EFFERENTS

The longitudinal subdivision of the cerebellum is closely related to its output. The output of the cerebellum begin as axons from the Purkinje[1] cells. The majority of these axons end on cerebellar nuclei, however a number of axons from the flocculonodular lobe (vestibulocerebellum) and from the lateral strip of the vermis of the rostral lobe synapse directly on vestibular nuclei. The signals from the Purkinje cells are inhibitory (GABA-ergic) whereas deep cerebellar nuclei receive excitatory imputs from mossy and climbing fibers, and send excitatory fibers to the cerebellar cortex and cerebrum and the brain stem nuclei. However, a subset of small neurons in cerebellar nuclei project inhibitory axons to the olivary nucleus providing a feedback.

 

The Purkinje cells from the vermis end in the fastigial nucleus. From this nucleus, axons leave the cerebellum through the corpus juxtarestiforme (the medial portion of the caudal cerebellar peduncle) to ipsi- and contralateral vestibular nuclei and through the corpus restiforme (the lateral portion of the caudal cerbellar peduncle) to other brain stem nuclei involved in maintaining the muscle tone, posture and eye movements. Lesions affecting this pathways produce and increased muscle tone and titubation[2].

 

Purkinje axons from the paravermis (the cortex of the cerebellar hemisphere close to the vermis) reach the interpositus nucleus. Purkinje axons from the rest of the cerebellar hemisphere cortex project to the dentate nucleus. From these two cerebellar nuclei axons leave the cerebellum through the rostral cerebellar peduncle (brachium conjuntivum) and cross the midline in the decussation of the rostral cebellar peduncles. The interpositus nucleus is connected with the red nucleus, and the dentate nucleus with the ventral lateral nucleus of the thalamus which relays to the cerebral cortex. They are involved in planning and initiation of movements involving multiple joints. Lesions affecting this pathways produce intention tremor and hypermetria[3].

 

Purkinje axons from the flocculonodular lobe (archicerebellum) and from the lateral strip of the vermis of the rostral lobe (paleocerebellum) leave the cerebellum directly through the corpus juxtarestiforme (the medial portion of the caudal cerebellar peduncle) to end in the vestibular nuclei to regulate equilibrium. Lesions affecting these pathways produce vestibular signs.

 

Many cerebellar neurons fire spontaneously. Neither Purkinje cells nor deep cerebellar nuclei cells have a true resting potential. A consequence of the spontaneous firing of the Purkinje neurons is that the cerebellar nuclei receive more basal inhibition than excitation. Most excitatory activity to the cerebellar nuclei arise from the mossy fibers. However, despite the large amount of inhibition they receive from the Purkinje cells, the cerebellar nuclei persist in firing tens of spikes per second[4].

CEREBELLAR SOMATOTOPY

 

It has been difficult to stablish a clear somatotopy of the cerebellar cortex as it has been done in the cerebral cortex because there are multiple representations of the same body parts in different sectors of the cerebellar cortex. However, in humans, the vermis of the rostral lobe of the cerebellum exerts its control over the shoulder, upper trunk and head, and the vermis of the caudal lobe exerts its control over lower trunk and pelvis. The fore limb is the most widely represented in the cerebellar hemisphere of the rostral lobe, whereas the hind limbs are widely represented in the cerebellar hemisphere of the caudal lobe. Disturbances of the rostral lobe tend to cause neurological signs in the head and neck, and control of the fore limbs. Disturbances of the caudal lobe may cause signs in the lower trunk and hind limb. The flocculonodular lobe is involved in equilibrium, so lesions affecting this lobe cause vestibular signs. (Manni, E. and Petrosini, L. Nature 246, Ma4rch 2004, Volume 5).

 

[1] Jan Evangelista Purkinje was a Czech physiologist that lived between 1787 and 1869. He described the cells that are now named after him.

[2] Rhythmic oscillation of the head or the trunk itself.

[3] Exaggerated movement of flexion and returned to ground with excessive extension.

[4] Pugh, J.R. and Raman, I.M. Nothing can be coincidence: synaptic inhibition and plasticity in the cerebellar nuclei. Trends in Neurosciences.