ELECTRICAL-STIMULATION OF THE RAT PERIVENTRICULAR NUCLEUS INFLUENCES THE ACTIVITY OF HYPOTHALAMIC ARCUATE NEURONS

Citation
Si. Dickson et al., ELECTRICAL-STIMULATION OF THE RAT PERIVENTRICULAR NUCLEUS INFLUENCES THE ACTIVITY OF HYPOTHALAMIC ARCUATE NEURONS, Journal of neuroendocrinology, 6(4), 1994, pp. 359-367
Citations number
26
Categorie Soggetti
Neurosciences,"Endocrynology & Metabolism
ISSN journal
09538194
Volume
6
Issue
4
Year of publication
1994
Pages
359 - 367
Database
ISI
SICI code
0953-8194(1994)6:4<359:EOTRPN>2.0.ZU;2-8
Abstract
In rats, the release of growth hormone (GH) is inhibited during electr ical stimulation of the periventricular nucleus but after the end of s timulation, there is a rebound 'hypersecretion' of GH. We examined the responses of arcuate neurones in pentobarbitone-anaesthetized male ra ts, following electrical stimulation of the periventricular nucleus to test the hypothesis that the effects of periventricular nucleus stimu lation on GH secretion are mediated via effects upon GH-releasing horm one (GRF) neurones in the arcuate nucleus. The electrical activity of 2 groups of arcuate neurones were analysed before, during and after pe riventricular nucleus stimulation (10 Hz, 5 min, 0.5 mA biphasic, 0.5/ 1.0 ms): a) putative neurosecretory cells which were antidromically id entified (AD) as projecting to the median eminence (n = 53) and b) non -neurosecretory cells, identified by their spontaneous 'bursting' patt ern of activity (n = 29), During stimulation predominantly inhibitory responses were observed in both AD and bursting cell groups. Of the 39 AD cells which were spontaneously active, 25 were inhibited during th e periventricular nucleus stimulation, and 10 of these showed a reboun d hyperactivation following the end of stimulation. Fifteen bursting c ells were inhibited during stimulation and 4 of these displayed a rebo und hyperactivation following the end of stimulation. Additional evide nce was sought for the identity of these cells by testing their respon se to electrical stimulation of the basolateral amygdala (which has pr eviously been shown to increase plasma GH concentration without influe ncing the release of other pituitary hormones). Six of the 10 AD cells which displayed the inhibition/rebound response to periventricular nu cleus stimulation were also excited following electrical stimulation o f the basolateral amygdala. We conclude that 1) electrical stimulation of the periventricular nucleus and the basolateral amygdala exert pre dominantly inhibitory and excitatory effects respectively upon the act ivity of arcuate neurones but for neither site were the effects of sti mulation exclusively upon GRF neurones, and 2) the rebound hypersecret ion of GH following PeN stimulation is likely to involve the rebound a ctivation of arcuate neurones.