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- W1997132021 abstract "The ventral tegmental area (VTA) is required for the rewarding and motivational actions of opioids and activation of dopamine neurons has been implicated in these effects. The canonical model posits that opioid activation of VTA dopamine neurons is indirect, through inhibition of GABAergic inputs. However, VTA dopamine neurons also express postsynaptic μ-opioid peptide (MOP) receptors. We report here that in Sprague Dawley rat, the MOP receptor-selective agonist DAMGO (0.5–3 μ m ) depolarized or increased the firing rate of 87 of 451 VTA neurons (including 22 of 110 dopamine neurons). This DAMGO excitation occurs in the presence of GABA A receptor blockade and its EC 50 value is two orders of magnitude lower than for presynaptic inhibition of GABA release on to VTA neurons. Consistent with a postsynaptic channel opening, excitations were accompanied by a decrease in input resistance. Excitations were blocked by CdCl 2 (100 μ m , n = 5) and ω-agatoxin-IVA (100 n m , n = 3), nonselective and Ca v 2.1 Ca 2+ channel blockers, respectively. DAMGO also produced a postsynaptic inhibition in 233 of 451 VTA neurons, including 45 of 110 dopamine neurons. The mean reversal potential of the inhibitory current was −78 ± 7 mV and inhibitions were blocked by the K + channel blocker BaCl 2 (100 μ m , n = 7). Blockade of either excitation or inhibition unmasked the opposite effect, suggesting that MOP receptors activate concurrent postsynaptic excitatory and inhibitory processes in most VTA neurons. These results provide a novel direct mechanism for MOP receptor control of VTA dopamine neurons." @default.
- W1997132021 created "2016-06-24" @default.
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- W1997132021 date "2014-10-29" @default.
- W1997132021 modified "2023-09-25" @default.
- W1997132021 title "Direct Bidirectional μ-Opioid Control of Midbrain Dopamine Neurons" @default.
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- W1997132021 doi "https://doi.org/10.1523/jneurosci.2144-14.2014" @default.
- W1997132021 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4212068" @default.
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