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SUMMARY1. In slices (300 stm) of rat hypothalamus maintained in vitro in isotonic (298 + 4 m-osmol/kg) medium, the median firing rate of twenty-four supraoptic (s.o.) neurones was 0.05 spikes/s, compared to 0-66 spikes/s for twenty-eight paraventricular (p.v.) 4. Mean durations of bursts and silent periods in phasic cells excited by perifused glutamate were 16-6 s and 13-2 s (calculated from normalized distributions of thirty values), compared to means of 41-7 s and 33-9 s (thirty-six values, P < 0-001 for each parameter) for cells excited by glutamate ionophoresis. The periodicity of phasic firing in vitro was unaffected by a change to hypertonic (340 m-osmol/kg) medium.5. From these in vitro results it is proposed that the excitation associated with osmotic stimuli in vivo does not originate within the p.v. and s.o. neurosecretory cells, but that it involves a separate osmoreceptor. However, the control of phasic firing, which is commonly found during osmotic excitation, would seem to involve a mechanism which lies within or in close proximity to, the neurosecretory neurones.

Experiments were conducted to determine if food intake and adrenalectomy influenced abnormal antioxidant defense mechanisms observed in obese mice. Paired male C57BL/6J mice of two genotypes, obese (ob/ob) and lean (+/?), were fed a nonpurified diet ad libitum or restricted (2.5 g/d) until 3 mo old. Obese mice had larger livers and kidneys but smaller brains than lean mice. Plasma ceruloplasmin activity of obese mice was 240% of that of lean mice. Restricting food intake but not adrenalectomy reduced this difference, but ceruloplasmin activity of obese mice was still 150% of that of restricted-fed lean mice. Glutathione peroxidase (GSH-Px) activity in liver of obese mice was 70% of that in control lean mice; however, in kidney GSH-Px activity was 135% of that in obese mice. Both liver and kidney GSH-Px differences were eliminated by food restriction but not by adrenalectomy. Blood and brain GSH-Px activity was not influenced by the mutation. Liver and kidney copper-zinc superoxide dismutase activity was lower in obese mice than in lean littermates, 30 and 20%, respectively. Food restriction eliminated this difference in liver but not in kidney. Glutathione S-transferase activity using 1-chloro-2,4-dinitrobenzene as substrate was 55% lower in liver (not kidney) of obese mice than in lean mice and this difference was not markedly influenced by food restriction. Obese mice have marked changes in the steady-state activities of a number of protective enzymes that are organ dependent and, in part, due to the hyperphagia associated with this mutation.

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