Matching dendritic neuron models to experimental data

Rall, W.F.; Burke, Robert E.; Holmes, William R.; Jack, J. J. B.; Redman, S. J.; Segev, Idan

doi:10.1152/physrev.1992.72.suppl_4.s159

Cited by 298 publications

(238 citation statements)

References 65 publications

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“…This conclusion is consistent with our observation that the membrane time constant, defined as the product of membrane resistance and capacitance per unit area where the capacitance is considered to be constant (Rall et al 1992), showed an increase (Fig. 4C) in association with the input resistance (Fig.…”

Section: Resting Potential Input Resistance and Membrane Time Constantsupporting

confidence: 93%

“…The voltage response of NGIs in this study could be expressed as a sum of two exponentials with different time constants. The slower time constant represented the membrane time constant whereas the faster one represented the equalizing time constant that was associated with rapid reduction of voltage differences between different membrane regions (Rall et al 1992). …”

Section: Intracellular Recording and Current Injectionmentioning

confidence: 99%

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Physiological changes of premotor nonspiking interneurons in the central compensation of eyestalk posture following unilateral sensory ablation in crayfish

Fujisawa

Takahata

2006

J Comp Physiol A

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AbstractsWe investigated how the physiological characteristics and synaptic activities of NGIs (Nonspiking Giant Interneurons), which integrate sensory inputs in the brain and send synaptic outputs to oculomotor neurons innervating eyestalk muscles, changed after unilateral ablation of the statocyst in order to clarify neuronal mechanisms underlying the central compensation process in crayfish. The input resistance and membrane time constant in recovered animals that restored the original symmetrical eyestalk posture two weeks after operation were significantly greater than those immediately after operation on the operated side whereas in non-recovered animals only the membrane time constant showed a significant increase. On the intact side, both recovered and non-recovered animals showed no difference. The frequency of synaptic activity showed a complex pattern of change on both sides depending on the polarity of the synaptic potential. The synaptic activity returned to the bilaterally symmetrical level in recovered animals while bilateral asymmetry remained in non-recovered ones. These results suggest that the central compensation of eyestalk posture following unilateral impairment of the statocyst is subserved by not only changes in the physiological characteristics of the NGI membrane but also the activity of neuronal circuits presynaptic to NGIs.Fujisawa and Takahata -3-

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Section: Resting Potential Input Resistance and Membrane Time Constantsupporting

confidence: 93%

Section: Intracellular Recording and Current Injectionmentioning

confidence: 99%

Physiological changes of premotor nonspiking interneurons in the central compensation of eyestalk posture following unilateral sensory ablation in crayfish

Fujisawa

Takahata

2006

J Comp Physiol A

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“…Synaptic inputs from many other association cortical regions converge in layer I-II, where the apical tuft of the layer V-VI pyramidal neurons extends (Peters 1987;van Eden et al 1992;Condé et al 1995;Mitchell and Cauller 1997; Table 2). Distal synaptic signals en route to the deep layer soma of these neurons can be greatly attenuated if the dendritic membrane is functionally passive in nature (Rall et al 1992;Cauller and Connors 1994). Moreover, recent evidence indicates that there are high densities of K ϩ and mixed cationic currents (I H ) in the dendrites (Hoffman et al 1997;Stuart and Spruston 1998), which produce even greater attenuation of synaptic signals than that expected for a passive dendrite.…”

Section: Apical Dendritic Compartment Of Deep Layer Pyramidal Corticamentioning

confidence: 99%

Developing a Neuronal Model for the Pathophysiology of Schizophrenia Based on the Nature of Electrophysiological Actions of Dopamine in the Prefrontal Cortex

Yang

Seamans

Gorelova

1999

Neuropsychopharmacology

164

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This review covers some recent findings of the electrophysiological mechanisms through which mesocortical dopamine modulates prefrontal cortical neurons. Dopamine has been shown to modulate several ionic conductances located along the soma-dendritic axis of prefrontal cortical pyramidal neurons. These ionic currents include high-voltage-activated calcium currents and slowly inactivating NaReceived May 12, 1998; revised May 27, 1998; accepted May 29, 1998. 162 C.R. Yang et al. N EUROPSYCHOPHARMACOLOGY 1999 -VOL . 21 , NO Schizophrenia strikes one in one hundred people worldwide, regardless of cultural or racial origins. As the illness progresses and if it remains unattended, patients are frequently trapped in psychological, social, and economic devastation (Gottesman 1991;Jablensky 1995). Currently, our incomplete understanding of the neurobiological bases of schizophrenia suggests that defects in the genetic controls of brain development in such limbic regions (including temporal lobe structures such as hippocampus and the amygdala) as well as the prefrontal cortex (PFC) lead to cell loss or deformation, cytoarchitectural disorganization, and abnormal innervation in these brain regions (Roberts and Bruton 1990;Stevens 1992; Bogerts 1993;Shapiro 1993; Akbarian et al. 1993 Akbarian et al. , 1996Ross and Pearlson 1996;Weinberger 1996; Karayiorgou and Gogos 1997; Lewis 1997;Selemon et al. 1995Selemon et al. , 1998.Some results from recent imaging studies of brains from living schizophrenics have suggested that there are defective functional communications between the interconnected cortical (PFC and cingulate cortex) and limbic subcortical structures (thalamus, striatum, and temporal lobe limbic structures)(see reviews of Liddle 1996; Pfefferbaum and Marsh 1995; Andreasen 1997; Heckers et al. 1998). Findings from these studies suggest that in schizophrenics, abnormal recruitment of several interconnected cortical and subcortical structures may underlie such symptom clusters as psychomotor poverty, thought disorganization, and reality distortion (Liddle et al. 1992; Liddle 1996; Fletcher 1998; Heckers et al. 1998).As noted in Figure 1, the PFC receives converging limbic, association cortical, and mesocortical dopamine inputs. These inputs interact in the PFC and are involved functionally in high-level cognitive processes (Fuster 1995). Among the many brain regions that PFC output innervates, two important subcortical regions are emphasized in this review. These are the nucleus accumbens (where mesoaccumbens dopamine neurons terminate) and the ventral tegmental area (VTA, where the midbrain dopamine neurons reside) Groenewegen et al. 1990; Berendse et al. 1992a Berendse et al. , 1992bSesack and Pickel 1992;Gorelova and Yang 1997b). Several of the interconnected limbic, cortical, and subcortical structures known to be affected in schizophrenia are targets of the ascending midbrain dopamine systems that normally provide functional modulation of neurotransmission (Björklund and Lindvall 1984;Mogenson et ...

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“…Although the axon contributes substantially to the time course of somatic EPSPs in cerebellar interneurons (13), its contribution in hippocampal BCs is not evident. Finally, the cable parameters, specific membrane resistance (R m ), membrane capacitance (C m ), and intracellular resistivity (R i ), will shape neuronal signaling (14)(15)(16)(17)(18)(19)(20)(21)(22). For example, a low value of R m , which may be generated by a high density of leak channels (23), would accelerate the decay of EPSPs by speeding up the membrane time constant.…”

mentioning

confidence: 99%

Distinct nonuniform cable properties optimize rapid and efficient activation of fast-spiking GABAergic interneurons

Nörenberg

Vida

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

121

166

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Fast-spiking, parvalbumin-expressing basket cells (BCs) play a key role in feedforward and feedback inhibition in the hippocampus. However, the dendritic mechanisms underlying rapid interneuron recruitment have remained unclear. To quantitatively address this question, we developed detailed passive cable models of BCs in the dentate gyrus based on dual somatic or somatodendritic recordings and complete morphologic reconstructions. Both specific membrane capacitance and axial resistivity were comparable to those of pyramidal neurons, but the average somatodendritic specific membrane resistance (R m ) was substantially lower in BCs. Furthermore, R m was markedly nonuniform, being lowest in soma and proximal dendrites, intermediate in distal dendrites, and highest in the axon. Thus, the somatodendritic gradient of R m was the reverse of that in pyramidal neurons. Further computational analysis revealed that these unique cable properties accelerate the time course of synaptic potentials at the soma in response to fast inputs, while boosting the efficacy of slow distal inputs. These properties will facilitate both rapid phasic and efficient tonic activation of BCs in hippocampal microcircuits.cable models | dendrites | hippocampus | basket cell F ast-spiking, parvalbumin-expressing basket cells (BCs) play an important role in feedforward and feedback inhibition, providing rapid control over the frequency and timing of action potential initiation in principal neuron ensembles (1-6). Although inhibition comprises several steps, including activation of excitatory input synapses on BCs, dendritic integration of excitatory postsynaptic potentials (EPSPs), action potential initiation and propagation, and GABA release from output synapses, the kinetics of disynaptic inhibition can be very rapid, with ≈2 ms total onset time at physiologic temperature (3, 7). Several synaptic specializations contribute to the remarkable speed of feedforward and feedback inhibition. At the glutamatergic input synapses of BCs, the fast clearance of transmitter from the synaptic cleft and the expression of molecularly specialized L-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptors (AMPARs) contribute to rapid signaling (8, 9). At the GABAergic output synapses of BCs, the use of rapidly gated P/Qtype Ca 2+ channels and the tight coupling of these channels to the Ca 2+ sensors of exocytosis may serve a similar function (10, 11). Thus, functional specializations at both input and output synapses maximize the speed of BC-mediated disynaptic inhibition.Synaptic location, dendritic structure, and electrical cable properties will also contribute to rapid signaling in GABAergic interneurons. For example, the proximal location of excitatory synapses may promote rapid activation of BCs. The significance of this factor, however, is unclear, because many glutamatergic synapses terminate on distal dendrites of BCs (12). Furthermore, rapid signaling could be promoted by the extensive axon, which may accelerate the somatic EPSP decay time course by ge...

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Matching dendritic neuron models to experimental data

Cited by 298 publications

References 65 publications

Physiological changes of premotor nonspiking interneurons in the central compensation of eyestalk posture following unilateral sensory ablation in crayfish

Physiological changes of premotor nonspiking interneurons in the central compensation of eyestalk posture following unilateral sensory ablation in crayfish

Developing a Neuronal Model for the Pathophysiology of Schizophrenia Based on the Nature of Electrophysiological Actions of Dopamine in the Prefrontal Cortex

Distinct nonuniform cable properties optimize rapid and efficient activation of fast-spiking GABAergic interneurons

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