Academic literature on the topic 'Ventrale tegmentale Area'
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Journal articles on the topic "Ventrale tegmentale Area"
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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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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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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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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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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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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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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.
Dissertations / Theses on the topic "Ventrale tegmentale Area"
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Jalabert, Marion. "Caractérisation des circuits neuronaux contrôlant l’activité des neurones dopaminergiques de l’aire tegmentale ventrale." Thesis, Bordeaux 2, 2011. http://www.theses.fr/2011BOR21824/document.
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Les neurones dopaminergiques (DA) de l’aire tegmentale ventrale (VTA) sont influencés par différents stimuli comme des récompenses naturelles et d’autres stimuli moins physiologiques tels que les drogues d’abus. Ces drogues agissent en détournant les mécanismes d’apprentissage qui sous-tendent normalement la motivation pour des renforçateurs naturels. Les neurones DA, en conditions physiologiques, sont subtilement régulés par une balance entre tonus GABA et glutamatergique. Ils sont soumis à de multiples sources inhibitrices dont le noyau accumbens, les interneurones locaux ou les neurones GABA de la queue de la VTA (tVTA). Le glutamate est également important dans leur modulation. Il contrôle leur activité en bursts, qui est le mode de décharge le plus efficace pour libérer de la dopamine et coder des informations associées à la récompense. Il permet des adaptations synaptiques à long terme qui se sont révélées importantes dans la prise de drogue. La connaissance des facteurs endogènes qui contrôlent l’excitabilité des cellules DA de la VTA est essentielle à la compréhension des processus physiologiques (recherche de plaisir…) mais aussi pathologiques (addiction…). L’objectif de mon travail a été de comprendre les circuits de régulation des neurones DA en conditions physiologiques et lors de l’exposition à la morphine. Dans un premier temps, nous avons étudié les mécanismes de régulation des neurones DA par la formation hippocampique ventrale incluant le subiculum ventral et l’aire CA1 ventrale (vSUB/CA1). Grâce à l’utilisation d’approches d’électrophysiologie in vivo chez le rat anesthésié, nous avons montré que le vSUB/CA1 exerce un contrôle excitateur glutamatergique des neurones DA. Nous avons mis en évidence que cette voie vSUB/CA1-VTA est polysynaptique, faisant intervenir le BNST comme relais. J’ai aussi pu confirmer le rôle fonctionnel de la tVTA en tant que nouvelle structure GABA modulant l’activité des neurones DA, renforçant ainsi l’idée d’une balance entre tonus GABA et glutamatergique régulant les neurones DA in vivo.La deuxième partie de ma thèse a consisté en l’étude des circuits neuronaux à l’origine des effets excitateurs de la morphine sur les neurones DA de la VTA in vivo. L’hypothèse actuelle est que la morphine excite les neurones DA par un mécanisme de désinhibition en inhibant les neurones GABA de la VTA. Grâce à l’utilisation d’approches multiples, nous avons proposé un nouveau circuit expliquant les effets de la morphine. Ces effets sont la conséquence d’une modification de la balance GABA/glutamate par la morphine. Elle se traduit par une diminution du tonus GABA et d’une augmentation du tonus glutamatergique. Enfin, nous avons pu démontrer qu’une seule exposition à la cocaïne augmente l’activité de base des neurones DA. Chez ces animaux, les effets excitateurs de la morphine sont potentialisés confirmant ainsi l’hypothèse que l’amplitude de l’activation des neurones DA par la morphine dépend de leur état d’excitabilitéDopaminergic (DA) neurons of the ventral tegmental area (VTA) are influenced by several stimuli such as natural rewards or drugs of abuse. Drugs shunt learning mechanisms which underlie motivation for natural reinforcers. Under physiological conditions, DA neurons are regulated by a balance between GABA and glutamatergic inputs. They receive several inhibitory inputs especially from the nucleus accumbens, VTA local interneurons and GABA neurons of the tail of the VTA (tVTA). Glutamate is also important in modulating DA neuron activity. It controls their bursting activity which is the most efficient way to release dopamine and to encode reward-associated informations. It allows long term synaptic adaptations important for addiction. Knowing how these endogenous factors control VTA DA neuron excitability is essential to understand physiological (search for pleasure…) and pathological (drug addiction…) processes.In the first part of my thesis, we studied the regulation of the VTA by the hippocampal formation including the ventral subiculum and the ventral CA1 area (vSUB/CA1). Using electrophysiological approaches in anesthetized animal, we showed that the vSUB/CA1 controls VTA DA neurons and that this input is glutamatergic. We also demonstrated that the vSUB/CA1-VTA pathway is polysynaptic implicating the BNST as a relay. I also confirmed the inhibitory control of the VTA by tVTA, new GABA input to DA neurons. Thus, in vivo, DA neurons are regulated by a balance between GABA and glutamatergic inputs. The second part of my research consisted in studying the neuronal circuits underlying excitatory effects of morphine on VTA DA neurons in vivo. The actual hypothesis is that morphine excites DA neurons by a disinhibition mechanism inhibiting VTA GABA neurons. Using several approaches (electrophysiological approaches in anesthetized animal, tract-tracing methods), we proposed a new circuitry explaining morphine effects. These excitatory effects result from a modification of the balance between GABA and glutamatergic inputs with a decrease of the GABA tone and an increase of the glutamatergic tone. Finally, we demonstrated that an acute cocaine exposure increases DA neuron activity. In animals exposed to cocaine, morphine excitatory effects are potentiated. This last experiment confirms the hypothesis that the amplitude of morphine-induced activation of VTA DA neurons depends on their excitability state
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Faivre, Fanny. "La queue de l’aire tegmentale ventrale : définition anatomo-moléculaire, implication dans la réponse aux stimuli aversifs et influence sur la voie nigrostriée." Thesis, Strasbourg, 2018. http://www.theses.fr/2018STRAJ082.
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La queue de l’aire tegmentale ventrale (tVTA) est le principal contrôle inhibiteur des neurones dopaminergiques du mésencéphale. Cette structure, bien qu’aujourd’hui très étudiée, n’est cependant pas encore référencée dans les atlas stéréotaxiques. Anatomiquement, nous avons pu apporter une définition de référence de la tVTA, à travers son analyse neurochimique, stéréologique, hodologique et génomique. Fonctionnellement, nous avons montré son rôle dans la réponse à des expériences émotionnelles aversives et nous avons testé son influence sur les symptômes moteurs et non-moteurs de la maladie de Parkinson. Nous avons ainsi montré qu’une co-lésion de la tVTA dans un modèle murin de la maladie permet une amélioration des performances motrices, des seuils nociceptifs et des symptômes de type dépressifs. Ce travail a ainsi participé au progrès de nos connaissances sur la tVTA et ouvre de nouvelles pistes d’exploration quant à son implication fonctionnelleThe tail of the ventral tegmental area (tVTA) is the major brake of the midbrain dopamine neurons. This structure although studied, is not yet referenced in stereotaxic atlases. Anatomically, this work allowed to obtain a reference definition of the tVTA through its neurochemical, stereological, connectivity-based and genomic analyses. Functionally, we studied its role for the response of aversive stimuli and we tested its influence on motor and non-motor symptoms of Parkinson’s disease. We observed that a co-lesion of the tVTA in a rodent model of the disease induce motor, nociceptive and depressive-like symptoms improvements. This work has thus contributed to the progress of our knowledge on the tVTA and opens new explorative track for its functional implication
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Baudonnat, Mathieu. "Rôle des récompenses dans la sélection et l'utilisation de différentes formes de mémoire : interactions entre l'hippocampe et le striatum." Thesis, Bordeaux 1, 2011. http://www.theses.fr/2011BOR14392/document.
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Il existe différents types de mémoire chez l’homme et l’animal. Chez les mammifères, on distingue principalement une mémoire relationnelle/spatiale reposant sur l’hippocampe et le cortex préfrontal, et une mémoire procédurale/indicée dépendante du striatum. Lors de nouveaux apprentissages, ces systèmes interagissent de manière coopérative et/ou compétitive en fonction de la nature de la tâche. S’il est connu que les émotions négatives et le niveau d’entraînement modulent ces interactions, peu de travaux ont étudié le rôle des récompenses dans la sélection et l’utilisation de ces deux formes principales de mémoire. Nous avons utilisé deux versions du test de discrimination spatiale dans un labyrinthe en Y afin de d’évaluer la mémoire spatiale d’une part, et la mémoire procédurale d’autre part. Nos résultats montrent que la stimulation pharmacologique du système de récompense par auto-injection de morphine au niveau de l’aire tegmentale ventrale (ATV), perturbe de manière spécifique l’apprentissage spatial reposant sur le fonctionnement hippocampo-préfrontal Ce déficit spatial s’accompagne d’une forte réduction de l’activité du facteur de transcription CREB (cAMP Response Element Binding) au sein de ce réseau. Au contraire, l’apprentissage indicé est préservé et l’activation de CREB est potentialisée par l’utilisation d’une récompense pharmacologique (injections de morphine). Nous mettons en évidence que la suractivation de la voie PKA/CREB, dans le striatum dorsal, est la cause de l’interférence observée lors de la formation de la mémoire spatiale. De plus, la stimulation répétée du système de récompense par la drogue lors de l’acquisition d’une stratégie indicée entraîne une persistance de l’activité réverbérante de la voie PKA/CREB dans le striatum dorsal. Cette persistance peut être révélée par l’utilisation préférentielle d’une stratégie indicée dans une nouvelle tâche ambigüe, le test de compétition en piscine de Morris. L’ensemble de ce travail éclaire, grâce aux effets différentiels de récompenses sensorielles et pharmacologiques sur l’apprentissage, la compréhension des interactions dynamiques entre les systèmes de mémoire. De plus, il suggère que l’hyperassociativité persistante consécutive à l’usage de drogue est à l’origine de déficits de type déclaratifs qui pourraient jouer un rôle clé dans l’installation d’un comportement addictifThere are different forms of memory proceeded in human’s and animal’s brain. At least two major systems can be defined. A spatial/declarative form of memory relies on the hippocampus and prefrontal cortex, and secondly, a more rigid, procedural/cued type of memory supported by striatal circuitry. Learning requires cooperative and/or competitive interactions between memory systems, depending on the nature of the task. It is well established that negative emotions and training modulate these interactions. However, little is known about the role of rewards on the selection and formation of these forms of memory.Using two versions (spatial or cue) of a Y-maze discrimination task, we show that drug reward, but not food reward, disrupts spatial learning while sparing the cued task. The spatial memory deficit relies on an decrease of CREB (cAMP Response Element Binding) activity within the hippocampus and the prefrontal cortex. Inhibition of the PKA/CREB signalling pathway restored spatial learning, suggesting that striatal overactivation of this pathway is responsible for the spatial memory deficit. The cued learning strategy elicits a strong CREB activitiy within the dorsal striatum which is further increased by morphine injections. We propose that drug-induced activation of the DA reward system induces abnormal reverberating activity of the PKA/CREB signalling pathway within the dorsal striatum, eventually leading to a preferential use of a striatum-dependent strategy during a new ambiguous learning task, the water maze competition task.In conclusion, our results points to a key role of rewards in the modulation of learning systems. Furthermore, we provide evidence that drug-induced striatal hyperactivity may underlie the declarative memory deficit reported here. This mechanism could represent an important early step toward the development of addictive behaviors by promoting conditioning to the detriment more flexible forms of memory
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Vitay, Julien, and Fred H. Hamker. "Timing and expectation of reward: a neuro-computational model of the afferents to the ventral tegmental area." Universitätsbibliothek Chemnitz, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:ch1-qucosa-147898.
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Neural activity in dopaminergic areas such as the ventral tegmental area is influenced by timing processes, in particular by the temporal expectation of rewards during Pavlovian conditioning. Receipt of a reward at the expected time allows to compute reward-prediction errors which can drive learning in motor or cognitive structures. Reciprocally, dopamine plays an important role in the timing of external events. Several models of the dopaminergic system exist, but the substrate of temporal learning is rather unclear. In this article, we propose a neuro-computational model of the afferent network to the ventral tegmental area, including the lateral hypothalamus, the pedunculopontine nucleus, the amygdala, the ventromedial prefrontal cortex, the ventral basal ganglia (including the nucleus accumbens and the ventral pallidum), as well as the lateral habenula and the rostromedial tegmental nucleus. Based on a plausible connectivity and realistic learning rules, this neuro-computational model reproduces several experimental observations, such as the progressive cancelation of dopaminergic bursts at reward delivery, the appearance of bursts at the onset of reward-predicting cues or the influence of reward magnitude on activity in the amygdala and ventral tegmental area. While associative learning occurs primarily in the amygdala, learning of the temporal relationship between the cue and the associated reward is implemented as a dopamine-modulated coincidence detection mechanism in the nucleus accumbens.
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Glangetas, Christelle. "The Bed Nucleus of the Stria Terminalis between Stress and Reward." Thesis, Bordeaux, 2014. http://www.theses.fr/2014BORD0419/document.
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L’objectif principal de mon projet de thèse a été d’identifier les mécanismes neuronaux adaptatifs se mettant en place au niveau des circuits de la récompense et des circuits activés en réponse à un stress aigu. Plus spécifiquement, nous avons étudié le rôle du noyau du lit de la strie terminale (BNST) au sein de ces deux circuits. Mon hypothèse est que le BNST appartient à un circuit de structures interconnectées dans lequel il intègre des informations contextuelles (hippocampe ventral) et des informations émotionnelles (cortex préfrontal médian) afin, d’une part, de réguler les niveaux d’anxiété innés ainsi que les réponses induites par les centres du stress suite à un épisode de stress aigu mais également, d’adapter l’activité des neurones dopaminergiques de l’aire tegmentale ventrale (VTA) en vue de motiver ou d’empêcher la reproduction d’un comportement associé à un stimulus récompensant ou aversif. Afin de tester cette hypothèse, nous avons mis en place et développé différents projets de recherche combinant des approches d’électrophysiologie in vivo, anatomiques et comportementales. Dans un premier temps, nous nous sommes intéressés au BNST en tant que structure clef participant à la régulation des centres de stress. Grâce à l’utilisation d’approches d’électrophysiologie in vivo chez la souris anesthésiée, nous avons montré qu’après l’exposition à un stress aigu, les neurones du BNST adaptent leur réponse suite à la stimulation du cortex préfrontal médian et passent d’une dépression à long terme (LTD) en situation contrôle à une potentialisation à long terme (LTP) après un stress aigu. Nous avons disséqué une partie des mécanismes permettant l’élaboration de ces plasticités grâce à l’utilisation de souris génétiquement modifiés pour le récepteur aux endocannabinoïdes de type 1 (CB1-R). Ainsi, nous avons trouvé que la LTD et la LTP mis en place dans le BNST sont médiées par le système endocannabinoïde via les récepteurs CB1. Ensuite, nous avons étudié le rôle du ventral subiculum (vSUB) dans la régulation des neurones du BNST ainsi que l’impact de l’activation de cette voie vSUB-BNST sur l’autre voie glutamatergique ILCx-BNST. Tout d’abord, nous avons montré par des approches électrophysiologiques et anatomiques, qu’un même neurone du BNST est capable d’intégrer des informations provenant à la fois du ventral subiculum et du cortex infralimbic (ILCx). Nous avons induit in vivo une LTP NMDA dépendante dans la voie vSUB-BNST suite à un protocole de stimulation haute fréquence dans le vSUB alors qu’en parallèle ce même protocole induit une LTD sur ces mêmes neurones dans la voie ILCx–BNST. Deplus, nous avons noté que ces adaptations plastiques se mettant en place dans le BNST suiteà une simple stimulation haute fréquence dans le vSUB permettent à long terme de diminuerles niveaux d’anxiété innés chez le rat. Enfin, nous avons mis en évidence que le BNST est un relai excitateur entre le vSUBet la VTA. Nous avons montré qu’une stimulation à haute fréquence dans le vSUBpotentialise in vivo l’activité des neurones dopaminergiques (DA) de la VTA. Or le vSUBne projette pas de manière directe sur les neurones DA de la VTA. Nous avons observé quece protocole de stimulation haute fréquence dans le vSUB induit dans un premier temps uneLTP NMDA dépendante dans les neurones du BNST projetant à la VTA qui est nécessairepour observer cette potentialisation des neurones DA. En dernier lieu, nous avons montréque cette potentialisation des neurones DA de la VTA augmente la réponse locomotrice à unchallenge avec de la cocaine.Ainsi, l’ensemble de ces projets nous ont permis de confirmer et de préciser lafonction majeure du BNST dans la régulation du stress et de l’anxiété ainsi que dans lecircuit de la motivationThe main goal of my PhD was to identify the adaptive neuronal mechanismsdeveloping in the reward circuit and in the circuit implicated in the regulation of stressresponses. More specifically, we have studied the function of the bed nucleus of the striaterminalis (BNST) in both circuits.My hypothesis was that, the BNST belongs to interconnected circuits in whichintegrates contextual (from ventral hippocampus) and emotional informations (from medialprefrontal cortex). Thus, the BNST diffuses these informations in order to regulate the basalinnate level of anxiety and stress centers responses induced after acute stress exposure, butalso to adapt the activity of dopaminergic neurons of the ventral tegmental area (VTA) thatcan promote or prevent a behavioral task associated with a rewarding or aversive stimulus.To test this hypothesis, we decided to develop several research projects usingelectrophysiological, anatomical and behavioral approaches.Firstly, we focused our interest on the stress circuit in which the BNST is a keystructure which participates in regulating the responses of stress centers after acute stressexposure. By using in vivo electrophysiology approach in anesthetized mice, we haveshown that after acute restraint stress, BNST neurons adapt their plastic responses inducedby the tetanic stimulation of the medial prefrontal cortex: switch from long term depression(LTD) under control condition to long term potentiation (LTP) after acute stress condition.Furthermore, we demonstrated that both LTD and LTP are endocannabinoid dependent byusing genetic modified mice for the type 1 endocannabinoid receptors and localpharmacological approach in the BNST.In a second step, we studied the function of the ventral subiculum (vSUB) in theregulation of BNST neurons and the impact of the vSUB-BNST pathway activation on theother glutamatergic ILCx-BNST pathway. In a first set of experiments, we showed that asame single BNST neuron could integrate informations from both vSUB and the infralimbiccortex. By using high frequency stimulation (HFS) protocols, we induced in vivo NMDAdependentLTP in the vSUB-BNST pathway whereas the same protocol led to LTD in thesame BNST neurons in the ILCx-BNST pathway. Moreover, we noted single application ofHFS protocol in the vSUB induced a long term decrease of the basal innate level of anxietyin rats.Lastly, we presented the BNST as a key excitatory relay between the vSUB and theVTA. Here, we have shown that in vivo HFS protocols in the vSUB potentiate the activity ofdopaminergic (DA) neurons of the VTA. However, the vSUB does not directly project to theVTA. We observed that a HFS protocol in the vSUB first induce NMDA-dependent LTP inBNST neurons that project to the VTA, which is necessary to promote the potentiation of7VTA DA neurons. In the last step, we demonstrated in vivo that the potentiation of VTA DAneurons increases the locomotor response to cocaine challenge.All together, these projects allow us to confirm and detail the major function of theBNST in the regulation of stress and anxiety and also in the motivational circuit
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Sheppard, Ashley B. "Role of the Ventral Tegmental Area and Ventral Tegmental Area Nicotinic Acetylcholine Receptors in the Incentive Amplifying Effect of Nicotine." Digital Commons @ East Tennessee State University, 2014. https://dc.etsu.edu/etd/2362.
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Nicotine has multiple behavioral effects as a result of its action in the central nervous system. Nicotine strengthens the behaviors that lead to nicotine administration (primary reinforcement), and this effect of nicotine depends on mesotelencephalic systems of the brain that are critical to goal directed behavior, reward, and reinforcement. Nicotine also serves as a ‘reinforcement enhancer’ – drug administration enhances behaviors that lead to other drug and nondrug reinforcers. Although the reinforcement enhancing effects of nicotine may promote tobacco use in the face of associated negative health outcomes, the neuroanatomical systems that mediate this effect of nicotine have never been described. The ventral tegmental area (VTA) is a nucleus that serves as a convergence point in the mesotelencephalic system, plays a substantial role in reinforcement by both drug and nondrug rewards and is rich in both presynaptic and postsynaptic nicotinic acetylcholine receptors (nAChRs). Therefore, these experiments were designed to determine the role of the VTA and nAChR subtypes in the reinforcement enhancing effect of nicotine. Transiently inhibiting the VTA with a gamma amino butyric acid (GABA) agonist cocktail (baclofen and muscimol) reduced both primary reinforcement by a visual stimulus and the reinforcement enhancing effect of nicotine, without producing nonspecific suppression of activity. Intra-VTA infusions of a high concentration of mecamylamine a nonselective nAChR antagonist, or methylycaconitine, an α7 nAChR antagonist, did not reduce the reinforcement enhancing effect of nicotine. Intra-VTA infusions of a low concentration of mecamylamine and dihydro-beta-erythroidine (DHβE), a selective antagonist of nAChRs containing the *β2 subunit, attenuated, but did not abolish, the reinforcement enhancing effect of nicotine. In follow-up tests replacing systemic nicotine injections with intra-VTA infusions (70mM, 105mM) resulted in complete substitution of the reinforcement enhancing effects – increases in operant responding were comparable to giving injections of systemic nicotine. These results suggest that *β2-subunit containing nAChRs in the VTA play a role in the reinforcement enhancing effect of nicotine. However, when nicotine is administered systemically these reinforcement enhancing effects may depend on the action of nicotine at nAChRs in multiple brain nuclei.
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Baimel, Corey. "Orexin modulation of ventral tegmental area dopamine neurons." Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/58211.
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Dopamine neurons in the ventral tegmental area (VTA) are critically involved in the expression of motivated behaviour. The activity of dopamine neurons is regulated by intrinsic conductances and by synaptic inputs, both of which are subject to neuromodulatory influences. This thesis explores how orexin signalling alters the synaptic regulation and the activity of VTA dopamine neurons. Chapter 1 describes a role for dopamine in motivated behaviour and highlights how drugs of abuse alter synaptic transmission in the mesocorticolimbic dopamine system to drive compulsive reward seeking. Moreover, it outlines how lateral hypothalamic orexin projections to the VTA alter synaptic transmission onto dopamine neurons to promote motivated behaviour. Chapter 2 examines how orexin signalling gates morphine-induced synaptic plasticity in the VTA. We demonstrate that inhibiting orexin receptor signalling in the VTA blocks morphine-induced increases and decreases in the strength of excitatory and inhibitory synaptic transmission respectively. Orexin neurons coexpress the inhibitory peptide dynorphin and the two are likely coreleased. In chapter 3 we demonstrate that orexin and dynorphin modulate the activity of dopamine neurons in a projection-target specific manner. Orexin preferentially increased the output of dopamine neurons that project to the lateral shell of the nucleus accumbens (NAc), while dynorphin was more effective at inhibiting the activity of dopamine neurons that project to the basolateral amygdala (BLA). Chapter 4 discusses the strength and weaknesses of these experiments and proposes future research to further enhance our understanding of orexin modulation of VTA dopamine neurons.Medicine, Faculty of
Anesthesiology, Pharmacology and Therapeutics, Department of
Graduate
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Reisiger, Anne-Ruth. "Pathologie du système de récompense : effets à long terme d’une exposition chronique à la nicotine et au sucrose." Thesis, Bordeaux 1, 2013. http://www.theses.fr/2013BOR14870/document.
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La prise volontaire de nicotine augmente l'excitabilité de la voie ILCx-BNST, entraînant une hyperactivité des neurones DA de l’ATV. Dans une première partie, l'objectif était d’étudier les neuroadaptations de la voie ILCx-BNST induites par l'auto-administration intraveineuse (AAIV) de nicotine. Les récepteurs cannabinoides CB1 contrôlent les propriétés renforçantes de la nicotine. Par conséquent, nous avons examiné le rôle des récepteurs CB1 du BNST. Nous montrons que l'acquisition de l’AAIV de nicotine est associée à une facilitation persistante de l'induction d’une potentialisation à long terme (LTP) CB1-dépendantes des synapses ILCx-BNST. La stimulation électrique du ILCx favorise également la persistance du comportement de recherche de nicotine pendant les périodes où la drogue n'est pas disponible. En outre, en utilisant la pharmacologie intra-BNST, nous montrons que la stimulation des récepteurs CB1 du BNST au cours de l’acquisition de lAAIV augmente la sensibilité aux stimuli associés à la nicotine. L’idée qu’il existe un appétit incontrôlable pour les aliments palatables, en dépit des conséquences négatives. Dans une seconde partie, notre projet a porté sur le rôle des neurones dopaminergiques (DA) de l’ATV dans la perception d’un stimulus aversif chez l’animal exposé au sucrose. Nos résultats indiquent que le sucrose augmente l'activité spontanée des neurones DA de la VTA. En outre, si un choc électrique provoque une inhibition presque complète de l'activité de VTA neurones DA chez les rats témoins, le sucrose perturbe la signalisation d'un stimulus aversif, indépendamment de l’état calorique du ratLearning mechanisms associated with active responding for nicotine enhanced the excitability of the ILCx-BNST pathway. The objective of this project was to better understand the involvement of the ILCx-BNST pathway in nicotine self-administration. Since the endocannabinoid system controls nicotine reinforcement and nicotine-induced synaptic modifications, we examined the role of CB1 receptors in the BNST. We showed that acquisition of nicotine IVSA was associated with a persistent facilitation of LTP induction at ILCx-BNST synapses. Behaviorally, electrical stimulation temporarily increased excessive responding to nicotine when nicotine was not available. Moreover, using intra-BNST pharmacology, we revealed that stimulation of BNST CB1 receptors enhanced sensitivity to nicotine-paired cue. In contrast, after a prolonged history of nicotine intake, it blocked drug-seeking in a reinstatement model of relapse. Drug addiction is partly due to the inability to stop using despite negative consequences. The hypothesis that palatable food induces similar uncontrolled consumption is becoming more widespread. As drug addiction is known to increases activity of VTA DA neurons, we aimed to examine whether exposure to sucrose would induce similar neuronal modifications and impair the capacity to respond to an aversive stimulus. We found that sucrose enhanced spontaneous activity of DA VTA neurons. In addition, while a footshock caused a nearly complete inhibition of activity of VTA DA neurons in control rats, sucrose disrupted signaling of an aversive stimulus. These modifications were independent from the caloric state of the rats
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Williams, Stephanie Bair. "Neuroimmune-Mediated Alcohol Effects on Ventral Tegmental Area Neurons." BYU ScholarsArchive, 2018. https://scholarsarchive.byu.edu/etd/7326.
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Dopamine (DA) transmission is a key player in the rewarding aspects of ethanol as well as ethanol dependence. The current dogma is that DA transmission is increased during ethanol via the inhibition of ventral tegmental area (VTA) GABA neurons and that excitation of VTA GABA neurons during withdrawal results in decreased DA transmission. Microglia, the major neuroimmune effector in the brain, may be a key mediator in this process by releasing cytokines following activation. We evaluated the effect of ethanol on cytokine concentrations in the VTA and NAc using a cytometric bead array, and found that low dose ethanol (1.0 g/kg) decreased interleukin (IL)-10 levels, but high dose ethanol increased IL-10 levels (4.0 g/kg). We also used standard cell-attached mode electrophysiological techniques to evaluate the effects of select cytokines on VTA neuron firing rate in vitro. We found no change in firing rate in response to IL-6, but an increase in firing rate in VTA DA neurons response to IL-10. Consistent with the changes in firing rate, optically-evoked IPSCs were also found to be decreased in response to IL-10. Ex vivo voltammetry and in vivo microdialysis were done to determine whether IL-10 can directly result in an increase in DA release. Although ex vivo voltammetry showed no change in DA release, IL-10 increased DA release in vivo. These findings suggest that the rewarding and/or addictive effects of ethanol are mediated by cytokines, specifically the anti-inflammatory cytokine IL-10.
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Taylor, Amanda Lee. "Elucidating the fear - maintaining properties of the Ventral Tegmental Area." Thesis, University of Canterbury. Psychology, 2008. http://hdl.handle.net/10092/2853.
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The ventral tegmental area (VTA) and its dopaminergic (DA) mesocorticolimbic projections are thought to be essential in the brain’s reward neurocircuitry. In humans and animal experimental subjects, mild electrical VTA stimulation increases dopamine levels and can induce euphoria. Paradoxically, aversive stimuli activate VTA neurons and forebrain DA activity, and excessive electrical stimulation of the VTA exaggerates fearfulness. Research suggests that experimental manipulation of either the amygdala or the VTA has similar effects on the acquisition and expression of Pavlovian conditioned fear. Recently it was demonstrated that electrical stimulation of the amygdala produced fear extinction deficits in rats. Fear extinction involves the progressive dissipation of conditioned fear responses by repeated non-reinforced exposure to a conditioned stimulus (CS). Maladaptive states of fear in fear-related anxiety disorders, such as post-traumatic stress disorders (PTSD) or specific phobias are thought to reflect fear extinction learning deficits. The primary purpose of the present study was to examine the effects of intra-VTA stimulation on fear extinction learning. Using fear-potentiated startle as a behavioural index of conditioned fear, it was found that 120 VTA stimulations paired or unpaired with non-reinforced CS presentations impaired the extinction of conditioned fear. This effect was not apparent in rats that received electrical stimulation of the substantia nigra (SN), suggesting that not all midbrain regions respond similarly. Electrical stimulation parameters did not have aversive affects because rats failed to show fear conditioning when electrical VTA stimulation was used as the unconditioned stimulus. Also, VTA stimulation did not alter conditioned fear expression in non-extinguished animals. Based on the results it is suggested that VTA activation disinhibited conditioned fear responding. Therefore, VTA neuronal excitation by aversive stimuli may play a role in fear-related anxiety disorders thought to reflect extinction learning deficits.
Books on the topic "Ventrale tegmentale Area"
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van Domburg, Peter Henricus Maria Franciscus, and Hendrik Jan ten Donkelaar. The Human Substantia Nigra and Ventral Tegmental Area. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75846-1.
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Donkelaar, H. J. ten 1946-, ed. The human substantia nigra and ventral tegmental area: A neuroanatomical study with notes on aging and aging diseases. Berlin: Springer-Verlag, 1990.
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Laviolette, Steven R. Identification of a GABAa receptor-mediated opiate addiction switch in the mammalian ventral tegmental area. 2002.
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The Human Substantia Nigra and Ventral Tegmental Area: A Neuroanatomical Study with Notes on Aging and Aging Diseases. Springer, 2012.
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Peter H.M.F. van Domburg and Hendrik J. ten Donkelaar. The Human Substantia Nigra and Ventral Tegmental Area: A Neuroanatomical Study with Notes on Aging and Aging Diseases. Springer Verlag, 1991.
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Modir, Shahla J., and George E. Muñoz. The Future of Addiction and Recovery Healing Arts. Edited by Shahla J. Modir and George E. Muñoz. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190275334.003.0032.
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This chapter peers into the future of addiction treatment. It begins with an exploration of repetitive transcranial magnetic brain stimulation or rTMS as a treatment for SUD. The evidence and clinical data is reviewed. Findings include outcome data on the use of rTMS. Furthermore, important brain regions central to the development of SUD are examined: the ventral tegmental area and ventral striatum appear to play a central role in the binge/intoxication stage, the extended amygdala in the withdrawal/negative affect stage, and the orbitofrontal cortex-dorsal striatum, prefrontal cortex, basolateral amygdala, hippocampus, and insula in craving. The role of genomics and gene-wide associations to deliver future personalized addiction treatments is discussed as is advanced functional neural imaging. Technology for patients and consumers, including relapse prevention apps and bidirectional biometric reading is mentioned. Breakthroughs in addiction immunology, both generalized and substance specific, are discussed as potential points of future study and interventions.
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Peter Henricus M. F. Van Domburg, H. J. Ten Donkelaar, and P. H. M. F. Van Domburg. The Human Substantia Nigra and Ventral Tegmental Area: A Neuroanatomical Study With Notes on Aging and Aging Diseases (Advances in Anatomy, Embryology and Cell Biology). Springer, 1991.
Find full textBook chapters on the topic "Ventrale tegmentale Area"
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Pentel, Paul R., Mark G. LeSage, Mark G. LeSage, Paul R. Pentel, Lawrence H. Price, Tomasz Schneider, Maria-Inés López-Ibor, et al. "Ventral Tegmental Area." In Encyclopedia of Psychopharmacology, 1359. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_760.
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Block, Michelle L. "Ventral Tegmental Area of Midbrain." In Encyclopedia of Clinical Neuropsychology, 3567. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_373.
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Block, Michelle L. "Ventral Tegmental Area of Midbrain." In Encyclopedia of Clinical Neuropsychology, 2597–98. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_373.
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Block, Michelle L. "Ventral Tegmental Area of Midbrain." In Encyclopedia of Clinical Neuropsychology, 1. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56782-2_373-2.
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van Domburg, Peter Henricus Maria Franciscus, and Hendrik Jan ten Donkelaar. "The Human Substantia Nigra and Ventral Tegmental Area." In Advances in Anatomy Embryology and Cell Biology, 32–69. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75846-1_4.
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Beckstead, Robert M., Valerie B. Domesick, and Walle J. H. Nauta. "Efferent Connections of the Substantia Nigra and Ventral Tegmental Area in the Rat." In Neuroanatomy, 449–75. Boston, MA: Birkhäuser Boston, 1993. http://dx.doi.org/10.1007/978-1-4684-7920-1_22.
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Corrigall, W. A. "Self-Administered Nicotine Acts Through the Ventral Tegmental Area: Implications for Drug Reinforcement Mechanisms." In Effects of Nicotine on Biological Systems II, 203–9. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-7445-8_26.
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Borgland, Stephanie L. "Effects of Orexin/Hypocretin on Ventral Tegmental Area Dopamine Neurons: An Emerging Role in Addiction." In Narcolepsy, 241–51. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-8390-9_22.
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Alasmari, Fawaz, Naif O. Al-Harbi, Mohammed M. Alanazi, Abdullah F. Alasmari, and Youssef Sari. "Memory Dysfunction Correlates with the Dysregulated Dopaminergic System in the Ventral Tegmental Area in Alzheimer’s Disease." In Application of Biomedical Engineering in Neuroscience, 85–98. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-7142-4_5.
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Rinne, Juha O., L. Paljärvi, J. Rummukainen, M. Röyttä, and U. K. Rinne. "Neuronal Loss in the Substantia Nigra and Ventral Tegmental Area in Parkinson’s Disease and Alzheimer’s Disease." In Basic, Clinical, and Therapeutic Aspects of Alzheimer’s and Parkinson’s Diseases, 377–80. Boston, MA: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4684-5844-2_77.
Full textConference papers on the topic "Ventrale tegmentale Area"
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Hakimi, Shabnam, Jeffrey MacInnes, Kathryn Dickerson, and Alison Adcock. "Temporal structure of learning to regulate ventral tegmental area using real-time fMRI neurofeedback." In 2018 Conference on Cognitive Computational Neuroscience. Brentwood, Tennessee, USA: Cognitive Computational Neuroscience, 2018. http://dx.doi.org/10.32470/ccn.2018.1204-0.
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"Transcriptional profiling of ventral tegmental area of male mice with alternative patterns of social behaviors." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-057.
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Chen, T. Y., A. Dragomir, D. Zhang, Y. Akay, and M. Akay. "Prefrontal cortex deletion affects the dopaminergic neural firing complexity in nicotine-treated ventral tegmental area." In 2010 32nd Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC 2010). IEEE, 2010. http://dx.doi.org/10.1109/iembs.2010.5626088.
Full textReports on the topic "Ventrale tegmentale Area"
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Bonci, Antonello. Plasticity of GABAergic Synapses in the Ventral Tegmental Area During Withdrawal from In Vivo Ethanol Administration. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada407409.
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