Developmental increase in D1-like dopamine receptor-mediated inhibition of glutamatergic transmission through P/Q-type channel regulation in the basal forebrain of rats.
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.
Momiyama
Toshihiko
T
Division of Cerebral Structure, National Institute for Physiological Sciences, Okazaki 444-8787, Japan. tmomi@jikei.ac.jp
D060848:Agatoxins; D000818:Animals; D001552:Benzazepines / Q000494:pharmacology; D020865:Calcium Channels, P-Type / Q000378:metabolism*; D020907:Calcium Channels, Q-Type / Q000378:metabolism*; D004298:Dopamine / Q000378:metabolism; D018491:Dopamine Agonists / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D018698:Glutamic Acid / Q000378:metabolism*; D007097:Imines / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D016548:Prosencephalon / Q000187:drug effects / Q000254:growth & development* / Q000378:metabolism*; D051381:Rats; D017447:Receptors, Dopamine D1 / Q000378:metabolism*; D013111:Spider Venoms / Q000494:pharmacology; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D020866:omega-Conotoxin GVIA / Q000494:pharmacology
D060848:Agatoxins; D001552:Benzazepines; D020865:Calcium Channels, P-Type; D020907:Calcium Channels, Q-Type; D018491:Dopamine Agonists; D007097:Imines; D017447:Receptors, Dopamine D1; D013111:Spider Venoms; C083855:omega-agatoxin-Aa4b; D018698:Glutamic Acid; C067113:SK&F 81297; C014925:RMI 12330A; D020866:omega-Conotoxin GVIA; D004298:Dopamine