ANALYSIS OF INDIVIDUAL RABBIT OLFACTORY BULB NEURON RESPONSES TO THE MICROELECTROPHORESIS OF ACETYLCHOLINE, NOREPINEPHRINE AND SEROTONIN SYNERGISTS AND ANTAGONISTS

¹ Clinical Neuropharmacology Research Center, National Institute of Mental Health, and Laboratory of Chemical Pharmacology, National Heart Institute, National Institutes of Health at Saint Elizabeths Hospital, Washington, D. C.

The reduction of spontaneous discharge rate of olfactory neurons by electrophoretic administrations of ACh, NE or 5-HT to individual nerve cells has been investigated in unanesthetized rabbits. Electrophoretic administration of dihydro--erythroidine, atropine, hexamethonium and chlorisondamine to ACh-sensitive units, blocked their response to ACh. Physostigmine prolonged the duration of the ACh response. Dihydro--erythroidine specifically blocked the effects of ACh, but not of NE or 5-HT administration. Both the ACh blocking agents and physostigmine temporarily suppressed discharge rate regardless of ACh responsiveness.

Electrophoretic administration of NE and 5-HT always resulted in slowing of the unit’s spontaneous discharge. Similar responses were seen after administration of tyramine and metaraminol. Dibenamine and phentolamine specifically blocked NE responses and did not interfere with the responses of 5-HT. LSD-25 and BOL-148 did interfere with responses to 5-HT, but never without prior or concurrent blockade of responses to NE. The spontaneous discharge rate was at times increased after the unit’s response to NE was blocked by Dibenamine.

The ability of ACh, NE or 5-HT to slow spontaneous discharge rate was qualitatively unchanged 4 hours after local administration or intravenous injections of reserpine or 7 to 11 days after intravenous injection of -MMT, suggesting that the amines are not dependent for their effect upon intact brain stores of NE, 5-HT or dopamine. In -MMT treated rabbits, the effect of tyramine was not apparent until after electrophoresis of NE.