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Results for “CEREBELLAR CORTEX”

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PubMed2000

Direct projection from the cardiovascular control region of the cerebellar cortex, the lateral nodulus-uvula, to the brainstem in rabbits.

In decerebrate unanesthetized rabbits, electrical stimulation of the lateral nodulus-uvula in the cerebellar vermal cortex evoked an increase in renal sympathetic nerve activity, an increase in blood pressure and a decrease in renal arterial blood flow, which were all in contrast to the effects reported previously in the anesthetized rabbits. In order to identify the pathway mediating these responses, we investigated the Purkinje cell projection from the lateral nodulus-uvula using both anterograde (biotinylated dextran amine, BDA) and retrograde (horseradish peroxidase, HRP) tracing methods in rabbits. When BDA was iontophoretically injected into the lateral nodulus-uvula, labeled Purkinje cell axons were found within and around the superior and inferior cerebellar peduncles (SCP and ICP, respectively). Furthermore, terminal-like fields were found in the dentate and vestibular nuclei as reported in previous studies. However, the terminal-like patterns that we observed in the parabrachial nucleus (PB) in the rabbit have not been reported yet. When HRP was microinjected into the lateral PB, retrogradely labeled Purkinje cells were found in the lateral nodulus-uvula. These results indicate that Purkinje cells in the lateral nodulus-uvula project into the vestibular nuclei via the ICP and to the lateral PB via the SCP. We suggest that these two pathways mediating cardiovascular responses have different sensitivities to anesthetics.

Animals↗
PubMed2001

Beta1-class integrins regulate the development of laminae and folia in the cerebral and cerebellar cortex.

Mice that lack all beta1-class integrins in neurons and glia die prematurely after birth with severe brain malformations. Cortical hemispheres and cerebellar folia fuse, and cortical laminae are perturbed. These defects result from disorganization of the cortical marginal zone, where beta1-class integrins regulate glial endfeet anchorage, meningeal basement membrane remodeling, and formation of the Cajal-Retzius cell layer. Surprisingly, beta1-class integrins are not essential for neuron-glia interactions and neuronal migration during corticogenesis. The phenotype of the beta1-deficient mice resembles pathological changes observed in human cortical dysplasias, suggesting that defective integrin-mediated signal transduction contributes to the development of some of these diseases.

Animals↗