Learning causes synaptogenesis, whereas motor activity causes angiogenesis, in cerebellar cortex of adult rats.

Abstract

The role of the cerebellar cortex in motor learning was investigated by comparing the paramedian lobule of adult rats given difficult acrobatic training to that of rats that had been given extensive physical exercise or had been inactive. The paramedian lobule is activated during limb movements used in both acrobatic training and physical exercise. Acrobatic animals had greater numbers ofsynapses per Purkin e cell than animals from the exercise or inactive groups. No significant difference in synapse number or size between the exercised and inactive groups was found. This indicates that motor learning required of the acrobatic animals, and not repetitive use of synapses during physical exercise, generates new synapses in cerebellar cortex. In contrast, exercise animals had a greater density ,f blood vessels in the molecular layer than did either the acrobatic or inactive animals, suggesting that increased Synaptic activity elicited compensatory angiogenesis.Although many aspects of experience can alter synaptic connectivity (1-5), it has-been difficult'to relate unequivocally these changes to learning and memory because the morphological effects of leaning could not be isolated from those of behaviors. required to perform the task. For example, maze training (3) and forelimb reach-training (5) can alter neuronal morpholoy, but substantia trepetition of movements is required fo arning these, tasks'. Thus it is not possible to ascrib~e te morphological effects to learning per se.The cerebellar cortex may be particularly appropriate for testing hypotheses about synaptic plasticity because empirical evidence has implicated cerebellar cortex in motor skill learning (6,7,36), and there is some indication that synapse formation underlies cerebellar cortical learning, as suggested by dendritic-field changes in Purkinje cells of rodents and monkeys exposed to challenging. sensory-motor environments (8-10). Synaptogenesis in adult rat cerebellar cortex also occurs when afferents are cut (11,12). Furthermore, theorists have noted the suitability of cerebellar cortex for motor learning, with its convergence of two afferent systems conveying extensive somatic and cerebral state information upon the Purkinje cell, a single-output neuron that modulates motor activity (13)(14)(15)(16)(17).The results of the present study show that learning, as opposed to the motor activity necessary for learning a complex motor task, is responsible for synapse formation in the cerebellar cortex. We report a dissociation oflearning and motor activity, in which animals provided with complex visuomotor learning and minimal motor activity (acrobatic training)-form substantial numbers of new synapses in cerebellar cortex, whereas animals given extensive locomotor exercise with minimal opportunities for learning (repetitive exercise) formed new blood vessels but formed no more new synapses than animals in an inactive control group. MATERIAL AND METHODSAnimals and Training. Thirty-eight adult Long-Evans hooded female rats, kept in small groups...

Chronic treadmill exercise in rats delicately alters the Purkinje cell structure to improve motor performance and toxin resistance in the cerebellum

“…In cerebellum-related studies, acrobat training (2,19) or an enriched environment (11), but not repeated running, induces synaptogenesis in Purkinje cells. The apparent discrepancy with regard to running-induced synaptogenesis between the present study and previous reports may be explained by the different running intensities and durations employed.…”

“…Later studies using young rats show that a complex paradigm of "acrobat" training or an enriched environment induces morphological changes in Purkinje cells, while repeated running without skill learning induces angiogenesis in the cerebellum (2,11,19). However, other animal studies reveal that repeated running with defined intensity and duration improves the motor function and prevents the decay of Purkinje cells under various pathological conditions.…”

Biology of Cerebral Arteriovenous Malformations with a Focus on Inflammation

“…52,53 Angiogenesis can occur later in life in response to certain physiologic conditions, such as chronic hypoxia, shear stress, exercise, or hormonal fluctuations, thereby altering AVM morphology. [54][55][56][57][58][59] Pathologic conditions such as tumor, stroke, or trauma can also drastically upregulate angiogenesis via VEGF and angiopoietins (Table 2). These factors cause the reactivation of quiescent endothelium, breakdown of vessel walls, and the fusion of perinidal capillaries with the nidus, enlarging the AVM.…”

Cerebral blood flow and cerebrovascular reactivity at rest and during sub-maximal exercise: Effect of age and 12-week exercise training

“…One cross-sectional study indicated that higher fitness is related to larger frontal and temporal volumes of grey matter (Colcombe et al 2006). Other potential mechanisms may involve more endotheliumdependent vasodilatation as a result of more NO bioavailability (Green et al 2004) and/or cerebral angiogenesis (Rhyu et al 2010;Swain et al 2003;Ding et al 2006;Black et al 1990). In support of this, ageinduced cerebral atrophy appears to be less marked in those with higher aerobic fitness (Colcombe et al 2003).…”