The mechanism by which sex steroids rapidly modulate the excitability of neurons was investigated by intracellular recording of neurons in rat medial amygdala brain slices. Brief hyperpolarization and increased potassium conductance were produced by 17 beta-estradiol. This effect persisted after elimination of synaptic input and after suppression of protein synthesis. Thus, 17 beta-estradiol directly changes the ionic conductance of the postsynaptic membrane of medial amygdala neurons. In addition, a greater proportion of the neurons from females than from males responded to 17 beta-estradiol.

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SUMMARY1. Intracellular recordings were made from vagal motoneurones identified by antidromic stimulation in the dorsal motor nucleus of the vagus (d.m.v.) in slice preparations of rat medulla oblongata.2. Noradrenaline (NA) applied by perfusion (0O01 /IM to 1 mM) depolarized 55%, hyperpolarized 32 % and produced a biphasic response (hyperpolarization followed by depolarization) in 9% of the d.m.v. neurones tested.3. The NA effects persisted after complete elimination of synaptic inputs during perfusion with Ca2+-free high-Mg2+ solution, and therefore probably resulted from a direct action on the postsynaptic membranes. 4. The NA depolarization was blocked by prazosin and the NA hyperpolarization by yohimbine, but neither was blocked by propranolol or timolol. Phenoxybenzamine blocked both responses. The results indicate that NA depolarization is mediated by a -adrenoceptors and hyperpolarization by a2-adrenoceptors.5. The neurones which were depolarized by NA were also hyperpolarized by NA when the a1-adrenoceptors were blocked by prazosin (all of seven neurones tested).This result suggests that most vagal motoneurones in the d.m.v. have both a,-and a2-adrenoceptors.6. The NA depolarization was accompanied by a decrease in membrane conductance and the hyperpolarization by an increase in membrane conductance, both of which were measured under manual-clamp conditions. 7. The reversal potentials for the NA responses were around -85 mV in normal Ringer solution, and shifted as predicted by the Nernst equation when the extracellular K+ concentration was changed.8. The inhibitory postsynaptic potentials evoked by focal electrical stimulation on the slice surface of the commissural part of the nucleus of the tractus solitarius (n.t.s.), which contains an A2 catecholaminergic cell group, were abolished by yohimbine.9. The results suggest that NA modulates vagal output by decreasing or increasing the K+ conductance of d.m.v. neurones through a,-or a2-adrenoceptors. In addition, the A2 noradrenergic cell group within the n.t.s. may send inhibitory inputs to the d.m.v.

SUMMARY1. The membrane properties of neurones in the guinea-pig ventromedial hypothalamic nucleus (v.m.h.) were studied in in vitro brain slice preparations.2. The average resting potential was -629 + 5-4 mV (mean ± S.D.), input resistance was 155 + 58 MQ, and action potential amplitude was 699 + 63 mV.3. Three types of neurone were identified. The type A neurones were characterized by a short membrane time constant (7 3 ± 2-0 ms) and a small after-hyperpolarization (a.h.p.) (2-0+ 1-2 mV) with a short half decay time of 67 + 55 ms after stimulation with a long outward current pulse. Type B had a long time constant (188 ± 57 ms) and a large a.h.p. (6-9 + 2-4 mV) with a medium half decay time of 203 + 90 ms. Type C was characterized by a long time constant (14-3 + 2-3 ms) and a large a.h.p.(65± + 1-5 mV) with a long half decay time of 478 + 230 ms.4. The slopes of the frequency-current (f-I) plots of the three types were different, particularly for the first spike interval. The slopes for the type A (414 + 102 impulses Sol nA-1) and type B neurones (480 ± 120 impulses s-1 nA-1) were steeper than that for the type C neurones (178+41 impulses sol nA-1). This difference is probably related to the relatively long first interval observed in the type C neurones.5. In all type B and a few type C neurones, when the membrane potential was hyperpolarized beyond -65 mV the application of orthodromic or direct stimulation generated a burst of spikes, consisting of a low-threshold response (l.t.r.) of low amplitude and superimposed high-frequency spikes. At the original resting potential, outward current pulses produced a train of low-frequency spikes.6. In type C neurones maintained in a depolarized state (about -50 mV), inward current pulses produced a specific delay of the return to the original membrane potential. This delayed return was thought to be generated by activation of a transient K+ (IA) conductance. T. MINAMI, Y. OOMURA AND M. SUGIMORI The mean reversal potential for the depolarization was -89-2 + 2-0 mV, indicating a decrease in K+ conductance.9. Horseradish peroxidase (HRP) injection after examination of the membrane properties revealed three types of neurone which were related morphologically, with good correlation to the A, B and C classification.10. From these results, it can be concluded that there iselectrophysical heterogeneity associated with anatomical differences in neurones in the v.m.h. Based on these differences, the neurones were classed into types A, B and C, with the type B neurones showing l.t.r. and the type C having IA current and glucose responsiveness.

Fetal behavioural patterns were examined to test whether they could be used to localise sites of brain damage antenatally. Decreased fetal movement, persistent nonreactive fetal heart rate (FHR) pattern, and/or central nervous system malformation were used as indicators of possible neurological impairment. Ten fetuses tested in this way underwent further ultrasound examination observing movement of the extremities, chest wail (breathing), and eye and mouth, and active/quiet FHR paterns. Eight of these 10 fetuses were found on postnatal examination to have a brain impairment. The fetuses having potential in utero brain impairment were divided into four groups: those with (1) lesion sites at, or caudal to, the ponsmedulla that were specifically identified by fetal behaviour, (2) diffuse lesions in the brain which, although resulting in abnormal behaviour, could not be localised by this behaviour, (3) lesions localised in the cerebral hemisphere(s) but with no abnormal behaviour, and (4) temporally abnormal behaviour in utero, finally ch g over to a normal pattern with no neonatal neurological abnormality. A screening system for the antenatal assessment of brain impairment is thus proposed.