A novel tetrodotoxin-insensitive, slow sodium current in striatal and hippocampal beurons

Hoehn, Katja; Watson, T.; MacVicar, Brian A.

doi:10.1016/0896-6273(93)90341-n

Cited by 82 publications

(42 citation statements)

References 63 publications

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“…2D of Wong & Prince, 1981). We attribute this to the model's lack of one or more slower membrane processes, such as 9K(DR) inactivation (Numann, Wadman & Wong, 1987), a TTX-resistant gNa (Hoehn, Watson & MacVicar, 1993) or a Ca2+-activated cation current (Caeser, Brown, Giihwiler & Knopfel, 1993 We showed previously ) that injection of depolarizing current into an apical dendritic compartment could elicit repeating Ca2+ spikes reminiscent of dendritic potentials recorded experimentally in stratum radiatum, presumably from a single dendritic branch (Traub et al 1993). Injection of current into the dendritic site in the cable model corresponds mathematically to injection of current into all of the branches at a given level, not a single branch.…”

Section: Resultsmentioning

confidence: 99%

A branching dendritic model of a rodent CA3 pyramidal neurone.

Traub

Jefferys

Miles

et al. 1994

The Journal of Physiology

277

200

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Section: Resultsmentioning

confidence: 99%

A branching dendritic model of a rodent CA3 pyramidal neurone.

Traub

Jefferys

Miles

et al. 1994

The Journal of Physiology

277

200

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“…For example, voltage-gated cation channels have been described in a variety of neuronal cell types (Hoehn et al, 1993;Alzheimer, 1994) and participate in afterpotential genesis after spike repolarization (Penington and Kelly, 1993). These depolarizing afterpotentials are not sensitive to [Ca 2ϩ ] i , are only milliseconds in duration, and mediate burst firing at rapid frequencies (Deisz, 1996).…”

Section: Discussionmentioning

confidence: 99%

Cholinergic-Dependent Plateau Potential in Hippocampal CA1 Pyramidal Neurons

1996

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Cholinergic stimulation of the hippocampal formation results in excitation and/or seizure. We report here, using whole-cell patch-clamp techniques in the hippocampal slice (34 -35°C), a cholinergic-dependent slow afterdepolarization (sADP) and long-lasting plateau potential (PP). In the presence of 20 M carbachol, action potential firing evoked by weak intracellular current injection elicited an sADP that lasted several seconds. Increased spike firing evoked by stronger depolarizing stimuli resulted in long-duration PPs maintained close to Ϫ20 mV. Removal of either Na ϩ or Ca 2ϩ from the external media, intracellular Ca 2ϩ ([Ca 2ϩ ] i ) chelation with 10 mM bis(2-aminophenoxy)ethane-N,N,NЈ,NЈ-tetra-acetic acid, or the addition of 100 M Cd 2ϩ to the perfusate abolished both the sADP and PP. The sADP was depressed and the PP was abolished by either 10 M nimodipine or 1 M -conotoxin, whereas 1.2 M tetrodotoxin was ineffective. The involvement of a Na ϩ /Ca 2ϩ exchanger was minimal because both the sADP and PP persisted after equimolar substitution of 50 mM Li ϩ for Na ϩ in the external media or reduction of the bath temperature to 25°C. Finally, in the absence of carbachol the sADP and PP could not be evoked when K ϩ channels were suppressed, suggesting that depression of K ϩ conductances alone was not sufficient to unmask the conductance. Based on these data, we propose that a Ca 2ϩ -activated nonselective cation conductance was directly enhanced by muscarinic stimulation. The sADP, therefore, represents activation of this conductance by residual [Ca 2ϩ ] i , whereas the PP represents a novel regenerative event involving the interplay between high-voltage-activated Ca 2ϩ channels and the Ca 2ϩ -activated nonselective cation conductance. This latter mechanism may contribute significantly to ictal depolarizations observed during cholinergic-induced seizures.

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“…In B and C, the error bar represents the standard deviation. (Nisenbaum et al 1996), I NaS (Hoehn et al 1993), and I NaP (Chao and Alzheimer 1995). Currents followed I = g m k h(V − E), in which E(mV) is the reversal potential.…”

Section: Computational Modelingmentioning

confidence: 99%

Role of a Striatal Slowly Inactivating Potassium Current in Short-Term Facilitation of Corticostriatal Inputs: A Computer Simulation Study

Mahon

Deniau²,

Charpier³

2000

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Striatal output neurons (SONs) integrate glutamatergic synaptic inputs originating from the cerebral cortex. In vivo electrophysiological data have shown that a prior depolarization of SONs induced a short-term (Յ1 sec) increase in their membrane excitability, which facilitated the ability of corticostriatal synaptic potentials to induce firing. Here we propose, using a computational model of SONs, that the use-dependent, short-term increase in the responsiveness of SONs mainly results from the slow kinetics of a voltage-dependent, slowly inactivating potassium A-current. This mechanism confers on SONs a form of intrinsic short-term memory that optimizes the synaptic input-output relationship as a function of their past activation.The striatum, the main input stage of the basal ganglia, provides a dynamic neural network that is involved in adaptive control of behavior (for review, see Graybiel 1995). To achieve this function, GABAergic striatal output neurons (SONs) integrate glutamatergic synaptic inputs from many converging cortical neurons (Wilson 1995). However, one of the main electrophysiological features of SONs that has been recorded in vivo is a low level of spontaneous firing (Wilson 1995;Charpier et al. 1999). It is now assumed that this weak excitability of SONs is due to nonlinear electrical membrane properties rather than to a mutual synaptic inhibition (Jaeger et al. 1994;Nisenbaum et al. 1994;Nisenbaum and Wilson 1995;Wilson 1995). The nonlinear properties of SONs result from a set of voltage-gated potassium and sodium currents, including an inwardly rectifying potassium current (I Kir ), a fast (I Af ), a slowly inactivating Acurrent (I As ), a persistent (I Krp ) potassium current, a slowly inactivating (I NaS ), and a persistent (I NaP ) sodium current (Hoehn et al. 1993;Nisenbaum et al. 1994;Chao and Alzheimer 1995;Nisenbaum and Wilson 1995;Nisenbaum et al. 1996;Gabel and Nisenbaum 1998;Nisenbaum et al. 1998). A distinctive voltage behavior of SONs is conferred by I As , which is responsible for a slowing of the rate of depolarization that is evident from membrane potentials near −60 mV Nisenbaum et al. 1994;Gabel and Nisenbaum 1998). When a depolarizing input is maintained, the slow ramp of depolarization in SONs can lead to a long latency of action potential discharge (Fig. 1A, part 1, crossed arrow; Nisenbaum et al. 1994).Recently, using in vivo intracellular recordings from anesthetized rats, we have investigated the role of intrinsic electrical properties of SONs in the temporal integration of their cortical synaptic inputs (Mahon et al. 2000). We showed that direct activation of SONs through intracellular injection of a depolarizing current pulse induced a shortterm (Յ1 sec) increase in their membrane excitability. This change in excitability facilitated the ability of corticostriatal excitatory postsynaptic potentials (EPSPs) to induce firing. In this study we attempted to specify the mechanisms involved in the use-dependent increase in SON excitability. To this end, we have now perfor...

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A novel tetrodotoxin-insensitive, slow sodium current in striatal and hippocampal beurons

Cited by 82 publications

References 63 publications

A branching dendritic model of a rodent CA3 pyramidal neurone.

A branching dendritic model of a rodent CA3 pyramidal neurone.

Cholinergic-Dependent Plateau Potential in Hippocampal CA1 Pyramidal Neurons

Role of a Striatal Slowly Inactivating Potassium Current in Short-Term Facilitation of Corticostriatal Inputs: A Computer Simulation Study

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