Neuroscience
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Xanthurenic acid (XA), formed from 3-hydroxykynurenine (3-HK) in the kynurenine pathway of tryptophan degradation, may modulate glutamatergic neurotransmission by inhibiting the vesicular glutamate transporter and/or activating Group II metabotropic glutamate receptors. Here we examined the molecular and cellular mechanisms by which 3-HK controls the neosynthesis of XA in rat, mouse and human brain, and compared the physiological actions of 3-HK and XA in the rat brain. In tissue homogenates, XA formation from 3-HK was observed in all three species and traced to a major role of kynurenine aminotransferase II (KAT II). ⋯ The effect of 3-HK was reduced in the presence of the KAT inhibitor aminooxyacetic acid. Finally, both 3-HK and XA reduced the power of gamma-oscillatory activity recorded from the hippocampal CA3 region. Endogenous XA, newly formed from 3-HK, may therefore play a physiological role in attentional and cognitive processes.
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Cluster of differentiation 36 (CD36) belongs to the class B scavenger receptor family. CD36 is a glycoprotein found on the surface of various cell types and has been implicated in the mechanism of numerous central nervous system (CNS) diseases. However, the relationship between CD36 and epilepsy remains unknown. ⋯ Whole-cell patch-clamp technique exhibited a decreased frequency of action potentials (APs) in the hippocampal slices of CD36-/- mice. In addition, local field potential (LFP) analysis further indicated that CD36 deletion reduced the frequency and duration of epileptiform-like discharges. These results revealed that CD36 deficiency could produce an antiepileptic effect and could provide new insight into antiepileptic treatment.
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I describe the origins of the British Neuroscience Association (BNA) based on new documents which I have discovered. The foundation of the Brain Research Association (BRA) on February 23rd 1968 was influenced by IBRO, notably its two UK Council members, and by many UK neuroscientists, especially the London-based Black Horse Group. The BRA changed its name to the BNA in 1996. The documents are in the Wellcome Trust Archives.
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If one eye is patched for a period of 2.5 h in human adults, transient changes in sensory eye dominance result with the previously patched eye's contribution being strengthened. Similar changes result from opaque and translucent occlusion suggesting that it is the deprivation of contrast not luminance information that drives these transient shift of sensory eye dominance. ⋯ With further control experiments we show that this deprivation effect critically depends on the absolute luminance of each eye rather than the relative interocular luminance imbalance. These results indicate that changes in contrast gain at an early, monocular stage of the pathway can result in the transient shift of sensory eye dominance.
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Recently, it has been shown that short-term monocular deprivation in adult humans can temporally shift the ocular dominance in favor of the deprived eye. It is not clear whether this form of ocular dominance plasticity can be explained by cortical contrast adaptation, which is known to be orientationally selective. Here we show that if only one eye is deprived of a limited band of orientations for a short period of 2.5 h, the deprived eye's contribution to binocular function at all orientations rather than just those corresponding to the previously deprived orientations is strengthened. This isotropic enhancement is quite different from the orientational enhancement previously reported and suggests a separate neuroplastic mechanism specific to binocular function.