Effects of acetylcholine on sodium-dependent high-affinity glutamate transport in rat striatal homogenates.
Incubation of rat striatal tissue in the presence of acetylcholine, carbachol, oxotremorine, or nicotine results in a significant decrease in the sodium-dependent high-affinity glutamate uptake (HAGU). The cholinergic inhibitory effect on glutamate transport is no more detectable in the presence of atropine, a cholinergic receptor antagonist. These data support the hypothesis that glutamatergic nerve ending activity in the striatum is modulated by cholinergic neurons. The effects would involve both muscarinic and nicotinic presynaptic receptors located on the corticostriatal glutamatergic terminals.
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001692:Biological Transport / Q000187:drug effects; D002217:Carbachol / Q000494:pharmacology; D003342:Corpus Striatum / Q000187:drug effects / Q000378:metabolism*; D005971:Glutamates / Q000378:metabolism*; D018698:Glutamic Acid; D007700:Kinetics; D008297:Male; D009538:Nicotine / Q000494:pharmacology; D010095:Oxotremorine / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000494:pharmacology*
D005971:Glutamates; D018698:Glutamic Acid; D010095:Oxotremorine; D009538:Nicotine; D001285:Atropine; D002217:Carbachol; D012964:Sodium; D000109:Acetylcholine