Neuron addition and enlargement in juvenile and adult animals

Locomotion requires bilateral symmetry of neural circuitry in the spinal cord. Although not well understood, the mechanisms responsible for establishing and maintaining this symmetry must balance the numbers, sizes, and connectivity of the neurons on both sides of the spinal cord. Those mechanisms do not cease to function after embryogenesis, since there is substantial evidence that these properties continue to change as juvenile animals grow to adult size. We review the evidence that spinal neuron number and size increase in growing juvenile frogs and mammals. We postulate that these increases are regulated by both local and systemic factors. In addition, we discuss evidence that axotomy of spinal sensory and motor neurons also enlists local and systemic regulatory factors, some of which may also be operative in normal growth and development.     

Mice deleted for the DiGeorge/velocardiofacial syndrome region show abnormal sensorimotor gating and learning and memory impairments.

Del22q11 syndrome is caused by heterozygous deletion of an approximately 3 Mb segment of chromosome 22q11.2. Children diagnosed with del22q11 syndrome commonly have learning difficulties, deficits of motor development, cognitive defects and attention deficit disorder. They also have a higher than normal risk for developing psychiatric disorders, mainly schizophrenia, schizoaffective disorder and bipolar disorder. Here, we show that mice that are heterozygously deleted for a subset of the genes that are deleted in patients have deficits in sensorimotor gating and learning and memory. The finding of sensorimotor gating deficits is particularly significant because patients with schizophrenia and schizotypal personality disorder show similar deficits. Thus, our deletion mouse models at least two major features of the del22q11-associated behavioral phenotype, and as such, represents an animal model of this complex behavioral phenotype. These findings not only open the way to pharmacological analyses that may lead to improved treatments, but also to the identification of gene/s that modulate these specific behaviors in humans.     

Saccadic eye movements evoked by electrical stimulation of the cat's visual cortex

Eye movements were recorded with the scleral search coil method while striate cortex (area 17) was stimulated in alert cats with their heads fixed. Regardless of where stimulation was applied in the retinotopic map, eye position at the onset of stimulation strongly affected the amplitudes of evoked saccades, but had much less influence on their directions. Application of long stimulus trains evoked repeated saccades at all sites tested. Highly convergent or goal-directed saccades were not observed. Cortically evoked saccades appeared to habituate with repeated stimulation and had higher thresholds and longer latencies that those reported for saccades evoked from the superior colliculus. The directions of cortically evoked saccades generally agreed with those predicted from the retinotopic coordinates of the stimulus sites, but saccade amplitudes were usually lower than expected. It is suggested that these findings are consistent with certain characteristics of eye-head coordination in the cat's normal visual orienting behavior. The results are difficult to reconcile with the hypothesis that goal-directed saccades are a normal response to targets outside the cat's oculomotor range.