Neuroscience
-
Traumatic brain injury (TBI) is known to impair synaptic function, and subsequently contribute to observed cognitive deficits. Retinoic Acid (RA) signaling modulates expression of synaptic plasticity proteins and is involved in hippocampal learning and memory. All trans-retinoic acid (ATRA), a metabolite of Vitamin A, has been identified as a potential pharmacotherapeutic for other neurological disorders due to this role. ⋯ ATRA treatment significantly recovered Ng synaptic protein expression, while having no effect on motor performance, spatial learning, and memory, and GluA1 expression after TBI. RA signaling protein expression is unchanged 2 weeks after TBI. Overall, ATRA administration after TBI showed limited therapeutic benefits compared to the vehicle.
-
Intralaminar thalamic nuclei, including the central medial nucleus (CMT), have been classically implicated in the control of attentional functional states such as sleep-wake transitions. In rodents, the CMT innervates large cortical and subcortical areas bilaterally, including sensorimotor regions of the cortex and striatum, but its contribution to motor function, which regularly develops in faster temporal scales than attentional states, is still far from being completely understood. Here, by using a novel behavioral protocol to evaluate bilateral coordination in rats, combined with electrophysiological recordings and optogenetic manipulations, we studied the contribution of the CMT to motor control and coordination. ⋯ The same type of stimulations produced a significant increase in bilateral movement coordination of the forelimbs accompanied by a decrease in movement trajectory variability. Optogenetic inactivation of the CMT did not affect motor execution but significantly increased execution times, suggesting less interest in the task. Altogether, our results indicate that brief CMT activations create windows of synchronized bilateral cortico-striatal activity, suitable to facilitate motor coordination in temporal scales relevant for motor execution.
-
Cognitive deficit remains an intractable symptom of schizophrenia, accounting for substantial disability. Despite this, little is known about the cause of cognitive dysfunction in schizophrenia. Recent studies suggest that schizophrenia patients show several changes in dentate gyrus structure and functional characteristic of immaturity. ⋯ Additionally, CaMKIIα-hKO mice showed spontaneous bursts of spike wave activity, possibly indicating absence seizures. The GABAB agonist baclofen increased, while the GABAB antagonist CGP35348 and the T-Type Ca2+ channel blocker Ethosuximide decreased spike wave burst frequency. None of these changes in event-related potentials or EEG oscillations are characteristic of those observed in general population of patients with schizophrenia; yet, CaMKIIα-hKO mice likely model a subpopulation of patients with schizophrenia.