Relevant bibliographies by topics / Ventral tegmental area (VTA)

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Ventral tegmental area (VTA)'

Author: Grafiati
Published: 4 June 2021
Last updated: 4 February 2022

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Journal articles on the topic "Ventral tegmental area (VTA)"

1

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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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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Kalivas, P. W., and R. Richardson-Carlson. "Endogenous enkephalin modulation of dopamine neurons in ventral tegmental area." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 251, no. 2 (August 1, 1986): R243—R249. http://dx.doi.org/10.1152/ajpregu.1986.251.2.r243.

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Many lines of evidence support the possibility that the opioid pentapeptides Met- and Leu-enkephalin can modulate dopamine neurons in the ventral tegmental area (VTA). Thus microinjection of enkephalin analogues into the VTA of rats produces a dopamine-dependent increase in spontaneous motor activity and an increase in dopamine metabolism in certain mesolimbic dopamine terminal fields, such as the nucleus accumbens. To determine if these effects can be produced by endogenous enkephalins, an enkephalinase A inhibitor, thiorphan, was microinjected into the VTA to inhibit enkephalin metabolism. Thiorphan produced a dose-dependent (0.3-3.33 micrograms) increase in spontaneous motor activity that was blocked by pretreatment with the opioid antagonist naloxone (2.0 mg/kg ip) or the dopamine antagonist haloperidol (0.1 mg/kg ip). Thiorphan injection into the VTA increased dopamine metabolism in the nucleus accumbens, prefrontal cortex, and septum but not in the striatum. In all brain regions the increase in dopamine metabolism was blocked by pretreatment with naloxone. These data demonstrate that endogenous enkephalin in the VTA can increase the activity of A10 dopamine neurons, supporting a physiological role for enkephalin in mesolimbic and mesocortical dopamine-mediated behaviors.
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Hung, Lin W., Sophie Neuner, Jai S. Polepalli, Kevin T. Beier, Matthew Wright, Jessica J. Walsh, Eastman M. Lewis, et al. "Gating of social reward by oxytocin in the ventral tegmental area." Science 357, no. 6358 (September 28, 2017): 1406–11. http://dx.doi.org/10.1126/science.aan4994.

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The reward generated by social interactions is critical for promoting prosocial behaviors. Here we present evidence that oxytocin (OXT) release in the ventral tegmental area (VTA), a key node of the brain’s reward circuitry, is necessary to elicit social reward. During social interactions, activity in paraventricular nucleus (PVN) OXT neurons increased. Direct activation of these neurons in the PVN or their terminals in the VTA enhanced prosocial behaviors. Conversely, inhibition of PVN OXT axon terminals in the VTA decreased social interactions. OXT increased excitatory drive onto reward-specific VTA dopamine (DA) neurons. These results demonstrate that OXT promotes prosocial behavior through direct effects on VTA DA neurons, thus providing mechanistic insight into how social interactions can generate rewarding experiences.
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Simmons, DeNard V., Alyssa K. Petko, and Carlos A. Paladini. "Differential expression of long-term potentiation among identified inhibitory inputs to dopamine neurons." Journal of Neurophysiology 118, no. 4 (October 1, 2017): 1998–2008. http://dx.doi.org/10.1152/jn.00270.2017.

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The in vivo firing pattern of ventral tegmental area (VTA) dopamine neurons is controlled by GABA afferents originating primarily from the nucleus accumbens (NAc), rostromedial tegmental nucleus (RMTg), and local GABA neurons within the VTA. Although different forms of plasticity have been observed from GABA inputs to VTA dopamine neurons, one dependent on cyclic GMP synthesis and the other on adenylyl cyclase activation, it is unknown whether plasticity is differentially expressed in each. Using an optogenetic strategy, we show that identified inhibitory postsynaptic currents (IPSCs) from local VTA GABA neurons and NAc afferents exhibit a cyclic GMP-dependent long-term potentiation (LTP) that is capable of inhibiting the firing activity of dopamine neurons. However, this form of LTP was not induced from RMTg afferents. Only an adenylyl cyclase-mediated increase in IPSCs was exhibited by all three inputs. Thus discrete plasticity mechanisms recruit overlapping but different subsets of GABA inputs to VTA dopamine neurons. NEW & NOTEWORTHY We describe a mapping of plasticity expression, mediated by different mechanisms, among three distinct GABA afferents to ventral tegmental area (VTA) dopamine neurons: the rostromedial tegmental nucleus, the nucleus accumbens, and the local GABA neurons within the VTA known to synapse on VTA dopamine neurons. This work is the first demonstration that discrete plasticity mechanisms recruit overlapping but different subsets of GABA inputs to VTA dopamine neurons.
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Lepack, Ashley E., Craig T. Werner, Andrew F. Stewart, Sasha L. Fulton, Ping Zhong, Lorna A. Farrelly, Alexander C. W. Smith, et al. "Dopaminylation of histone H3 in ventral tegmental area regulates cocaine seeking." Science 368, no. 6487 (April 9, 2020): 197–201. http://dx.doi.org/10.1126/science.aaw8806.

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Vulnerability to relapse during periods of attempted abstinence from cocaine use is hypothesized to result from the rewiring of brain reward circuitries, particularly ventral tegmental area (VTA) dopamine neurons. How cocaine exposures act on midbrain dopamine neurons to precipitate addiction-relevant changes in gene expression is unclear. We found that histone H3 glutamine 5 dopaminylation (H3Q5dop) plays a critical role in cocaine-induced transcriptional plasticity in the midbrain. Rats undergoing withdrawal from cocaine showed an accumulation of H3Q5dop in the VTA. By reducing H3Q5dop in the VTA during withdrawal, we reversed cocaine-mediated gene expression changes, attenuated dopamine release in the nucleus accumbens, and reduced cocaine-seeking behavior. These findings establish a neurotransmission-independent role for nuclear dopamine in relapse-related transcriptional plasticity in the VTA.
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Chen, Li, and Daniel J. Lodge. "The lateral mesopontine tegmentum regulates both tonic and phasic activity of VTA dopamine neurons." Journal of Neurophysiology 110, no. 10 (November 15, 2013): 2287–94. http://dx.doi.org/10.1152/jn.00307.2013.

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Anatomic studies have demonstrated that the mesolimbic dopamine system receives a substantial afferent input from a variety of regions ranging from the prefrontal cortex through to the brain stem. However, how these afferents regulate dopamine neuron activity is still largely unknown. The mesopontine tegmentum provides a significant input to ventral tegmental area (VTA) dopamine neurons, and it has been demonstrated that discrete subdivisions within this region differentially alter dopamine neuron activity. Thus the laterodorsal tegmental nucleus provides a tonic input essential for maintaining burst firing of dopamine neurons, whereas the pedunculopontine tegmental (PPTg) nucleus regulates a transition from single-spike firing to burst firing. In contrast, the recently identified rostromedial tegmental nucleus provides an inhibitory input to the VTA and decreases spontaneous dopamine neuron activity. Here, we demonstrate that an area adjacent to the PPTg regulates both population activity as well as burst firing of VTA dopamine neurons. Specifically, N-methyl-d-aspartic acid (NMDA) activation of the lateral mesopontine tegmentum produces an increase in the number of spontaneously active dopamine neurons and an increase in the average percentage of burst firing of dopamine neurons. This increase in neuronal activity was correlated with extracellular dopamine efflux in the nucleus accumbens, as measured by in vivo microdialysis. Taken together, we provide further evidence that the mesopontine tegmentum regulates discrete dopamine neuron activity states that are relevant for the understanding of dopamine system function in both normal and disease states.
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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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Brodie, M. S., and E. B. Bunney. "Serotonin potentiates dopamine inhibition of ventral tegmental area neurons in vitro." Journal of Neurophysiology 76, no. 3 (September 1, 1996): 2077–82. http://dx.doi.org/10.1152/jn.1996.76.3.2077.

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1. The ventral tegmental area (VTA) has been implicated in both the rewarding effects of drugs of abuse and the etiology of schizophrenia. We report here that serotonin (5-HT) potentiates the inhibitory effect of dopamine on dopaminergic VTA neurons. Dopamine (0.5-10 microM) inhibited the spontaneous firing of putative dopamine-containing neurons of the VTA. 5-HT (5-10 microM) itself did not significantly alter the spontaneous firing rate; however, in the presence of 5-HT, the inhibitory potency of dopamine was significantly increased. 2. The inhibitory potency of the dopamine agonist quinpirole was also increased by 5-HT. 3. 5-HT-induced potentiation was also produced by the selective 5-HT2 agonist (+/-)-2,5-dimethoxy-4-iodoamphetamine, and was reversed by the selective 5-HT2 antagonist ketanserin. 4. This novel action of 5-HT on dopaminergic neurons has important implications for the development of drugs to treat schizophrenia, and for the identification of agents that will be useful in treating drug abuse disorders like alcoholism.
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Dissertations / Theses on the topic "Ventral tegmental area (VTA)"

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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.
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Weed, Jared Mark. "Endocannabinoid-Dependent Long-Term Depression of Ventral Tegmental Area GABA Neurons." BYU ScholarsArchive, 2013. https://scholarsarchive.byu.edu/etd/4287.

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GABA neurons in the ventral tegmental area of the midbrain are important components in the brain's reward circuit. Long term changes in this circuit occur through the process of synaptic plasticity. It has been shown that high frequency stimulation, as well as treatment with endocannabinoids, can cause GABA neurons in the ventral tegmental area to undergo long term depression, a form of synaptic plasticity that decreases excitability of cells. The present study elaborates on the mechanism whereby high frequency stimulation can result in long term depression of ventral tegmental area GABA neurons. Using the whole cell patch clamp technique in acute brain slices, we recorded excitatory currents from ventral tegmental area GABA neurons in GAD-GFP expressing CD1 mice and observed how the excitatory currents changed in response to different treatments. We confirm that high frequency stimulation causes long term depression, and the cannabinoid type 1 receptor antagonist AM-251 blocks this effect. Long term depression is also elicited by treatment with the cannabinoid type 1 receptor agonist 2-arachidonylglycerol. It is inconclusive whether treatment with 2-arachidonylglycerol occludes further long term depression by high frequency stimulation. We also demonstrate that activation of group I metabotropic glutamate receptors by DHPG produces long term depression. These results support the model that at these excitatory synapses, high frequency stimulation causes the release of glutamate from presynaptic terminals, activating group I metabotropic glutamate receptors, causing production of 2-arachidonylglycerol. 2-arachidonylglycerol in turn acts on presynaptic cannabinoid type 1 receptors to decrease release of glutamate onto GABA neurons. This model can be tested by further research, which should include cannabinoid type 1 receptor knockout mice. This study provides more insight into how drugs of abuse such as tetrahydrocannabinol, the active component of marijuana that activate cannabinoid type I receptors, can corrupt the natural reward mechanisms of the brain.
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Sandoval, Philip J. "Long-Term Depression of Excitatory Inputs to GABAergic Neurons in the Ventral Tegmental Area." BYU ScholarsArchive, 2012. https://scholarsarchive.byu.edu/etd/3911.

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Dopamine cells within the ventral tegmental area of the brain are involved in motivation and reward. Drugs of abuse target these dopamine cells altering their activity and plasticity resulting in addiction. While dopamine cell activity is primarily involved in addiction, the GABA neurons in the VTA have also been shown to have an indirect role. By decreasing the activity of the inhibitory GABA inputs onto dopamine neurons abusive drugs can indirectly increase dopamine cell activity resulting in addictive behaviors. However, although GABA neurons are important in the perception of reward, much less is known about how the excitatory inputs to these cells are regulated and possibly altered by drugs of abuse. Using transgenic mice expressing GFP attached to the GAD promoter, GABA cells were located and patched using whole cell voltage clamp and EPSCs were measured. High frequency stimulation induced LTD of the excitatory inputs to GABA neurons. The endocannabinoid analogue R- methanandamide also induced LTD at these excitatory synapses. These results suggest that endocannabinoids could potentially regulate the activity of GABA cells and as a result the activity of dopamine neurons. The endocannabinoid receptor involved is likely CB1, but not TRPV1 as only the CB1 antagonist AM-251 blocked this high frequency stimulus-induced LTD. Future research could then determine if the pathways involved in this LTD could potentially be altered by drugs of abuse contributing to addiction.
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Taylor, Devin Hardy. "The Effects of Acute and Chronic Nicotine on GABA and Dopamine Neurons in the Midbrain Ventral Tegmental Area." BYU ScholarsArchive, 2011. https://scholarsarchive.byu.edu/etd/2951.

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Nicotine (NIC) abuse involves activation of midbrain dopamine (DA) neurons and NIC addiction involves neuroadaptive changes in the mesolimbic DA reward system. GABA neurons in the midbrain ventral tegmental area (VTA) express α4β2-containing nicotinic acetylcholine receptors (nAChRs), whose activation increases GABAergic input to DA neurons. However, this initial effect is decreased after chronic NIC treatment (as in the case of smokers) by inducing nAChR desensitization. Thus, GABA neuron inhibition results in increased DA release in limbic structures such as the nucleus accumbens. To support this hypothesis, we evaluated the effects of acute and chronic NIC on GAD-67 positive neurons in the VTA of GAD GFP mice using in vivo and in vitro electrophysiological methods. In in vivo studies in naïve mice, stimulation of the peduncopontine tegmental nucleus (PPT) activated VTA GABA neurons orthodromically and antidromically. Orthodromic activation of VTA GABA neuron spikes by PPT stimulation was blocked by the nAChR mecamylamine (1 mg/kg). Acute systemic NIC (0.15-0.5 mg/kg IV) had mixed overall effects on VTA GABA neuron firing rate, but in situ microelectrophoretic application of NIC produced a brisk and consistent enhancement (200-500 %) of VTA GABA neuron firing rate that showed no acute tolerance or sensitization with repeated, periodic current application. Local NIC activation was blocked by systemic administration of mecamylamine. Compared to 12 day chronic saline injections, chronic NIC injections (2 mg/kg IP/day) significantly increased VTA GABA neuron firing rate. In in vitro studies, compared to 12 day chronic saline injections, chronic NIC injections decreased DA neuron firing rate. In addition, chronic NIC increased DA neuron, but decreased GABA neuron GABA-mediated sIPSCs. These findings demonstrate that there is reciprocal innervation between the PPT and VTA and that cholinergic input from the PPT is excitatory on VTA GABA neurons. Moreover, VTA GABA neurons are excited by acute NIC and sensitize to chronic NIC, suggesting that α4β2 nAChR subunits on these neurons may play an important role in the adaptations to chronic NIC. Thus, quantitative molecular studies are ongoing to determine specific alterations in nAChRs on VTA GABA neurons to chronic NIC.
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Allison, David Wilbanks. "Cocaine and Mefloquine-induced Acute Effects in Ventral Tegmental Area Dopamine and GABA Neurons." BYU ScholarsArchive, 2009. https://scholarsarchive.byu.edu/etd/2362.

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The aim of the two studies presented here was to evaluate the effects of cocaine and mefloquine (MFQ) on γ-aminobutyric acid (GABA) and dopamine (DA) neurons in the ventral tegmental area (VTA). Cocaine: In vivo, lower doses of intravenous cocaine (0.25-0.5 mg/kg), or methamphetamine (METH), enhanced VTA GABA neuron firing rate via D2/D5 receptor activation. Higher cocaine doses (1.0-2.0 mg/kg) inhibited their firing rate. Cocaine and lidocaine inhibited the firing rate and spike discharges induced by stimulation of the internal capsule (ICPSDs) at dose levels 0.25-2 mg/kg (IC50 1.2 mg/kg), but neither DA nor METH reduced ICPSDs. In VTA GABA neurons in vitro, cocaine reduced (IC50 13 µM) current-evoked spikes and sodium currents in a use-dependent manner. In VTA DA neurons, cocaine reduced IPSCs (IC50 13 µM), increased IPSC paired-pulse facilitation, and decreased sIPSC frequency, without affecting mIPSC frequency or amplitude. These findings suggest cocaine reduces activity-dependent GABA release on DA neurons in the VTA, and that cocaine's use-dependent blockade of VTA GABA neuron voltage-sensitive sodium channels (VSSCs) may synergize with its DAT inhibiting properties to enhance mesolimbic DA transmission implicated in cocaine reinforcement. Mefloquine: Mefloquine (MFQ) is an anti-malarial agent, Connexin-36 (Cx36) gap junction blocker, 5-HT3 antagonist, and calcium ionophore. Mounting evidence of a Cx36-mediated VTA GABA neuron syncytium suggests MFQ-related dysphoria may attribute to its gap junction blocking effects on VTA synaptic homeostasis. We observed that MFQ (25 µM) increased DA neuron spontaneous IPSC frequency 6 fold, and mIPSC 3 fold. Carbenoxolone (CBX, 100 µM) only increased sIPSC frequency 2 fold, and did not affect DA mIPSC frequency. Ondansetron did not mimic MFQ. Additionally, MFQ did not affect VTA DA evoked IPSC paired pulse ratio (PPR). However, Mefloquine did induce a 3.5 fold increase in bath-applied GABA current. Remarkably, MFQ did not affect VTA GABA neuron inhibition. At VTA DA neuron excitatory synapses MFQ increased sEPSC frequency in-part due to an increase in the AMPA/NMDA ratio. These finding suggest MFQ alters VTA synapses differentially depending on neuron and synapse type, and that these alterations appear to involve MFQ's gap junction blocking and calcium ionophore actions.
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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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Ferreira, Jozélia Gomes Pacheco. "Organização das projeções da área tegmental ventral para o complexo VTA-substância negra e para o hipotálamo no rato e estudo da expressão dos substratos do receptor de insulina em neurônios da VTA que se projetam para o estriado." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/42/42137/tde-25032010-144241/.

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Numa primeira etapa, estudamos as conexões da VTA para o complexo VTA-substância negra (SN) utilizando a leucoaglutinina do Phaseolus vulgaris (PHA-L). Estas conexões são substanciais, topograficamente organizadas, com destaque para o pólo caudal da VTA que inerva bilateralmente toda a extensão deste complexo. Numa segunda etapa, estudamos as projeções da VTA para o hipotálamo. A VTA se projeta principalmente para a área pré-óptica lateral e área hipotalâmica lateral, a região subfornical posterior e o núcleo dorsomedial. Foram vistas poucas aposições entre varicosidades PHA-L+ e neurônios imunorreativos para orexina ou para hormônio concentrador de melanina. Por fim, estudamos a colocalização do substrato do receptor de insulina (IRS-1), IRS-1 fosforilado e fosfatidilinositol-3 quinase (PI3K) com tirosina hidroxilase (TH) ou com a subunidade B da toxina colérica (CTb) injetada no estriado. A maioria dos neurônios TH+ da VTA-SN expressa IRS-1; injeções de CTb no estriado resultaram em células duplamente marcadas para CTb/IRS-1, CTb/PI3K e CTb/IRS-1 fosforilado.
In a first step, we studied the connections of the VTA to the complex VTA-substantia nigra (SN) using the Phaseolus vulgaris leucoagglutinin (PHA-L). These connections are substantial, topographically organized, especially the caudal pole of the VTA, which innervates bilaterally throughout the length of this complex. In a second step, we studied the projections of the VTA to the hypothalamus. The VTA projected mainly to the lateral preoptic area, lateral hypothalamic area, posterior subfornical region and dorsomedial nucleus. Were observed few appositions between PHA-L+ varicosities and neurons immunoreactive for orexin or melanin-concentrating hormone. Finally, we studied the co-localization of the insulin receptor substrate-1 (IRS-1), IRS-1-phosphorylated and phosphatidylinositol-3 kinase (PI3K) with tyrosine hydroxylase (TH) or cholera toxin B subunit (CTb) injected into the striatum. Most TH+ neurons of the VTA-SN expressed IRS-1; CTb injections in the striatum resulted in cells double-labeled for CTb/IRS-1, CTb/PI3K and CTb/IRS-1 phosphorylated.
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Degroot, Steven R. "The Role of Mesointerpeduncular Circuitry in Anxiety." eScholarship@UMMS, 2019. https://escholarship.umassmed.edu/gsbs_diss/1060.

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Anxiety is an affective state defined by heightened arousal and unease in the absence of a clear and present fear-inducing stimulus. Chronic and inappropriate anxiety leads to anxiety disorders, the most common class of human mental disorder. Recent work suggests projections to the ventral tegmental area (VTA), are critical for anxiety behavior expression. However, the relationship between efferent VTA projections and anxiety is unclear. This thesis resolves anxiety circuitry connecting the dopaminergic (DAergic) VTA to the interpeduncular nucleus (IPN), coined the mesointerpeduncular circuit. I hypothesize the mesointerpeduncular circuit affects anxiety through the release of anxiogenic corticotropin releasing factor (CRF) during nicotine withdrawal and anxiolytic dopamine (DA) during drug naïve behavior. Electrophysiological and pharmacological data suggest CRF release from the DAergic VTA during nicotine withdrawal activates CRF receptor 1 (CRFR1) potentiating the glutamatergic activation of “Type 2” neurons and anxiety-like behavior in mice. However, in nicotine naïve conditions CRF production is negligible. Instead, in vivo DA release is anticorrelated with anxiety-like behaviors. Optogenetic stimulation and inhibition drives decreased and increased anxiety-like behaviors, respectively. Electrophysiological experiments reveal a complex interpeduncular microcircuit where D1-like DA receptor expressing “Type C” neurons in the caudal IPN (cIPN) regulate glutamatergic release in the ventral IPN (vIPN) through presynaptic GABA receptors. The result is propagation of the signal to excite “Type A” and inhibit “Type B” vIPN neurons. Finally, pharmacological activation or inhibition of interpeduncular D1-like DA receptors is sufficient to decrease and increase anxiety-like behaviors respectively. Thus, this circuit is important for modulating anxiety-like behavior.
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9

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 motivation
The 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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Books on the topic "Ventral tegmental area (VTA)"

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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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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.

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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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Book chapters on the topic "Ventral tegmental area (VTA)"

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Nishino, Seiji, and Noriaki Sakai. "Modulations of Ventral Tegmental Area (VTA) Dopaminergic Neurons by Hypocretins/Orexins: Implications in Vigilance and Behavioral Control." In Dopamine and Sleep, 65–89. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-46437-4_5.

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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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Conference papers on the topic "Ventral tegmental area (VTA)"

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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.

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Reports on the topic "Ventral tegmental area (VTA)"

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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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