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• W2170264841 abstract "Whole-cell patch-clamp recordings of non-N-methyl-d-aspartate glutamatergic excitatory postsynaptic currents (EPSCs) were carried out from cholinergic neurons in slices of basal forebrain (BF) of developing rats aged 21-42 postnatal days to elucidate postnatal developmental change in Ca(2+) channel subtypes involved in the transmission as well as that in dopamine D(1)-like receptor-mediated presynaptic inhibition. The amplitude of EPSCs was inhibited by bath application of omega-conotoxin GVIA (omega-CgTX; 3 microM) or omega-agatoxin-TK (omega-Aga-TK; 200 nM) throughout the age range examined, suggesting that multiple types of Ca(2+) channel are involved in the transmission. The EPSC fraction reduced by omega-CgTX decreased with age, whereas that reduced by omega-Aga-TK increased. Inhibition of the EPSCs by a D(1)-like receptor agonist, SKF 81297 (SKF; 30 microM) increased with age in parallel with the increase in omega-Aga-TK-induced inhibition. An activator of the adenylyl cyclase (AC) pathway, forskolin (FK; 10 microM) inhibited the EPSCs, and FK-induced inhibition also increased with age in parallel with the increase in SKF-induced inhibition. Throughout the age range examined, SKF showed no further inhibitory effect on the EPSCs after omega-Aga-TK- or FK-induced effect had reached steady-state. These findings suggest that D(1)-like receptor-mediated presynaptic inhibition of glutamate release onto cholinergic BF neurons increases with age, and that the change is coupled with a developmental increase in the contribution of P/Q-type Ca(2+) channels as well as a developmental increase in AC pathway contribution." @default.
• W2170264841 created "2016-06-24" @default.
• W2170264841 creator A5088889563 @default.
• W2170264841 date "2010-07-06" @default.
• W2170264841 modified "2023-09-27" @default.
• W2170264841 title "Developmental increase in D1-like dopamine receptor-mediated inhibition of glutamatergic transmission through P/Q-type channel regulation in the basal forebrain of rats" @default.
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• W2170264841 doi "https://doi.org/10.1111/j.1460-9568.2010.07306.x" @default.
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