Pharmacologic sensitivity of amino acid responses and synaptic activation of in vitro prepyriform neurons

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Abstract
In an effort to identify the neurotransmitter released from terminals of the lateral olfactory tract (LOT), the exitatory amino acid agonist and antagonist actions were studied on population and single-unit responses in submerged and perfused slices of rat prepyriform cortex. Previous studies suggest that the transmitter at this synapse is either Asp or Glu. The field potential reflecting the monosynaptic activation of pyramidal neurons after stimulation of the LOT was reversibly depressed by bath perfusion of agonists, with an order of potency being kainic acid (KA) > N-methyl-DL-aspartate (NMDA) > homocysteic acid (HC) > Asp = Glu. The synaptic field potential was essentially unaffected by DL-.alpha.-aminoadipic acid (AA), 2-amino-3-phosphonopropionic acid (APP) and DL-.alpha.-diaminopimelic acid (DAPA), all presumed to be selective for Asp receptors, and by L-glutamic acid diethyl ester (GDEE), presumed to be specific for Glu receptors. The field potential was depressed or abolished by 2-amino-4-phosphonobutyric acid (APB), an agent known to block Glu responses in insect muscle. The effects of ionophoretic application of agonists were studied on single neurons recorded extracellularly. While there was some variability among neurons in relative agonist potency, all neurons were excited by the 5 agonists with relative potencies in general similar to those observed for the field potentials. Responses to Glu and Asp were unaffected by AA, GDEE and APB at concentrations up to 5 .times. 10-3 M. Responses to KA, NMDA and HC were often depressed by APB but were unaffected by the other antagonists. The excitation on stimulation of the LOT was consistently, rapidly and reversibly blocked by APB. These observations are not consistent with either Glu or Asp being the neurotransmitter of the LOT.