Current source density correlates of cerebellar Golgi and Purkinje cell responses to tactile input

Abstract

Tahon K, Wijnants M, De Schutter E, Maex R. Current source density correlates of cerebellar Golgi and Purkinje cell responses to tactile input. J Neurophysiol 105: 1327-1341, 2011. First published January 12, 2011 doi:10.1152/jn.00317.2010The overall circuitry of the cerebellar cortex has been known for over a century, but the function of many synaptic connections remains poorly characterized in vivo. We used a one-dimensional multielectrode probe to estimate the current source density (CSD) of Crus IIa in response to perioral tactile stimuli in anesthetized rats and to correlate current sinks and sources to changes in the spike rate of corecorded Golgi and Purkinje cells. The punctate stimuli evoked two distinct early waves of excitation (at Ͻ10 and ϳ20 ms) associated with current sinks in the granular layer. The second wave was putatively of corticopontine origin, and its associated sink was located higher in the granular layer than the first trigeminal sink. The distinctive patterns of granular-layer sinks correlated with the spike responses of corecorded Golgi cells. In general, Golgi cell spike responses could be linearly reconstructed from the CSD profile. A dip in simple-spike activity of coregistered Purkinje cells correlated with a current source deep in the molecular layer, probably generated by basket cell synapses, interspersed between sparse early sinks presumably generated by synapses from granule cells. The late (Ͼ30 ms) enhancement of simple-spike activity in Purkinje cells was characterized by the absence of simultaneous sinks in the granular layer and by the suppression of corecorded Golgi cell activity, pointing at inhibition of Golgi cells by Purkinje axon collaterals as a likely mechanism of late Purkinje cell excitation. in vivo electrophysiology; local field potential; microcircuit; multielectrode recording; synaptic current FOR A LONG TIME, THE CEREBELLUM has been considered to be primarily, if not exclusively, a motor organ as lesions cause symptoms such as ataxia, dysmetria, tremor, and hypotonia (Holmes 1939). Research of the past decades revealed more of its true nature: a neural substrate processing massive sensory information and serving not only motor, but also nonmotor regions

Power Spectral Density Analysis of Purkinje Cell Tonic and Burst Firing Patterns From a Rat Model of Ataxia and Riluzole Treated

“…In this study, a PC model (De Schutter & Bower, 1994a; De Schutter & Bower 1994b) was used in order to explore the effect of ion channels blockade in the spectral analysis of the PC output. This model is a multi-compartmental Purkinje cell model with soma and active dendrites, and has been previously described in detail (De Schutter & Bower, 1994a; De Schutter & Bower 1994b).…”

“…This model is a multi-compartmental Purkinje cell model with soma and active dendrites, and has been previously described in detail (De Schutter & Bower, 1994a; De Schutter & Bower 1994b). The model contains 10 ion channels consisting of fast sodium (NaF), persistent sodium (NaP), delayed rectifier potassium (Kdr), P-type calcium (CaP), T-type calcium (CaT), anomalous rectifier h-current (Kh), persistent potassium current (KM), A-type potassium (KA), BK calcium-activated potassium current (KC), K 2 calcium-activated potassium current (K 2 ).…”

“…Normal PCs spontaneously fire action potentials, and provide the single output of the cerebellar cortex (De Schutter & Bower, 1994a; De Schutter & Bower 1994b; Miyasho et al, 2001). Four representative Purkinje cell firing patterns were reported in the experimental studies: Simple spikes (contain high frequency sodium spikes), Na + spike bursts (are separated by near-random pauses), trimodal state (includes a tonic segment of simple spikes, followed by a period of Ca 2+ spike bursts, and finished with a quiescent period, in a highly cyclic pattern.…”

Golgi Neurons

“…34.3g) Tahon et al 2005;Vos et al 1999b;Xu and Edgley 2008). When stimulating the whiskers or the mystacial pad, short-latency excitation consisted of one or two early spikes (5-10 ms) eventually followed by a later component (13-26 ms), probably of cortical origin Tahon et al 2005; Tahon et al 2011;Vos et al 1999b;Vos et al 2000). The early response is sometimes composed of two spikes: the first is probably triggered by direct MF inputs and is followed in less than 4 ms by a second, interpreted as disynaptic inputs from the PF (Vos et al 1999b;Vos et al 2000) (Fig.…”

Balanced excitation and inhibition: Model based analysis of local field potentials

“…However the CSD analysis alone is not sufficient at disambiguating EPSC and IPSC from net current flows (Mitzdorf, 1985). With additional anatomical and spike rate information, previous modelling studies have attempted to provide coherent interpretations of CSD analysis in terms of neural excitation and inhibition (Ketchum and Haberly, 1993a,b;Tahon et al, 2011).…”