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|Title:||THE RATE AND TEMPORAL CODING PROPERTIES OF THE DEEP CEREBELLAR NUCLEUS NEURONS|
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|Authors/Affiliations:||1 R. Tadayon Nejad *; 1 M. Molineux; 1 WH. Mehaffey; 1 K. Jayasuriya; 1 R. Turner; |
1 Hotchkiss Brain Institute, University of Calgary, AB, Canada
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|Content:||Ojectives: The cerebellum coordinates movement by providing precise control over the magnitude and timing of motor commands. Cerebellar output is highly dependent on the intrinsic properties of deep cerebellar nuclear (DCN) neurons that receive and translate information from the cerebellar cortex. DCN cells respond to Purkinje cell-evoked IPSPs with a rebound increase in spike frequency. We have shown that DCN cells fall into two burst phenotypes that generate either a high frequency Transient Burst or Weak Burst in relation to the expression of T type calcium channel isoforms. This study tests the hypothesis that Transient and Weak Burst cell phenotypes establish differential rate and temporal coding of Purkinje cell input.|
Methods and Materials: Cerebellar slices were prepared from P12-P18 rats to be maintained at 32°C in vitro and patch clamp recordings obtained from large diameter cells in all three DCN (medial, interpositus, lateral). Varying amplitudes and durations of current-evoked membrane hyperpolarizations were applied to compare the rebound spike response and coding properties of Transient and Weak Burst cells. The response to physiological patterns of Purkinje cell input was tested by time-stamping spike trains from rat Purkinje cells recorded in vivo (E. deSchutter) and applied as TTL stimulus pulse trains to Purkinje cell axons entering the DCN. Drugs were either bath applied or focally ejected from a pressure electrode.
Results: Transient and Weak Burst cells displayed distinctly different rate coding responses to membrane hyperpolarizations in terms of rebound frequency and number of spikes per burst. In general, Transient Burst cells required a greater level of hyperpolarization (<-65 mV) before producing a near maximal spike frequency and number per burst. Weak Burst cells instead responded in a graded fashion in rebound spike frequency and number over a wider range of membrane potentials than Transient Burst cells. Both cell types generate a graded first spike latency to membrane hyperpolarizations, revealing a previously unrecognized temporal code in DCN cells. Pharmacological tests indicate that the rebound burst frequency and gain of rate coding in Transient and Weak Burst cells reflect different contributions of T-type calcium and calcium-dependent potassium channels. In contrast, the inward current IH underlies the graded shift in first spike latency in relation to membrane hyperpolarizations in both cell types. Physiological trains of Purkinje cell inhibitory input indicate that the extent to which rate and temporal coding properties of Transient and Weak Burst cells are recruited vary according to the precise pattern of presynaptic input and resting membrane potential.
Conclusions: The two DCN cell burst phenotypes create different strategies for encoding membrane hyperpolarizations and thus cerebellar cortical input across DCN nuclei.
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