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
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.