Cerebellar Modulation of Trigeminal Reflex Blinks: Interpositus Neurons

Abstract

Because of its simplicity, blinking is a prominent model system in analysis of adaptation and conditioning with the cerebellum. Nevertheless, data on the role of the cerebellum in modulation of normal reflex blinks are limited. We correlated the discharge of interpositus (IP) neurons with normal trigeminal reflex blinks and blink adaptation in urethane-anesthetized rats. Two groups of IP neurons responded to cornea stimulation. One group, pause neurons, showed a long cessation of their tonic discharge beginning 6 ms before the end of lid closure. The second group, burst neurons, exhibited a transient increase in firing frequency at a constant interval after the cornea stimulus. The cessation of pause neuron activity appeared to contribute to the termination of blinks. The tonic discharge rate increased and the cessation of pause neuron activity was delayed coincident with increased amplitude and duration of reflex blinks produced by blink adaptation. There was a coincident increase in the amplitude and duration of reflex blinks with increased tonic activity and delayed pause in pause neurons treated with the GABA A antagonist, gabazine. Burst neurons did not appear to modulate reflex blinks. Burst neuron discharge correlated neither with blink characteristics normally nor with blink adaptation. These findings indicated that pause neurons affect reflex blinks by providing a tonic excitatory input to facial motoneurons during lid closure and then disfacilitating those motoneurons to adjust the termination of lid closure. Burst neurons may play a role in eyelid conditioning.

The Cerebellar Interpositus Nucleus and the Dynamic Control of Learned Motor Responses

“…Their discharge rates were related to eyelid position (with a gain of 0.1-8.0 spikes/°; r Ͻ 0.7; p Յ 0.05) and/or to eyelid velocity (0.05-0.25 spikes/°per second; r Ͻ 0.7; p Յ 0.05). In accordance with previous reports (Van Kan et al, 1993;Gruart and DelgadoGarcía, 1994;Chen and Evinger, 2006), the recorded neurons (n ϭ 131) were classified as type A. Posterior interpositus type B neurons (n ϭ 43) were also antidromically activated from the red nucleus (0.85-1.25 ms) but presented a noticeable inhibition in their firing coinciding exactly with the downward displacement of the upper eyelid during reflexively evoked blinks (Gruart and Delgado-García, 1994;Gruart et al, 2000). Only those neurons located in the posterior interpositus nucleus, antidromically activated from the red nucleus and classified as type A, were included in this study.…”

“…In this regard, the eyelid motor system appears a suitable model for the study of cerebellar function in the acquisition of new motor abilities, because the brainstem and cerebellar circuits involved have been described precisely (Krupa et al, 1993;Llinás and Welsh, 1993;Mauk, 1997;Bracha et al, 2001;Carey and Lisberger, 2002;Delgado-García and Gruart, 2002;Morcuende et al, 2002;Christian and Thompson, 2003), the inputs and outputs of the system can be presented and/or measured quantitatively (Evinger et al, 1991;Gruart et al, 1995), and the neuronal activity of the relevant centers can be recorded in vivo during the actual performance of associative learning tasks (Trigo et al, 1999;Gruart et al, 2000;Chen and Evinger, 2006). Moreover, this motor system can be easily trained using classical conditioning paradigms (Gormezano et al, 1983).…”

Ionic Factors Governing Rebound Burst Phenotype in Rat Deep Cerebellar Neurons

“…A spontaneous, tonic discharge is present in DCN neurons at rest that is independent of synaptic input (Raman et al 2000). Alternatively, DCN cells can fire bursts of action potentials that can be correlated with specific movements (Chen and Evinger 2006;Ohtsuka andNoda 1991, 1992;Raman et al 2000). The ability to generate a rebound depolarization in vitro can show considerable variability but has been reported for large diameter cells (Aizenman and Linden 1999;Czubayko et al 2001;Jahnsen 1986).…”

Animal Models for Investigating Benign Essential Blepharospasm

“…[22-24] In the Schicatano et al (1997) animal model, [100] the predisposing condition distorts trigeminal blink circuit activity patterns so that maladaptive modifications occur in response to eye irritation [35]. The cerebellum is also critical in blink adaptation processes [101, 108, 109]. Trigeminal inputs to the cerebellum through mossy and climbing fibers [110-117] enable the cerebellum to support and maintain blink adaptations through indirect modulation of OO motoneuron depolarization and trigeminal system activity [68, 108, 117].…”

“…The cerebellum is also critical in blink adaptation processes [101, 108, 109]. Trigeminal inputs to the cerebellum through mossy and climbing fibers [110-117] enable the cerebellum to support and maintain blink adaptations through indirect modulation of OO motoneuron depolarization and trigeminal system activity [68, 108, 117]. If the cerebellum receives abnormal trigeminal inputs from maladaptive learning processes, then the cerebellum will support and maintain this abnormal motor learning that originated in trigeminal blink circuits.…”