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Both in vivo and ex vivo electrophysiological studies of VTA neurons have been instrumental in forwarding our understanding of motivation and reinforcement, however, approximately 45% of VTA neurons are not DAergic [1].
The results suggest that activation of VTA 5-HT1B receptors increases mesolimbic DA neuron activities.
However, little is known about the effect of methylphenidate (MPD) on the electrophysiological properties of VTA and NAc neurons.
Opioid inhibition of GABA neurons in these sites is hypothesized to lead to arousing and rewarding effects through disinhibition of VTA DA neurons.
The increased DA neuron activity may be associated, at least in part, with the 5-HT1B receptor-mediated inhibitiof of VTA GABA release.
After cell-cycle exit, Sox6 selectively localizes to SNc neurons, while Otx2 and Nolz1 are expressed in a subset of VTA neurons.
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Identification of VTA-DA neurons in rats.
(A ) Electrophysiological properties of VTA-DA neurons.
Vglut2 was identified as gene targeted (knocked out) within all three populations of VTA-VGLUT2 neurons.
(A ) Effect of morphine on spontaneous firing of VTA-DA neurons.
To test whether morphine has a disinhibitory effect on the presynaptic glutamate release of VTA-DA neurons, the presence of an inhibitory circuit from neighboring GABA neurons to the presynaptic glutamatergic terminals of VTA-DA neurons must first be demonstrated.
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