Programmable nanoampere constant current sources for iontophoresis.
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A group of neurons in the pigeon's lateral geniculate equivalent nucleus (LGNe) shows associative enhancement of their response to light during visually conditioned heart rate change. The source of the relevant unconditioned stimulus input to LGNe for this enhancement has been identified as the locus coeruleus (LC). Thus, we have begun to examine neurotransmitters synthesized in LC for possible involvement in associative modification of neuronal discharge in LGNe. As a first step, we have examined the responses of LGNe neurons to iontophoretic application of norepinephrine (NE) and identified the receptor mediating one response class. The majority of neurons in LGNe show inhibition of maintained activity in response to iontophoretic application of NE or its agonists. The potency of the NE agonists is alpha-methyl NE greater than epinephrine greater than NE greater than phenylephrine greater than isoproterenol. This profile is characteristic of an alpha 2-adrenoceptor. The alpha 2-agonist clonidine also induces inhibition of maintained activity. The alpha 2-antagonists WB-4101 and yohimbine block the NE-inhibition while the alpha 1-antagonist prazosin and beta-antagonist sotalol do not. It is thus suggested that the receptor mediating the NE-inhibition of maintained activity has the characteristics of an alpha 2-adrenoceptor.
Responses of paraventricular nucleus (PVN) neurones were examined following stimulation of the sciatic nerve, and concomitant with iontophoretic application of cortisol. Sciatic nerve stimulation excited the majority of cells (22/24, 92%) and iontophoretic application of cortisol reduced the spontaneous activity of 16 of the cells tested (67%). Cortisol prevented neuronal responses to sciatic nerve stimulation in 11 cases (50%) but some of the cells inhibited by the steroid still responded to the stimulation, whilst some cells unaffected by cortisol alone were found not to respond during exposure to the stimulus. These results indicate an inhibitory role for glucocorticoids in the regulation of PVN neuronal activity and responses to afferent neural stimuli.