Oxytocin and ADH secretion in relation to electrical activity in antidromically identified supraoptic and paraventricular units

Abstract

SUMMARY1. Electrical recordings were made from antidromically identified supraoptic and paraventricular units during intracarotid injections of hypertonic and isotonic sodium chloride solutions in rats.2. The blood concentrations of vasopressin and oxytocin were estimated by bio-assay before and at different intervals after similar injections.3. Although a significant change in the action potential activity of the supraoptic nucleus was associated with hormone release, the results were not entirely consistent with a simple relationship between action potential activity and hormone secretion. Firstly, although some units were excited by the stimulus a substantial number were inhibited. Secondly, the blood concentration of the hormones, particularly ADH, remained elevated for longer than might have been expected if additional hormone had ceased to be secreted as soon as firing rates had returned to control values.4. There were substantial differences between the initial blood concentrations of vasopressin and oxytocin but the firing rates of units in the supraoptic and paraventricular nuclei appeared to be the same.5. Although significantly less paraventricular than supraoptic units were affected by hypertonic injections the blood concentration of oxytocin was increased bv a factor of 8 whereas that of vasopressin was increased by a factor of 2-7.

Studies of antidromically identified neurosecretory cells of the hypothalamus by intracellular and extracellular recordings

“…The existence of such a system in mammalian neurosecretory cells of the SON and PVN has also been indicated, first by Koizumi & Yamashita in 1969. Inhibition of cell activity by antidromic stimulation of the posterior pituitary has been demonstrated now in the rat SON (Kelly & Dreifuss, 1970), and cat SON and PVN and in the SON and PVN of the dog , 1971. The IPSPs recorded intracellularly from the dog SON and evoked by antidromic stimulation is good evidence to suggest the existence of a recurrent collateral system in these nuclei , 1971. The demonstrated presence ofsmall cells which resemble Renshaw cells (the recurrent collateral cells of the spinal cord) provides additional evidence of interaction through recurrent collaterals.…”

“…Several papers have now appeared describing studies of neurosecretory cells of the SON and the PVN which were identified by antidromic excitation (Kelly & Dreifuss, 1970;Yamashita, Koizumi & Brooks, 1970;Barker, Crayton & Nicoll, 1971;Dyball, 1971). However, none of these publications were concerned with the neural control of neurosecretory cell activity from other structures nor did they report intracellular recordings from mammalian neurosecretory cells.…”

“…Many neural and chemical stimuli have been shown to evoke changes m rate of neurone discharges in the SON and PVN (Suda et al 1963;Koizumi et al 1964;Ishikawa, Koizumi & Brooks, 1966;Brooks et al 1966;Dyball & Koizumi, 1969) as well as in ADH and oxytocin release (Dyball, 1968(Dyball, , 1971. Originally, cells were considered to be neurosecretory cells when they were anatomically located in the PVN and SON and were osmosensitive (Koizumi et al 1964;Brooks et al 1966;Ishikawa et al 1966 (Harris, 1955).…”

“…Our preliminary studies (Koizumi & Yamashita, 1969;, 1971 Following completion of this dissection, the animal was mounted in a stereotaxic instrument (Narishige SN-3), held in a supine position and suspended in the air. The instrument had been adjusted for use with the stereotaxic atlas of Bleier (1961) and of Snider & Niemer (1961).…”

A microinjection study of the control of antidiuretic hormone release by the supraoptic nucleus of the hypothalamus in the cat

“…The osmoreceptors, have not been identified, but evidence from unit recordings suggests that the neurosecretory cells themselves may respond to a rise in the osmolarity of the blood. The firing rate of these cells is frequently accelerated by hypertonic stimuli (Koizumi, Ishikawa & Brooks, 1964;Wang, 1969), although this effect is not necessarily accompanied by a rise in hormone output (Dyball, 1971). It is possible that a process involving neurotransmitters, intervenes between the stimulus and the release of APR (Bridges & Thorn, 1970).…”