Asymmetric distribution of acetylcholine receptors and M channels on prepyriform neurons.
The responses of pyramidal neurons of rat prepyriform cortex to ionophoretic application of acetylcholine (ACh) were studied in a submerged, perfused brain slice. ACh excited some neurons but only if applied to an area near to the cut surface of the slice. This area contained the basal dendrites of the pyramidal cells and some cell bodies. No excitation was seen if ACh was applied at depths of 250 microns or more from the cut surface, an area which contained only apical dendrites, although the apical dendrites were very sensitive to excitatory amino acids such as aspartate (Asp) and glutamate (Glu). On all neurons which did not discharge to ionophoretic application of ACh, ACh potentiated the response to Glu and Asp. No potentiation of amino acid responses was obtained on apical dendrites. The potentiation had a time course similar to that of the discharge of neurons which fired to ACh. This observation suggests that pyramidal neurons have receptors for ACh on basal but not apical dendrites. The ACh response in the basal dendrite-soma region was elicted by pilocarpine and blocked by atropine but not curare. This was true whether the response studied was direct excitation or potentiation of the response to an amino acid. The ACh response was associated with a voltage-dependent increase in membrane resistance which had a slow time course and appeared to be due to a turning off of an M current, as described by Brown and Adams (1980) in sympathetic ganglion cells. The effects of ACh were minimal at the resting potential but increased with depolartization. ACh had no effect on the current-voltage relation of the cell, except at depolarized potentials of less than -60 mV. Ionophoretic application of Ba2+ to the basal dendritic region resulted in potentiation of the amino acid responses and sometimes induced a discharge similar to that of ACh. Since Ba2+ mimics the ACh response, presumably by a direct blockade of the M channel, the effects of Ba2+ on apical dendrites were tested to determine whether these dendrites contain M channels associated with a transmitter receptor other than ACh. However, Ba2+ did not induce potentiation in apical dendrites, suggesting that M channels are also restricted to the basal dendrites or cell bodies.(ABSTRACT TRUNCATED AT 400 WORDS)
D000109:Acetylcholine / Q000494:pharmacology*; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001224:Aspartic Acid / Q000494:pharmacology; D001931:Brain Mapping; D002118:Calcium / Q000502:physiology; D002540:Cerebral Cortex / Q000502:physiology*; D005971:Glutamates / Q000494:pharmacology; D018698:Glutamic Acid; D006710:Homocysteine / Q000031:analogs & derivatives / Q000494:pharmacology; D010862:Pilocarpine / Q000494:pharmacology; D051381:Rats; D011950:Receptors, Cholinergic / Q000502:physiology*; D011976:Receptors, Muscarinic / Q000502:physiology
D005971:Glutamates; D011950:Receptors, Cholinergic; D011976:Receptors, Muscarinic; D010862:Pilocarpine; D006710:Homocysteine; C007956:homocysteic acid; D001224:Aspartic Acid; D018698:Glutamic Acid; D000109:Acetylcholine; D002118:Calcium