Evidence for an agonist independent down regulation of hippocampal muscarinic receptors in kindling.
Kindling induces a decline of hippocampal muscarinic cholinergic receptors. To test the hypthesis that the decline was mediated by the agonist, acetylcholine, adult male Sprague--Dawley rats were lesioned in the medial septum prior to kindling. Despite the marked destruction of presynaptic cholinergic terminals in the hippocampus, amygdala kindling proceeded normally and the hippocampal muscarinic receptor decline was not blocked. A small but significant decline in choline acetyltransferase activity was demonstrated in non-lesioned kindled rats. It is proposed that the kindling induced decline of hippocampal muscarinic receptors is mediated by repeated neuronal depolarization.
D000109:Acetylcholine / Q000502:physiology*; D000679:Amygdala / Q000502:physiology; D000818:Animals; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D004558:Electric Stimulation; D006624:Hippocampus / Q000502:physiology*; D008297:Male; D009434:Neural Pathways / Q000502:physiology; D011813:Quinuclidinyl Benzilate / Q000378:metabolism; D051381:Rats; D011950:Receptors, Cholinergic / Q000502:physiology*; D011976:Receptors, Muscarinic / Q000502:physiology*; D012640:Seizures / Q000503:physiopathology*; D012686:Septal Nuclei / Q000502:physiology
D011950:Receptors, Cholinergic; D011976:Receptors, Muscarinic; D011813:Quinuclidinyl Benzilate; D002795:Choline O-Acetyltransferase; D000109:Acetylcholine