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Journal of Neurophysiology, Vol 55, Issue 6 1295-1307, Copyright © 1986 by APS
ARTICLES |
D. C. McIntyre and R. K. Wong
The evoked and spontaneous activity of neurons in the pyriform cortex of control and kindled rats was examined using a coronal slice preparation containing the amygdala-pyriform region. Electrical stimulation of the amygdala nuclei elicited synchronized burst responses in pyriform cells of slices from both control and kindled animals. The mean duration of the burst was greatly prolonged in cells from kindled preparations. The depolarizing synaptic events underlying the burst response in the kindled and control animals could be examined when Mg2+ was increased to suppress but not block synaptic transmission. Electrical stimulation evoked a short-latency graded synaptic depolarization, followed by a long-latency all-or-none depolarizing event, which appeared to be involved in generating the burst response. Norepinephrine (NE), in a 4-microM concentration, reversibly blocked the burst responses in the control preparation. Burst responses elicited from kindled preparations were also suppressed by NE. For the latter cases, higher concentrations of NE were required to produce this effect. The alpha-2-agonist clonidine mimicked the suppressive action of NE on the evoked events. In contrast the beta-agonist isoproterenol facilitated the occurrence of spontaneous synchronous bursts and prolonged evoked burst discharges in both the control and kindled preparations. NE and clonidine block the burst response by suppressing the underlying synaptic events. The facilitatory action of isoproterenol on spontaneous and evoked responses suggests that NE may also exert an excitatory effect.
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