Inactivation of ventral tegmental area influences long term potentiation in the rat hippocampus

Previous work has shown that a single dose of cocaine can produce long-term potentiation (LTP) of the glutamatergic synapses received by dopamine neurons in the ventral tegmental area (VTA). This and other plastic changes in the brain's reward circuitry have been suggested to underlie addiction. A recent study has provided new insights into cocaine-induced LTP, showing that it begins 3–5 h after exposure, requires activation of a dopamine D5/NMDA receptor cascade, and can be evoked by cocaine application directly to the VTA.

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Dopamine and reward seeking: the role of ventral tegmental area

Reviews in the Neurosciences ◽

10.1515/revneuro-2014-0019 ◽

2014 ◽

Vol 0 (0) ◽

Cited By ~ 8

Author(s):

Robert Ranaldi

Keyword(s):

Ventral Tegmental Area ◽

Long Term Potentiation ◽

Positive Relation ◽

Conditioned Stimuli ◽

Neurochemical Mechanisms ◽

Reward Seeking ◽

Term Potentiation ◽

Ventral Tegmental

AbstractReward seeking is controlled by conditioned stimuli (CSs). There is a positive relation between mesocorticolimbic dopamine (DA) and the performance of learned reward-directed behavior. The mechanisms by which reward-, including drug-, associated stimuli come to acquire the capacity to activate the DA systems are not fully understood. In this review, we discuss the possible neurochemical mechanisms within the ventral tegmental area that may be involved in how CSs acquire the capacity to activate ventral tegmental area (VTA) DA neurons based on principles of long-term potentiation in the VTA and the role of mesocorticolimbic DA in reward-related learning. We propose that CSs function as such because they acquire the capacity to activate VTA DA neurons. Furthermore, CSs come to acquire this control of VTA DA cells when there is coincident

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Ethanol Blocks Long-Term Potentiation of GABAergic Synapses in the Ventral Tegmental Area Involving μ-Opioid Receptors

Neuropsychopharmacology ◽

10.1038/npp.2010.51 ◽

2010 ◽

Vol 35 (9) ◽

pp. 1841-1849 ◽

Cited By ~ 33

Author(s):

Yan-zhong Guan ◽

Jiang-Hong Ye

Keyword(s):

Ventral Tegmental Area ◽

Opioid Receptors ◽

Long Term Potentiation ◽

Term Potentiation ◽

Gabaergic Synapses ◽

Ventral Tegmental ◽

Μ Opioid Receptors

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High-Frequency Afferent Stimulation Induces Long-Term Potentiation of Field Potentials in the Ventral Tegmental Area

Neuropsychopharmacology ◽

10.1038/sj.npp.1301561 ◽

2007 ◽

Vol 33 (7) ◽

pp. 1704-1712 ◽

Cited By ~ 17

Author(s):

Fereshteh S Nugent ◽

Alison R Hwong ◽

Yoko Udaka ◽

Julie A Kauer

Keyword(s):

Ventral Tegmental Area ◽

High Frequency ◽

Long Term Potentiation ◽

Field Potentials ◽

Afferent Stimulation ◽

Term Potentiation ◽

Ventral Tegmental

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Spike Timing-Dependent Long-Term Potentiation in Ventral Tegmental Area Dopamine Cells Requires PKC

Journal of Neurophysiology ◽

10.1152/jn.01384.2007 ◽

2008 ◽

Vol 100 (1) ◽

pp. 533-538 ◽

Cited By ~ 31

Author(s):

Percy Luu ◽

Robert C. Malenka

Keyword(s):

Protein Kinase ◽

Ventral Tegmental Area ◽

Drugs Of Abuse ◽

Long Term Potentiation ◽

Spike Timing ◽

Term Potentiation ◽

Nmdar Activation ◽

Ventral Tegmental ◽

Underlying Mechanisms

Long-term potentiation (LTP) of excitatory synapses on ventral tegmental area (VTA) dopamine (DA) cells is thought to play an important role in mediating some of the behavioral effects of drugs of abuse yet little is known about its underlying mechanisms. We find that spike timing-dependent LTP (STD LTP) in VTA DA cells is absent in slices prepared from mice previously administered cocaine, suggesting that cocaine-induced LTP and STD LTP share underlying mechanisms. This form of STD LTP is dependent on NMDA receptor (NMDAR) activation and a rise in postsynaptic calcium but surprisingly was not affected by an inhibitor of calcium/calmodulin-dependent protein kinase II (CaMKII). It was blocked by antagonists of conventional isoforms of PKC, whereas activation of protein kinase C (PKC) using a phorbol ester enhanced synaptic strength. These results suggest that NMDAR-mediated activation of PKC, but not CaMKII, is a critical trigger for LTP in VTA DA cells.

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