 receptor, tyrosine hydroxylase, phosphorylated extracellular regulated kinase, and phosphorylated cyclic adenosine monophosphate response element binding protein were examined by using Western blot analysis. Results: Thioredoxin-1 downregulation in the ventral tegmental area delayed methamphetamine-conditioned place preference extinction. The expression of thioredoxin-1 was decreased in the ventral tegmental area of mice in control and negative groups after methamphetamine-conditioned place preference extinction, but not in the thioredoxin-1 siRNA group. The levels of dopamine D1 receptor, tyrosine hydroxylase, phosphorylated extracellular regulated kinase, and phosphorylated cyclic adenosine monophosphate response element binding protein were decreased in the ventral tegmental area, nucleus accumbens, and prefrontal cortex of mice in the control and negative groups after methamphetamine-conditioned place preference extinction, but were inversely increased in thioredoxin-1 siRNA group. Conclusions: The results suggest that downregulation of thioredoxin-1 in the ventral tegmental area may delay methamphetamine-conditioned place preference extinction by regulating the mesocorticolimbic dopaminergic signaling pathway.

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14

Coimbra, B., C. Soares-Cunha, S. Borges, N. Sousa, and A. Rodrigues. "Modulation of the laterodorsal tegmental area inputs to the ventral tegmental area by prenatal stress." European Neuropsychopharmacology 26 (October 2016): S193—S194. http://dx.doi.org/10.1016/s0924-977x(16)31032-x.

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Trutti, Anne C., Martijn J. Mulder, Bernhard Hommel, and Birte U. Forstmann. "Functional neuroanatomical review of the ventral tegmental area." NeuroImage 191 (May 2019): 258–68. http://dx.doi.org/10.1016/j.neuroimage.2019.01.062.

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Langlois, Ludovic D., and Fereshteh S. Nugent. "Opiates and Plasticity in the Ventral Tegmental Area." ACS Chemical Neuroscience 8, no. 9 (August 16, 2017): 1830–38. http://dx.doi.org/10.1021/acschemneuro.7b00281.

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17

Morales, Marisela, and Elyssa B. Margolis. "Ventral tegmental area: cellular heterogeneity, connectivity and behaviour." Nature Reviews Neuroscience 18, no. 2 (January 5, 2017): 73–85. http://dx.doi.org/10.1038/nrn.2016.165.

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Margolis, Elyssa B., Brian Toy, Patricia Himmels, Marisela Morales, and Howard L. Fields. "Identification of Rat Ventral Tegmental Area GABAergic Neurons." PLoS ONE 7, no. 7 (July 31, 2012): e42365. http://dx.doi.org/10.1371/journal.pone.0042365.

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Ting-A-Kee, Ryan, Hector Vargas-Perez, Jennifer K. Mabey, Samuel I. Shin, Scott C. Steffensen, and Derek van der Kooy. "Ventral tegmental area GABA neurons and opiate motivation." Psychopharmacology 227, no. 4 (February 8, 2013): 697–709. http://dx.doi.org/10.1007/s00213-013-3002-3.

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Alberico, Stephanie L., Martin D. Cassell, and Nandakumar S. Narayanan. "The vulnerable ventral tegmental area in Parkinson’s disease." Basal Ganglia 5, no. 2-3 (August 2015): 51–55. http://dx.doi.org/10.1016/j.baga.2015.06.001.

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Glimcher, Paul W., Adrienne A. Giovino, and Bartley G. Hoebel. "Neurotensin self-injection in the ventral tegmental area." Brain Research 403, no. 1 (February 1987): 147–50. http://dx.doi.org/10.1016/0006-8993(87)90134-x.

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Hjelmstad, G. O., Y. Xia, E. B. Margolis, and H. L. Fields. "Opioid Modulation of Ventral Pallidal Afferents to Ventral Tegmental Area Neurons." Journal of Neuroscience 33, no. 15 (April 10, 2013): 6454–59. http://dx.doi.org/10.1523/jneurosci.0178-13.2013.

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Brown, P. Leon, and Paul D. Shepard. "Functional evidence for a direct excitatory projection from the lateral habenula to the ventral tegmental area in the rat." Journal of Neurophysiology 116, no. 3 (September 1, 2016): 1161–74. http://dx.doi.org/10.1152/jn.00305.2016.

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The lateral habenula, a phylogenetically conserved epithalamic structure, is activated by aversive stimuli and reward omission. Excitatory efferents from the lateral habenula predominately inhibit midbrain dopamine neuronal firing through a disynaptic, feedforward inhibitory mechanism involving the rostromedial tegmental nucleus. However, the lateral habenula also directly targets dopamine neurons within the ventral tegmental area, suggesting that opposing actions may result from increased lateral habenula activity. In the present study, we tested the effect of habenular efferent stimulation on dopamine and nondopamine neurons in the ventral tegmental area of Sprague-Dawley rats using a parasagittal brain slice preparation. Single pulse stimulation of the fasciculus retroflexus excited 48% of dopamine neurons and 51% of nondopamine neurons in the ventral tegmental area of rat pups. These proportions were not altered by excision of the rostromedial tegmental nucleus and were evident in both cortical- and striatal-projecting dopamine neurons. Glutamate receptor antagonists blocked this excitation, and fasciculus retroflexus stimulation elicited evoked excitatory postsynaptic potentials with a nearly constant onset latency, indicative of a monosynaptic, glutamatergic connection. Comparison of responses in rat pups and young adults showed no significant difference in the proportion of neurons excited by fasciculus retroflexus stimulation. Our data indicate that the well-known, indirect inhibitory effect of lateral habenula activation on midbrain dopamine neurons is complemented by a significant, direct excitatory effect. This pathway may contribute to the role of midbrain dopamine neurons in processing aversive stimuli and salience.

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Ewan, Eric E., and Thomas J. Martin. "Opioid Facilitation of Rewarding Electrical Brain Stimulation Is Suppressed in Rats with Neuropathic Pain." Anesthesiology 114, no. 3 (March 1, 2011): 624–32. http://dx.doi.org/10.1097/aln.0b013e31820a4edb.

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Introduction Opioids are powerful analgesics, but are also common drugs of abuse. Few studies have examined how neuropathic pain alters the pharmacology of opioids in modulating limbic pathways that underlie abuse liability. Methods Rats with or without spinal nerve ligation (SNL) were implanted with electrodes into the left ventral tegmental area and trained to lever press for electrical stimulation. The effects of morphine, heroin, and cocaine on facilitating electrical stimulation of the ventral tegmental area and mechanical allodynia were assessed in SNL and control subjects. Results Responding for electrical stimulation of the ventral tegmental area was similar in control and SNL rats. The frequency at which rats emitted 50% of maximal responding was 98.2 ± 5.1 (mean ± SEM) and 93.7 ± 2.8 Hz in control and SNL rats, respectively. Morphine reduced the frequency at which rats emitted 50% of maximal responding in control (maximal shift of 14.8 ± 3.1 Hz), but not SNL (2.3 ± 2.2 Hz) rats. Heroin was less potent in SNL rats, whereas cocaine produced similar shifts in control (42.3 ± 2.0 Hz) and SNL (37.5 ± 4.2 Hz) rats. Conclusions Nerve injury suppressed potentiation of electrical stimulation of the ventral tegmental area by opioids, suggesting that the positive reinforcing effects are diminished by chronic pain. Given concerns regarding prescription opioid abuse, developing strategies that assess both analgesia and abuse liability within the context of chronic pain may aid in determining which opioids are most suitable for treating chronic pain when abuse is a concern.

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You, Chang, Bertha J. Vandegrift, and Mark S. Brodie. "KCNK13 potassium channels in the ventral tegmental area of rats are important for excitation of ventral tegmental area neurons by ethanol." Alcoholism: Clinical and Experimental Research 45, no. 7 (June 2, 2021): 1348–58. http://dx.doi.org/10.1111/acer.14630.

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Airapetov, M. I., S. O. Eresko, E. A. Sekste, A. A. Lebedev, E. R. Bychkov, and P. D. Shabanov. "Ethanol withdrawal leads to an increase in the CRFR2 mRNA level in the ventricular tegmental region of the rat brain." Biomeditsinskaya Khimiya 65, no. 5 (2019): 385–87. http://dx.doi.org/10.18097/pbmc20196505385.

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The neurotransmitter systems of the brain are exposed to dysregulation during alcohol withdrawal. This contributes to the development of the pathological craving for alcohol in which corticotropin-releasing hormone receptors are may be involved. During the period of alcohol withdrawal, the level of CRFR2 mRNA in the ventral tegmental area of the brain on the seventh day of abstinence was significantly increased in comparison with the control group. This supports existing concepts on possible participation in the modulation of dopaminergic and GABA-neural neurons in the ventral tegmental area the brain.

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Chen, Shiouh-Yi, Robert L. Burger, and Maarten E. A. Reith. "Extracellular dopamine in the rat ventral tegmental area and nucleus accumbens following ventral tegmental infusion of cocaine." Brain Research 729, no. 2 (August 1996): 294–96. http://dx.doi.org/10.1016/0006-8993(96)00671-3.

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Omelchenko, Natalia, and Susan R. Sesack. "Laterodorsal tegmental projections to identified cell populations in the rat ventral tegmental area." Journal of Comparative Neurology 483, no. 2 (2005): 217–35. http://dx.doi.org/10.1002/cne.20417.

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Schifirneţ, E., S. E. Bowen, and G. S. Borszcz. "Separating analgesia from reward within the ventral tegmental area." Neuroscience 263 (March 2014): 72–87. http://dx.doi.org/10.1016/j.neuroscience.2014.01.009.

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Sanchez-Catalan, M. J., J. Kaufling, F. Georges, P. Veinante, and M. Barrot. "The antero-posterior heterogeneity of the ventral tegmental area." Neuroscience 282 (December 2014): 198–216. http://dx.doi.org/10.1016/j.neuroscience.2014.09.025.

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Brodie, Mark S., Christine Pesold, and Sarah B. Appel. "Ethanol Directly Excites Dopaminergic Ventral Tegmental Area Reward Neurons." Alcoholism: Clinical and Experimental Research 23, no. 11 (November 1999): 1848–52. http://dx.doi.org/10.1111/j.1530-0277.1999.tb04082.x.

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Hnasko, T. S., G. O. Hjelmstad, H. L. Fields, and R. H. Edwards. "Ventral Tegmental Area Glutamate Neurons: Electrophysiological Properties and Projections." Journal of Neuroscience 32, no. 43 (October 24, 2012): 15076–85. http://dx.doi.org/10.1523/jneurosci.3128-12.2012.

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Bariselli, Sebastiano, Christelle Glangetas, Stamatina Tzanoulinou, and Camilla Bellone. "Ventral tegmental area subcircuits process rewarding and aversive experiences." Journal of Neurochemistry 139, no. 6 (October 3, 2016): 1071–80. http://dx.doi.org/10.1111/jnc.13779.

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Wang, Huikun, Tyler Treadway, Daniel P. Covey, Joseph F. Cheer, and Carl R. Lupica. "Cocaine-Induced Endocannabinoid Mobilization in the Ventral Tegmental Area." Cell Reports 12, no. 12 (September 2015): 1997–2008. http://dx.doi.org/10.1016/j.celrep.2015.08.041.

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Adcock, Rachel, Kathryn Dickerson, Jeff MacInnes, and R. Alison Adcock. "144. Cognitive Neurostimulation: Volitional Regulation of Ventral Tegmental Area." Biological Psychiatry 85, no. 10 (May 2019): S60. http://dx.doi.org/10.1016/j.biopsych.2019.03.158.

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Trulson, Michael E., Tamella J. Trulson, and Kamyar Arasteh. "Recording of mouse ventral tegmental area dopamine-containing neurons." Experimental Neurology 96, no. 1 (April 1987): 68–81. http://dx.doi.org/10.1016/0014-4886(87)90169-5.

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Perez-Bonilla, Patricia, Krystal Santiago-Colon, and Gina M. Leinninger. "Lateral hypothalamic area neuropeptides modulate ventral tegmental area dopamine neurons and feeding." Physiology & Behavior 223 (September 2020): 112986. http://dx.doi.org/10.1016/j.physbeh.2020.112986.

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38

Espinosa, Pedro, Roxana A. Silva, Nicole K. Sanguinetti, Francisca C. Venegas, Raul Riquelme, Luis F. González, Gonzalo Cruz, Georgina M. Renard, Pablo R. Moya, and Ramón Sotomayor-Zárate. "Programming of Dopaminergic Neurons by Neonatal Sex Hormone Exposure: Effects on Dopamine Content and Tyrosine Hydroxylase Expression in Adult Male Rats." Neural Plasticity 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/4569785.

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We sought to determine the long-term changes produced by neonatal sex hormone administration on the functioning of midbrain dopaminergic neurons in adult male rats. Sprague-Dawley rats were injected subcutaneously at postnatal day 1 and were assigned to the following experimental groups: TP (testosterone propionate of 1.0 mg/50 μL); DHT (dihydrotestosterone of 1.0 mg/50 μL); EV (estradiol valerate of 0.1 mg/50 μL); and control (sesame oil of 50 μL). At postnatal day 60, neurochemical studies were performed to determine dopamine content in substantia nigra-ventral tegmental area and dopamine release in nucleus accumbens. Molecular (mRNA expression of tyrosine hydroxylase) and cellular (tyrosine hydroxylase immunoreactivity) studies were also performed. We found increased dopamine content in substantia nigra-ventral tegmental area of TP and EV rats, in addition to increased dopamine release in nucleus accumbens. However, neonatal exposure to DHT, a nonaromatizable androgen, did not affect midbrain dopaminergic neurons. Correspondingly, compared to control rats, levels of tyrosine hydroxylase mRNA and protein were significantly increased in TP and EV rats but not in DHT rats, as determined by qPCR and immunohistochemistry, respectively. Our results suggest an estrogenic mechanism involving increased tyrosine hydroxylase expression, either by direct estrogenic action or by aromatization of testosterone to estradiol in substantia nigra-ventral tegmental area.

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Andino, Lourdes M., Daniel J. Ryder, Alexandra Shapiro, Michael K. Matheny, Yi Zhang, Melanie K. Judge, K. Y. Cheng, Nihal Tümer, and Philip J. Scarpace. "POMC overexpression in the ventral tegmental area ameliorates dietary obesity." Journal of Endocrinology 210, no. 2 (May 12, 2011): 199–207. http://dx.doi.org/10.1530/joe-10-0418.

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The activation of proopiomelanocortin (POMC) neurons in different regions of the brain, including the arcuate nucleus of the hypothalamus (ARC) and the nucleus of the solitary tract curtails feeding and attenuates body weight. In this study, we compared the effects of delivery of a recombinant adeno-associated viral (rAAV) construct encoding POMC to the ARC with delivery to the ventral tegmental area (VTA). F344×Brown Norway rats were high-fat (HF) fed for 14 days after which self-complementary rAAV constructs expressing either green fluorescent protein or the POMC gene were injected using coordinates targeting either the VTA or the ARC. Corresponding increased POMC levels were found at the predicted injection sites and subsequent α-melanocyte-stimulating hormone levels were observed. Food intake and body weight were measured for 4 months. Although caloric intake was unaltered by POMC overexpression, weight gain was tempered with POMC overexpression in either the VTA or the ARC compared with controls. There were parallel decreases in adipose tissue reserves. In addition, levels of oxygen consumption and brown adipose tissue uncoupling protein 1 were significantly elevated with POMC treatment in the VTA. Interestingly, tyrosine hydroxylase levels were increased in both the ARC and VTA with POMC overexpression in either the ARC or the VTA. In conclusion, these data indicate a role for POMC overexpression within the VTA reward center to combat HF-induced obesity.

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Vinish, Monika. "Acute electrical stimulation of ventral tegmental area improves depressive behavior." Annals of Neurosciences 16, no. 01 (January 1, 2009): 14–15. http://dx.doi.org/10.5214/ans.0972.7531.2009.160106.

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MacInnes, Jeff J., Kathryn C. Dickerson, Nan-kuei Chen, and R. Alison Adcock. "Cognitive Neurostimulation: Learning to Volitionally Sustain Ventral Tegmental Area Activation." Neuron 89, no. 6 (March 2016): 1331–42. http://dx.doi.org/10.1016/j.neuron.2016.02.002.

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Mullis, Kiersten, Kristen Kay, and Diana L. Williams. "Oxytocin action in the ventral tegmental area affects sucrose intake." Brain Research 1513 (June 2013): 85–91. http://dx.doi.org/10.1016/j.brainres.2013.03.026.

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Grant, Alanna, Colleen Manitt, and Cecilia Flores. "Haloperidol treatment downregulates DCC expression in the ventral tegmental area." Neuroscience Letters 575 (July 2014): 58–62. http://dx.doi.org/10.1016/j.neulet.2014.05.030.

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Jo, Yong Sang, and Sheri J. Y. Mizumori. "Prefrontal Regulation of Neuronal Activity in the Ventral Tegmental Area." Cerebral Cortex 26, no. 10 (September 22, 2015): 4057–68. http://dx.doi.org/10.1093/cercor/bhv215.

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DOMESICK, VALERIE B. "Neuroanatomical Organization of Dopamine Neurons in the Ventral Tegmental Area." Annals of the New York Academy of Sciences 537, no. 1 The Mesocorti (October 1988): 10–26. http://dx.doi.org/10.1111/j.1749-6632.1988.tb42094.x.

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Thomas, Taylor S., Corey Baimel, and Stephanie L. Borgland. "Opioid and hypocretin neuromodulation of ventral tegmental area neuronal subpopulations." British Journal of Pharmacology 175, no. 14 (September 26, 2017): 2825–33. http://dx.doi.org/10.1111/bph.13993.

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47

Xia, Yan-Fang, Elyssa B. Margolis, and Gregory O. Hjelmstad. "Substance P inhibits GABABreceptor signalling in the ventral tegmental area." Journal of Physiology 588, no. 9 (April 30, 2010): 1541–49. http://dx.doi.org/10.1113/jphysiol.2010.188367.

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48

Koyama, Susumu, and Sarah B. Appel. "Characterization of M-Current in Ventral Tegmental Area Dopamine Neurons." Journal of Neurophysiology 96, no. 2 (August 2006): 535–43. http://dx.doi.org/10.1152/jn.00574.2005.

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M-current ( IM) is a voltage-gated potassium current (KCNQ type) that affects neuronal excitability and is modulated by some drugs of abuse. Ventral tegmental area (VTA) dopamine (DA) neurons are important for the reinforcing effects of drugs of abuse. Therefore we studied IM in acutely dissociated rat DA VTA neurons with nystatin-perforated patch recording. The standard deactivation protocol was used to measure IM during voltage-clamp recording with hyperpolarizing voltage steps to −65 mV (in 10-mV increments) from a holding potential of −25 mV. IM amplitude was voltage dependent and maximal current amplitude was detected at −45 mV. The deactivation time constant of IM was voltage dependent and became shorter at more negative voltages. The IM/KCNQ antagonist XE991 (0.3–30 μM) caused a concentration-dependent reduction in IM amplitude with an IC50 of 0.71 μM. Tetraethylammonium (TEA, 0.3–10 mM) caused a concentration-dependent inhibition of IM with an IC50 of 1.56 mM. In current-clamp recordings, all DA VTA neurons were spontaneously active. Analysis of evoked action potential shape indicated that XE991 (1–10 μM) reduced the fast and slow components of the spike afterhyperpolarization (AHP) without affecting the middle component of the AHP. Action potential amplitude, duration, and threshold were not affected by XE991. In addition, 10 μM XE991 significantly shortened the interspike intervals in evoked spike trains. In conclusion, IM is active near threshold in DA VTA neurons, is blocked by XE991 (10 μM) and TEA (10 mM), may contribute to the shape of the AHP, and may decrease excitability of these neurons.

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Li, Wei, William M. Doyon, and John A. Dani. "Quantitative unit classification of ventral tegmental area neurons in vivo." Journal of Neurophysiology 107, no. 10 (May 15, 2012): 2808–20. http://dx.doi.org/10.1152/jn.00575.2011.

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Neurons in the ventral tegmental area (VTA) synthesize several major neurotransmitters, including dopamine (DA), GABA, and glutamate. To classify VTA single-unit neural activity from freely moving rats, we used hierarchical agglomerative clustering and probability distributions as quantitative methods. After many parameters were examined, a firing rate of 10 Hz emerged as a transition frequency between clusters of low-firing and high-firing neurons. To form a subgroup identified as high-firing neurons with GABAergic characteristics, the high-firing classification was sorted by spike duration. To form a subgroup identified as putative DA neurons, the low-firing classification was sorted by DA D2-type receptor pharmacological responses to quinpirole and eticlopride. Putative DA neurons were inhibited by the D2-type receptor agonist quinpirole and returned to near-baseline firing rates or higher following the D2-type receptor antagonist eticlopride. Other unit types showed different responses to these D2-type receptor drugs. A multidimensional comparison of neural properties indicated that these subgroups often clustered independently of each other with minimal overlap. Firing pattern variability reliably distinguished putative DA neurons from other unit types. A combination of phasic burst properties and a low skew in the interspike interval distribution produced a neural population that was comparable to the one sorted by D2 pharmacology. These findings provide a quantitative statistical approach for the classification of VTA neurons in unanesthetized animals.

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Yamaguchi, Tsuyoshi, Whitney Sheen, and Marisela Morales. "Glutamatergic neurons are present in the rat ventral tegmental area." European Journal of Neuroscience 25, no. 1 (January 12, 2007): 106–18. http://dx.doi.org/10.1111/j.1460-9568.2006.05263.x.

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