PubMed · 4131124
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R H Davis, S B Knoebel, C Fisch. 1970. Pacemaker-induced arrhythmias.. https://pubmed.ncbi.nlm.nih.gov/4131124/
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Experience-dependent potentiation and depression of synaptic strength has been proposed to subserve learning and memory by changing the gain of signals conveyed between neurons. Here we examine synaptic plasticity between individual neocortical layer-5 pyramidal neurons. We show that an increase in the synaptic response, induced by pairing action-potential activity in pre- and postsynaptic neurons, was only observed when synaptic input occurred at low frequencies. This frequency-dependent increase in synaptic responses arises because of a redistribution of the available synaptic efficacy and not because of an increase in the efficacy. Redistribution of synaptic efficacy could represent a mechanism to change the content, rather than the gain, of signals conveyed between neurons.
Magnocellular oxytocin (OT) and vasopressin (VP) neurons adopt different firing patterns in response to relevant physiological stimuli. OT neurons selectively display short (2-4 sec), high-frequency bursts of action potentials that are highly synchronized and correlated with OT release during lactation. The present experiments were done to determine whether the electrophysiological properties of OT neurons differ from those of VP neurons, and whether these properties are modulated during lactation to support short bursting activity. Intracellular recordings in vitro were obtained from immunochemically identified supraoptic neurons of diestrous or lactating female rats. Resting membrane potential, input resistance, membrane time constant, and the depolarizing afterpotential did not differ among groups. However, near spike threshold, OT, but not VP, neurons expressed a sustained outward rectification that was removed by small hyperpolarizing pulses and a rebound depolarization that occurred at the offset of these hyperpolarizing pulses. The rebound depolarization was short ( < 2 sec), supported brief bursts of action potentials, and was significantly larger during lactation. Neurons expressing the outward rectification also exhibited strong spike frequency adaptation during prolonged (1-4 sec) depolarization. Spike width, the Ca(2+)- dependent afterhyperpolarization, and the degree of spike broadening of OT, but not VP, neurons were also larger during lactation, suggesting an increase in Ca2+ influx per spike. The results indicate that OT neurons possess properties favoring the expression of short spike trains, and that some of these properties are enhanced during lactation. In addition, spikes in OT neurons may promote more Ca2+ influx in this state.
Leech heart interneurons were voltage-clamped with realistic waveforms to investigate the currents underlying the oscillation in the cells. By estimating the leak current parameters in regions in which there was little contamination by voltage-gated currents, it was possible to measure the Ca2+ current, the persistent Na+ current, Ip, and the hyperpolarization-activated inward current, Ih. The experiments verified a prediction of a computer model of HN cells that the shape of the typical waveform was such that the low-threshold Ca2+ currents were partially inactivated during a slow up-ramp to a plateau potential. A step within the same range of the membrane potential as the realistic waveform produced > 4 times as much Ca2+ current. In two-cell voltage-clamp experiments, the step produced 20 times more graded inhibition than the normal presynaptic waveform. When the presynaptic heart interneuron oscillated with spikes, the graded inhibition was larger. The difference may arise from integration of a slowly decaying component of the spike-mediated inhibition. The persistent Na+ current had a very low threshold. During the most hyperpolarized phase of the waveform, Ip deactivated to 50% of its maximum conductance. A substantial part of Ip, therefore, was effectively contributing to the leak current in the HN cells. The h-current increased for waveforms that had longer periods, whereas increasing the h-current in the model reduced the period. The h-current thus provides negative feedback to perturbations that alter the period of the oscillation.