SUMMARYThe effects of a synthetic and an endogenous steroid were studied on the GABAA receptors of isolated mouse spinal neurones, maintained in culture. Low doses of alphaxalone reversibly increased GABA-evoked whole-cell currents. Alphaxalone at higher doses (10-50 'M), when pressure ejected onto spinal neurones, also directly evoked a membrane chloride current. Such currents were reversibly suppressed by bicuculline (a GABAA antagonist) and enhanced by phenobarbitone. 5,/-Pregnan-3a-ol-20-one, a progesterone metabolite, dose-dependently potentiated the amplitude of GABA-evoked whole-cell currents. The mechanism of potentiation was examined at the single-channel level using outside-out patches from spinal neurones. The main action of the steroid on the GABAA receptor appears to be similar to that found for barbiturates, in that they prolonged GABA-activated bursts of channel openings. Bemegride had an antagonistic action on the GABAA receptor, suppressing both GABA-and pentobarbitone-evoked whole-cell currents to similar extents.
SUMMARYThe stellate ganglion of the squid Loligo peallei contains the neuropeptides Phe-Met-Arg-Phe-NH2 (FMRFamide), Phe-Leu-Arg-Phe-NH2 (FLRFamide) and at least one N-terminally extended FMRFamide-related peptide that is yet to be fully characterized. Both local application and arterial perfusion of FLRFamide potentiate transmission at the giant synapse. The N-terminally related peptide Ser-Asp-Pro-Phe-Leu-Arg-Phe-NH2 (SDPFLRFamide) produced a similar effect. The threshold for both the tetra-and the hepta-peptides was less than 10 /aM. Potentiation could be detected as an increase in rate of rise of the EPSPs, as an increase in amplitude of the EPSP in the absence of spikes, or under voltage clamp as an increase in the EPSC. The effect was most pronounced when the synapse was fatigued by high frequency stimulation. Another molluscan peptide, eledoisin and also leucine enkephalin were without effect. In the absence of any detectable effects of FLRFamide on the resting membrane potential of either pre-or postsynaptic terminals or on the presynaptic spike, it is suggested that the peptide influences transmitter mobilization. However, the peptide could also exert small changes in preterminal calcium currents, which so far we have been unable to detect.
SUMMARYIn Helix aspersa, activation of the cerebral giant serotonin neurones (GSNs) evokes a biphasic, excitatory synaptic response in the M neurones of the buccal ganglia. Local application of serotonin to the current-clamped M neurones also evokes fast and slow depolarizing responses.The slow response is thought to be dependent on calcium ions, whereas sodium ions have been implicated in the fast response. Here we provide further evidence that the slow response results from an increase in conductance to calcium ions, and show that okadaic acid, an antagonist of protein phosphatases 1 and 2A, potentiates the effect of serotonin, suggesting that the response is phosphorylation dependent. Further, agents known to activate protein kinase C, such as 1-oleoyl-2-acetyl-rac-glycerol and active phorbol esters (but not an inactive one) were found to increase the calcium current (actually carried by barium ions) of the M neurones. Such data suggest that the slow synaptic response mediated by serotonin can occur by activation of protein kinase C and phosphorylation of the affected voltage-sensitive calcium channels, or some closely associated protein(s).
SUMMARYThe giant neurone in the left pedal ganglion of the snail Helisoma trivoli'is is homologous with the giant dopaminergic neurone of Planorbis corneus, because the neurones have a very similar location and morphology, and react similarly with glyoxylic acid to produce an intense blue fluorescence, indicating the presence of dopamine. Each of these neurones is therefore referred to as a giant dopaminergic neurone, or GDN. Conditions for the extension of neurites and formation of chemical junctions in culture have been determined for the H. trivolvis GDN, and compared with other neurones from this species. The pattern of neurites that extended from the neurone was indistinguishable from that of another identified aminergic neurone, the large serotonergic neurone (LSN), but differed markedly from many other central neurones. However, the type of substrate also greatly affected the pattern of the neurites observed. Some of the electrical properties of the GDN in culture differed from those recorded in situ: peak spike amplitude was increased, spike half-width reduced and the firing pattern of the neurone was altered. However, the resting membrane potential was very similar. The GDN formed chemical and electrical junctions in culture. The chemical junctions formed were of the same type as those found in situ. They formed rapidly, within 18 h after plating, but were not stable and were lost within 48 h, to be replaced by a non-rectifying electrical junction. A chemical junction may form in either direction between the GDN and the LSN, but only rarely did such junctions allow transmission in both directions, as observed in situ. Experiments in which neurones were plated out at different times suggested that the direction of formation of the chemical junction was not dependent on the degree or state of neurite extension.
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