Ramification and termination of single axons in the cerebellothalamic pathway of the rat

Abstract

There is increasing speculation that individual neurones in the cerebellar nuclei are involved in the control of complex multi-joint movements rather than simple movements about a single-joint. These neurones project predominantly to the primary motor cortex after relaying in the motor thalamus. Given a) that localised regions of the motor cortex control individual muscles which generally act about single joints and b) the relatively tight topographical arrangement of thalamocortical connections, it is reasonable to hypothesise that if cerebellar output neurones control single-joint movements they are likely to project to localised areas of the motor thalamus, whereas if they project to more widespread regions they are likely to influence movements involving multiple joints. In this context, we have examined the ramifications and terminations of single anterogradely labelled axons in the cerebellothalamic pathway of the rat. A total of nine axons were traced (by using a 100 x oil objective) through serial sections from the caudal end of the thalamus to their terminations in the motor thalamus. Each of these axons gave off one or more collaterals which terminated in the intralaminar or other associated groups of thalamic nuclei, implying simultaneous activation of two functionally separate cerebellothalamic pathways. In the relay nucleus or motor thalamus, four axons formed either a single focal group of terminals or multiple groupings of terminals within a localised region, and five terminated over widespread regions including one which terminated bilaterally. These results show that a large proportion of cerebellar output neurones may be in a position to influence multi-joint or even bimanual movements.

The nondecussating pathway of the dentatorubrothalamic tract in humans: human connectome-based tractographic study and microdissection validation

“…Thus, the results need to be critically evaluated in the light of current neurophysiological data obtained in humans and animals and of histological studies in animals. In the present study, the existence of the nd-DRTT is in full agreement with previous anatomical and histological studies in animals 6,9,18,40 and with radiological 17 and neurophysiological data 10 obtained in humans, suggesting that the DN and its projections constitute the "missing ring" in the interaction between the cerebellar hemisphere and the bilateral cerebral cortex.…”

Cerebellar output controls generalized spike‐and‐wave discharge occurrence

“…59 CN axons that project to the thalamus have been shown to originate from glutamatergic neurons, which synapse predominantly perisomatically and evoke substantial excitatory responses. 4,6,[23][24][25][26][27][28][29] Upon CN injections with muscimol, we must in effect have substantially reduced the level of excitation of thalamic neurons and thereby disturbed the balance of inhibition and excitation in thalamocortical networks in favor of inhibition. One of the main consequences of hyperpolarizing the membrane potential of thalamic neurons through this inhibition is activation of hyperpolarization-activated depolarizing cation currents (I h ) and Ca V 3.1 (T-type) Ca 21 channel currents, which typically results in the burstlike action potential firing that can drive GSWDs in thalamocortical networks.…”

“…[12][13][14][15][16][17][18] Yet, as shown in 3 controlled, blind studies, [19][20][21] the impact of these cerebellar surface stimulations was highly variable and probably reflects irregularities in the converging inputs from superficial and deeper parts of the cerebellar cortex neurons to the cerebellar nuclei (CN). 22 Given the considerable divergence of excitatory axonal projections from the CN to a wide range of motor, associative, and intralaminar thalamic nuclei, 4,6,[23][24][25][26][27][28][29] we considered this region an ideal candidate to effectively modulate thalamocortical oscillations. We hypothesized that altering the firing patterns of CN neurons should affect GSWD occurrence.…”

Cerebellar involvement in migraine

“…Thalamic structures implicated in migraine pathophysiology include the zona incerta and ventral posteromedial, posterior, and parafascicular thalamic nuclei (7,28,40,41). Cerebellar nuclei neurons send divergent, excitatory axonal projections to various thalamic nuclei that include extensive innervation of all these migraine-related thalamic areas (24,42–45). Through these connections, the cerebellum has been shown to robustly affect thalamocortical network activity (45,46).…”