Neuroscience
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Stimulation of neurons in the ventrolateral periaqueductal gray (PAG) produces antinociception as well as cardiovascular depressor responses that are mediated in part by pontine noradrenergic neurons. A previous report using light microscopy has described a pathway from neurons in the ventrolateral PAG to noradrenergic neurons in the A5 cell group that may mediate these effects. The present study used anterograde tracing and electron microscopic analysis to provide more definitive evidence that neurons in the ventrolateral PAG form synapses with noradrenergic and non-catecholaminergic A5 neurons in Sasco Sprague-Dawley rats. ⋯ In both rostral and caudal subdivisions of the A5, nearly 40% of the anterogradely-labeled terminals formed synapses with non-catecholaminergic dendrites, and about 45% formed axoaxonic synapses. These results provide direct evidence for a monosynaptic pathway from neurons in the ventrolateral PAG to noradrenergic and non-catecholaminergic neurons in the A5 cell group. Further studies should evaluate if this established monosynaptic pathway may contribute to the cardiovascular depressor effects or the analgesia produced by the activation of neurons in the ventrolateral PAG.
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After trauma brain injury, a large number of cells die, releasing neurotoxic chemicals into the extracellular medium, decreasing cellular glutathione levels and increasing reactive oxygen species that affect cell survival and provoke an enlargement of the initial lesion. Alpha-lipoic acid is a potent antioxidant commonly used as a treatment of many degenerative diseases such as multiple sclerosis or diabetic neuropathy. Herein, the antioxidant effects of lipoic acid treatment after brain cryo-injury in rat have been studied, as well as cell survival, proliferation in the injured area, gliogenesis and angiogenesis. ⋯ All those facts allow the formation of new neural tissue. In view of the results herein, lipoic acid might be a plausible pharmacological treatment after brain injury, acting as a neuroprotective agent of the neural tissue, promoting angiogenesis and reducing the glial scar formation. These findings open new possibilities for restorative strategies after brain injury, stroke or related disorders.
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Retinogenesis is a developmental process that involves the sequential formation of neurons and glia from retinal progenitors. Once retinogenesis is completed, Müller glial cells can be stimulated to differentiate into neuronal lineages and constitute a retina-intrinsic source of neural progenitors. The identification of the intrinsic and extrinsic factors that control proliferation and differentiation of Müller cells or retinal progenitors is needed in order to fully define their potential therapeutic use in regenerative approaches. ⋯ Furthermore, consistent with the role of CREB as a histone acetyltransferase recruiter, we demonstrate that GABA induces the modification of histone H4 acetylation pattern in these cells suggesting that epigenetic alterations participate in the differentiation process. Our results support the notion that postnatal retinal progenitors derived from Müller glia primary cell cultures respond to GABA through the same molecular pathway previously characterized in hippocampal progenitors and developing neurons. We speculate that the induction of GABA receptor signaling could represent a novel strategy to enhance neural versus glial specification from these cells through genetic and epigenetic mechanisms.
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Motor learning adjusts movement size and direction to keep movements accurate. A useful model of motor learning, saccade adaptation, uses intra-saccade target movement to make saccades seem inaccurate and elicit adaptive changes in saccades. In the most studied saccade adaptation procedure, which we call short-term saccade adaptation (STSA), monkeys decrease or increase the size of their saccades by tracking 1000-2000 adapting target movements in a single saccade session. ⋯ In contrast to a single size-decreasing STSA, a single size-increasing STSA does not prevent additional saccade size increase at the normal rate when a monkey continues to track adapting target movements. We conclude that size-increasing LTSA is slower than size-decreasing LTSA but can make larger changes in saccade size. Size-increasing and size-decreasing LTSA use distinct mechanisms with different performance characteristics.
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In two related experiments, neurotoxic lesions were placed in the anterior thalamic nuclei of adult rats. The rats were then trained on behavioral tasks, immediately followed by the immunohistochemical measurement of molecules linked to neural plasticity. These measurements were made in limbic sites including the retrosplenial cortex, the hippocampal formation, and parahippocampal areas. ⋯ No changes in GAP-43 were detected. The results not only point to changes in several limbic sites (retrosplenial cortex and hippocampus) following anterior thalamic damage, but also indicate that these changes include decreased levels of pCREB. As pCREB is required for neuronal plasticity, partly because of its regulation of immediate early-gene expression, the present findings reinforce the concept of an 'extended hippocampal system' in which hippocampal function is dependent on distal sites such as the anterior thalamic nuclei.