| First Author | Chen M | Year | 2015 |
| Journal | Elife | Volume | 4 |
| PubMed ID | 26208338 | Mgi Jnum | J:226331 |
| Mgi Id | MGI:5697100 | Doi | 10.7554/eLife.09275 |
| Citation | Chen M, et al. (2015) Morphine disinhibits glutamatergic input to VTA dopamine neurons and promotes dopamine neuron excitation. Elife 4 |
| abstractText | One reported mechanism for morphine activation of dopamine (DA) neurons of the ventral tegmental area (VTA) is the disinhibition model of VTA-DA neurons. Morphine inhibits GABA inhibitory neurons, which shifts the balance between inhibitory and excitatory input to VTA-DA neurons in favor of excitation and then leads to VTA-DA neuron excitation. However, it is not known whether morphine has an additional strengthening effect on excitatory input. Our results suggest that glutamatergic input to VTA-DA neurons is inhibited by GABAergic interneurons via GABAB receptors and that morphine promotes presynaptic glutamate release by removing this inhibition. We also studied the contribution of the morphine-induced disinhibitory effect on the presynaptic glutamate release to the overall excitatory effect of morphine on VTA-DA neurons and related behavior. Our results suggest that the disinhibitory action of morphine on presynaptic glutamate release might be the main mechanism for morphine-induced increase in VTA-DA neuron firing and related behaviors. |
