Electrophysiological characteristics of immunochemically identified rat oxytocin and vasopressin neurones in vitro.

Abstract

1. Intracellular recordings were made from supraoptic neurones in vitro from hypothalamic explants prepared from adult male rats. Neurones were injected with biotinylated markers, and of thirty-nine labelled neurones, nineteen were identified immunocytochemically as containing oxytocin-neurophysin and twenty as containing vasopressin-neurophysin. 2. Vasopressin and oxytocin neurones did not differ in their resting membrane potential, input resistance, membrane time constant, action potential height from threshold, action potential width at half-amplitude, and spike hyperpolarizing after-potential amplitude. Both cell types exhibited spike broadening during brief, evoked spike trains (6-8 spikes), but the degree of broadening was slightly greater for vasopressin neurones. When hyperpolarized below -75 mV, all but one neurone exhibited a transient outward rectification to depolarizing pulses, which delayed the occurrence of the first spike.3. Both cell types exhibited a long after-hyperpolarizing potential (AHP) following brief spike trains evoked either with a square wave pulse or using 5 ms pulses in a train. There were no significant differences between cell types in the size of the AHP evoked with nine spikes, or in the time constant of its decay. The maximal AHP evoked by a 180 ms pulse was elicited by an average of twelve to thirteen spikes, and neither the size of this maximal AHP nor its time constant of decay were different for the two cell types.4. In most oxytocin and vasopressin neurones the AHP, and concomitantly spike frequency adaptation, were markedly reduced by the bee venom apamin and by d-tubocurarine, known blockers of a Ca2+-mediated K+ conductance. However, a minority of neurones, of both cell types, were relatively resistant to both agents.

Somato-dendritic mechanisms underlying the electrophysiological properties of hypothalamic magnocellular neuroendocrine cells: A multicompartmental model study

“…Figure 4 shows the voltage-gated currents and action potentials generated in the different compartments of the model MNC. In the model, spikes have a peak amplitude of 75 mV and a duration at the half-maximum spike amplitude of 1.2 ms, which are values close to the average values measured experimentally (Armstrong et al 1994;Stern and Armstrong 1996;Tasker and Dudek 1991;Teruyama and Armstrong 2002). In the model, action potentials and ionic currents have different characteristics in the soma, primary dendrite and secondary dendrite.…”

“…The DAP is expressed in the majority (75%) of VP neurons, whereas it is present in only a minority (32%) of OT neurons recorded in the brain slice preparation (Armstrong et al 1994). The findings of Greffrath et al (1998) suggest that the induction, maintenance and termination of the plateau potential underlying bursting in MNCs are regulated by the balance between the DAP and the slow AHP.…”

“…Activation of the SK channels is voltage independent and highly sensitive to intracellular Ca 2+ (Hille 2001;Sah and Davies 2000); BK channel activation is both voltage-and Ca 2+ -dependent (Vergara et al 1998;Dopico et al 1999). While activation of BK channels contributes to the falling phase of individual action potentials and the generation of the fast after hyperpolarizing potential (AHP) or hyperpolarizing after potential in many types of neurons (Lancaster and Adams 1986;Lancaster and Nicoll 1987;MacDermott and Weight 1982;Womack and Khodakhah 2002), including MNCs (Dopico et al 1999), SK channel activation is responsible for the generation of the AHP following a train of action potentials (Armstrong et al 1994;Bourque and Brown 1987;Greffrath et al 1998;Kirkpatrick and Bourque 1996;Lancaster and Adams 1986;Lancaster and Nicoll 1987;Sah and Bekkers 1996). This apamin-sensitive AHP is intermediate between the fast AHP (~50 ms) and "slow" AHP (lasting >5 s) (GhamariLangroudi and Bourque 2004).…”

“…The selected set of conductances provided a spike amplitude and duration similar to those recorded with somatic recordings from MNCs. Magnocellular neurons have action potentials with a fast ascending phase that provides a peak amplitude of 77.8±2.0 mV in VP neurons and 73.2±1.8 mV in OT neurons and a duration at the half-maximum spike amplitude of 1.5±0.1 ms (Armstrong et al 1994). Figure 4 shows the voltage-gated currents and action potentials generated in the different compartments of the model MNC.…”

“…However, the best characterized mechanism for burst termination is an activity-dependent inhibition of the DAP (Brown and Bourque 2004;Brown et al 2006), which was incorporated in the model of Roper et al (2004). In slice experiments, about half of the MNCs encountered in the SON displayed a DAP (Armstrong et al 1994;Li et al 1995). Only a small proportion (16%) of dissociated MNCs isolated from the rat SON displayed DAPs or spontaneous bursting activity following brief current-evoked trains (Oliet and Bourque 1992).…”