Neuroscience
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Adolescence is a critical developmental stage of life during which the prefrontal cortex (PFC) matures, and binge drinking and alcohol abuse are common. Recent studies have found that ethanol increases neuroinflammation via upregulated high-mobility group box 1 (HMGB1) signaling through Toll-like receptors (TLRs). HMGB1/TLR 'danger signaling' induces multiple brain innate immune genes that could alter brain function. ⋯ Adolescent intermittent ethanol treatment did not alter adult spatial learning on the Barnes maze, but did cause reversal learning deficits and increased perseverative behavior. Barnes maze deficits correlated with the expression of danger signal receptors in the PFC. Taken together, these findings provide evidence that adolescent binge drinking leads to persistent upregulation of innate immune danger signaling in the adult PFC that correlates with adult neurocognitive dysfunction.
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Opiates disrupt neural functions in many brain areas, including visual cortex. Previous studies have indicated substantial changes of many neuronal response properties induced by chronic morphine exposure in the visual information processing system. ⋯ Our results indicated significantly lower contrast sensitivity in morphine-treated cats than in saline-treated cats and V1 neurons in morphine-treated cats exhibited enhanced maximum visual responses, higher baseline responses and lower signal-to-noise ratios compared with saline-treated cats. These findings provide some neurobiological evidence for the morphine-mediated degenerations of the visual cortex, which could underlie the opiate-induced deficits in visual function.
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Thalamic cell activity is under a significant influence of inhibition from the thalamic reticular nucleus (TRN) that is composed of domains connected with first and higher order thalamic nuclei, which are thought to subserve transmission of sensory inputs to the cortex and cortico-thalamo-cortical transmission of cortical outputs, respectively. Provided that TRN cells have distinct activities along with their projections to first and higher order thalamic nuclei, TRN cells could shape cell activities of the two thalamic nuclei in different manners for the distinct functions. In anesthetized rats, visual response and spontaneous activity were recorded from TRN cells projecting to the dorsal lateral geniculate (first order) and lateral posterior (higher order) nuclei (TRN-DLG and TRN-LP cells), using juxta-cellular recording and labeling techniques. ⋯ Further, the features of burst spiking were related with the locations of topographically connected cell bodies and terminal fields. The difference in burst spiking contrasts with the difference between thalamic cells in the DLG and LP, which show low and high levels of burst spiking, respectively. The synergy between thalamic and TRN cell activities with their contrasting features of burst spiking may compose distinctive sensory processing and attentional gating functions of geniculate and extra-geniculate systems.
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The anterior and rostral paracapsular intercalated islands (AIC and PIC, respectively) were studied in the context of the amygdaloid modulation of fear/anxiety using horizontal sections. The structural analysis carried out using silver-impregnated specimens revealed that the AIC is composed of tightly packed, medium-sized spiny neurons with distinct dendritic and axonal patterns that send projecting axons to the central nucleus of the amygdala. The AIC occupies a strategic position between the basolateral amygdaloid complex and the caudal limb of the anterior commissure from which it receives fibers en passage and axon terminals. ⋯ Immunohistochemical analysis indicated that, within the AIC and rostral PIC, the distance between tyrosine hydroxylase-immunoreactive terminals and the punctate dopamine D(1) receptor immunoreactivity, was in the micrometer range. These results indicate a short distance and a rapid extrasynaptic form of dopamine volume transmission mediated via D(1) receptors in the AIC and PIC which may enhance fear and anxiety by suppressing feed-forward inhibition in the basolateral and central amygdaloid nuclei. The strong suggestion for a commissural axon projection to the AIC documented here, coupled with the previous evidences indicting an isocortical and amygdalar contributions to the anterior commissure, opens the possibility that the AIC may be involved in decoding nerve impulses arising from both the ipsi- and contra-lateral forebrain to, in turn, modulate the homolateral amygdala.
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Neurons of the ventral tegmental area (VTA) are critical in the rewarding and reinforcing properties of drugs of abuse. Desensitization of VTA neurons to moderate extracellular concentrations of dopamine (DA) is dependent on protein kinase C (PKC) and intracellular calcium levels. This desensitization is called DA inhibition reversal, as it requires concurrent activation of D2 and D1-like receptors; activation of D2 receptors alone does not result in desensitization. ⋯ Desensitization to baclofen was dependent on PKC. Dopamine inhibition was reduced for 30 min after baclofen-induced desensitization and conversely, the magnitude of baclofen inhibition was reduced for 30 min by long-duration application of dopamine, but not quinpirole. These results indicate that D2 and GABA(B) receptors share some PKC-dependent mechanisms of receptor desensitization.