Properties of Slow, Cumulative Sodium Channel Inactivation in Rat Hippocampal CA1 Pyramidal Neurons

Mickus, Timothy; Jung, Hae‐Yoon; Spruston, Nelson

doi:10.1016/s0006-3495(99)77248-6

Cited by 138 publications

(148 citation statements)

References 36 publications

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“…Such fatigue can be modeled by shifting the activation curve of the sodium current to larger voltages, which effectively raises the action potential threshold . It is thus likely that threshold fatigue is due to cumulative sodium channel desensitization (Mickus et al 1999). Multiple biophysical mechanisms can thus give rise to negative ISI correlations at lag 1.…”

Section: Mechanisms That Give Rise To a Single Negative Isi Correlatimentioning

confidence: 99%

Nonrenewal spike train statistics: causes and functional consequences on neural coding

Ávila-Ǻkerberg

Chacron

2011

Exp Brain Res

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Many neurons display significant patterning in their spike trains (e.g. oscillations, bursting), and there is accumulating evidence that information is contained in these patterns. In many cases, this patterning is caused by intrinsic mechanisms rather than external signals. In this review, we focus on spiking activity that displays nonrenewal statistics (i.e. memory that persists from one firing to the next). Such statistics are seen in both peripheral and central neurons and appear to be ubiquitous in the CNS. We review the principal mechanisms that can give rise to nonrenewal spike train statistics. These are separated into intrinsic mechanisms such as relative refractoriness and network mechanisms such as coupling with delayed inhibitory feedback. Next, we focus on the functional roles for nonrenewal spike train statistics. These can either increase or decrease information transmission. We also focus on how such statistics can give rise to an optimal integration timescale at which spike train variability is minimal and how this might be exploited by sensory systems to maximize the detection of weak signals. We finish by pointing out some interesting future directions for research in this area. In particular, we explore the interesting possibility that synaptic dynamics might be matched with the nonrenewal spiking statistics of presynaptic spike trains in order to further improve information transmission.

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Section: Mechanisms That Give Rise To a Single Negative Isi Correlatimentioning

confidence: 99%

Nonrenewal spike train statistics: causes and functional consequences on neural coding

Ávila-Ǻkerberg

Chacron

2011

Exp Brain Res

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“…Electrophysiological analysis of ND7-23 cells indicated accelerated slow inactivation in the absence AQP1, which occurred after prolonged depolarization in the seconds-to-minutes range. Slow inactivation has been reported in various mammalian neuronal cells including rat hippocampal neurons (48), tetrodotoxin-resistant DRG neurons (23), and cultured neuroblastoma cells (49) and is important to firing adaptation. Several molecular partners and membrane proteins have been reported to modulate Na ϩ channel slow inactivation, including ␤ 1-4 subunits, ankyrin G (50), and calmodulin (25).…”

Section: Discussionmentioning

confidence: 99%

Aquaporin-1 Tunes Pain Perception by Interaction with Nav1.8 Na+ Channels in Dorsal Root Ganglion Neurons

Zhang

Verkman

2010

Journal of Biological Chemistry

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Aquaporin-1 (AQP1) water channels are expressed in the plasma membrane of dorsal root ganglion (DRG) neurons. We found reduced osmotic water permeability in freshly isolated DRG neurons from AQP1 Aquaporins (AQPs) 2 are water-transporting proteins expressed in epithelial, endothelial, and other cell types. In the central nervous system AQP4 is expressed in glial cells, where it plays a role in cerebral edema (1, 2), glial cell migration (3, 4), and neuroexcitation (5, 6). The mechanisms of AQP4 modulation of seizure dynamics (5), cortical spreading depression (6), vision (7), hearing (8), and olfaction (9) remain unclear. AQP4-dependent Kir4.1 K ϩ channel function has been suggested from delayed K ϩ reuptake from brain extracellular space after neuroexcitation (6, 10); however, patch clamp analysis showed AQP4-independent Kir4.1 K ϩ channel function (11). Extracellular space expansion, which has been found AQP4-deficient brain (12, 13), may contribute to the altered neuroexcitation phenotype. Neurons in the central nervous system do not express AQPs.Water channel AQP1 is abundant in hematopoietic cells and kidney. In normal brain AQP1 expression is restricted to the choroid plexus, where it facilitates the secretion of cerebrospinal fluid (14). In the spinal cord and peripheral nervous system, AQP1 is expressed in sensory neurons in dorsal root ganglia (DRG) that are associated with pain nociception (15-17). These neurons, whose cell bodies reside in the DRG, carry sensory signals from the periphery through small diameter, non-myelinated fibers that synapse in the superficial lamina of the dorsal horn in the spinal cord (18). Two prior studies on pain phenotype in AQP1 Ϫ/Ϫ mice have reported conflicting behavioral findings. Oshio et al. (16) reported mild impairment in pain nociception in AQP1 Ϫ/Ϫ mice after thermal (tail flick) and chemical (capsaicin) stimuli, with no differences in response to mechanical stimuli. Shields et al. (15) confirmed AQP1 expression in DRG neurons and partially colocalization with TRPV1 and substance P; however, they reported no significant differences in behavioral pain tests. The role of AQP1 in neuronal function in the DRG has, thus, remained unclear, as does its role in neurons in trigeminal and nodose ganglia, where it is also expressed.To clarify the role of AQP1 in pain physiology, we did more extensive behavioral testing as well as immunolocalization, water permeability, and patch clamp studies on freshly isolated, dissociated DRG neurons from wild type (AQP1 ϩ/ϩ ) and AQP1 null (AQP1 Ϫ/Ϫ ) mice. We found greatly reduced behavioral response to inflammatory thermal and cold pain in littermatched AQP1 Ϫ/Ϫ mice and distinct electrophysiological defects related to impaired Na v 1.8 Na ϩ channel functioning in AQP1-deficient DRG neurons. Patch clamp, immunoprecipitation, and single particle tracking studies in transfected cell models suggested a novel AQP1-Na v 1.8 interaction as responsible, in part, for the impairment in pain-sensing in AQP1 deficiency. EXPERIMENTAL PROCEDURES...

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“…Although we did not attempt to build a complete biophysical model of a CA1 pyramidal neuron, the conductance distributions in the dendrites for the two active conductances included in these models were consistent with experimental findings. In other words, within the apical dendrites, sodium conductance density was constant (Magee and Johnston 1995;Mickus et al 1999), and persistent potassium conductance density was also constant throughout the dendrites (Chen and Johnston 2004;Hoffman et al 1997).…”

Section: Ca1 Pyramidal Morphology Modelsmentioning

confidence: 99%

Synaptic Democracy in Active Dendrites

Rumsey

Abbott²

2006

Journal of Neurophysiology

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Rumsey, Clifton C. and L. F. Abbott. Synaptic democracy in active dendrites. J Neurophysiol 96: 2307-2318, 2006. First published July 12, 2006 doi:10.1152/jn.00149.2006. Given the extensive attenuation that can occur along dendritic cables, location within the dendritic tree might appear to be a dominant factor in determining the impact of a synapse on the postsynaptic response. By this reasoning, distal synapses should have a smaller effect than proximal ones. However, experimental evidence from several types of neurons, such as CA1 pyramidal cells, indicates that a compensatory strengthening of synapses counteracts the effect of location on synaptic efficacy. A form of spike-timing-dependent plasticity (STDP), called anti-STDP, combined with non-Hebbian activity-dependent plasticity can account for the equalization of synaptic efficacies. This result, obtained originally in models with unbranched passive cables, also arises in multicompartment models with branched and active dendrites that feature backpropagating action potentials, including models with CA1 pyramidal morphologies. Additionally, when dendrites support the local generation of action potentials, anti-STDP prevents runaway dendritic spiking and locally balances the numbers of dendritic and backpropagating action potentials. Thus in multiple ways, anti-STDP eliminates the location dependence of synapses and allows Hebbian plasticity to operate in a more "democratic" manner.

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Properties of Slow, Cumulative Sodium Channel Inactivation in Rat Hippocampal CA1 Pyramidal Neurons

Cited by 138 publications

References 36 publications

Nonrenewal spike train statistics: causes and functional consequences on neural coding

Nonrenewal spike train statistics: causes and functional consequences on neural coding

Aquaporin-1 Tunes Pain Perception by Interaction with Nav1.8 Na+ Channels in Dorsal Root Ganglion Neurons

Synaptic Democracy in Active Dendrites

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