Neuroscience
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Peripherally restricted analgesics are desirable to avoid central nervous system (CNS) side effects of opioids. Nonsteroidal anti-inflammatory drugs produce peripheral analgesia but have significant toxicity. GABA(B) receptors represent peripheral targets for analgesia but selective GABA(B) agonists like baclofen cross the blood-brain barrier. ⋯ In a mouse model of osteoarthritis, isovaline restored performance during forced exercise to baseline values. Immunohistochemical staining of cutaneous layers of the analgesic test site demonstrated co-localization of GABA(B1) and GABA(B2) receptor subunits on fine nerve endings and keratinocytes. Isovaline represents a new class of peripherally restricted analgesics without CNS effects, mediated by cutaneous GABA(B) receptors.
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It is well known that after cerebral ischemia, brain suffers blood flow changes over time that have been correlated with inflammation, angiogenesis and functional recovery processes. Nevertheless, post-ischemic spatiotemporal changes of brain perfusion have not been fully investigated to date. Here we tested whether PET with [¹³N]ammonia would evidence the perfusion changes presented by different brain regions in an experimental model of brain ischemia. ⋯ [¹³N]ammonia shows hemodynamic changes after stroke involving hyperperfusion that might be related to angiogenesis and functional recovery. Long-term blood hyperperfusion is found both in ischemic and remote areas to infarction. These results may contribute to a better understanding of the evolution of cerebral ischemic lesion in animal models.
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Although short-term synaptic plasticity (STP) is ubiquitous in neocortical synapses its functional role in neural computations is not well understood. Critical to elucidating the function of STP will be to understand how STP itself changes with development and experience. Previous studies have reported developmental changes in STP using acute slices. ⋯ Importantly, despite the change in the PPR we did not observe changes in the time constant governing STP. Since these experiments were conducted in vitro our results indicate that the shift in STP does not depend on in vivo sensory experience. Although sensory experience may shape STP, we suggest that developmental shifts in STP are at least in part ontogenetically determined.
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Alcoholism is a chronic disorder characterized by the appearance of a withdrawal syndrome following the abrupt cessation of alcohol intake that includes symptoms of physical and emotional disturbances, anxiety being the most prevalent symptom. In humans, it was shown that anxiety may increase the probability of relapse. In laboratory animals, however, the use of anxiety to predict alcohol preference has remained difficult. ⋯ Unconditioned and conditioned anxiety-like behavior was assessed by the use of the fear-potentiated startle procedure (FPS). Data collected showed that anxiety and alcohol drinking in HA animals are positively correlated in animals that were made previously familiarized with the anxiolytic effects of alcohol. In addition, anxiety-like behavior induced during alcohol hangover seems to be an effect of changes in glutamatergic neurotransmission into DPAG possibly involving AMPA/kainate and NMDA receptors, among others.
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Previous research has demonstrated that diabetes induced learning and memory deficits. However, the mechanism of memory impairment induced by diabetes is poorly understood. Dietary fatty acids, especially polyunsaturated fatty acids (PUFA), have been shown to enhance learning and memory and prevent memory deficits in various experimental conditions. ⋯ Fish oil dietary supplementation decreased the transient currents and Kv4.2 expression in the hippocampus and partially improved learning performance of diabetic rats. The results of the present study suggested that sodium and potassium currents contributed to the inhibitory effect of diabetes on neuron excitability, further influencing learning and memory processing. Dietary fish oil may modulate the membrane excitability and is a possible strategy for preventing the impairments of diabetes on hippocampal function.