Neuroscience
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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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Afferent chorda tympani (CT) fibers innervating anterior tongue fungiform papillae have neuron cell bodies in the geniculate ganglion (GG). To characterize electrophysiological and receptive field properties, we recorded extracellular responses from single GG neurons to lingual application with chemical, thermal and mechanical stimuli. Receptive field size was mapped by electrical stimulation of individual fungiform papillae. ⋯ The receptive field sizes for CHEMICAL, and CHEMICAL/THERMAL neurons averaged five papillae exceeding the field size of THERMAL and TACTILE neurons which averaged about two papillae. Detailed analysis of the receptive field of CHEMICAL/THERMAL neurons revealed that within one field only a subset of the fungiform papillae making up the receptive field responded to the cold stimuli, whereas the other papillae responded only to chemical stimuli. These finding demonstrate that fungiform papilla are complex sensory organs with a multisensory function suggesting a unique role in detecting and sampling food components prior to ingestion.
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The neuroimmune factor IL-6 has been shown to regulate hippocampal long-term potentiation (LTP), an activity-dependent enhancement of synaptic transmission that plays a central role in memory and learning. This IL-6 action was demonstrated with relatively short IL-6 exposure, and may reflect physiological actions of IL-6. IL-6 is also expressed chronically at elevated levels in the central nervous system (CNS) under pathological conditions such as neurological disorders. ⋯ An inhibitor of mTOR, rapamycin, reduced L-LTP in slices from both genotypes, and eliminated the difference in magnitude of L-LTP between IL-6 and non-tg hippocampus. There were no genotypic effect of rapamycin on basal synaptic transmission, but synaptic responses during the LTP induction protocol were reduced in IL-6 tg slices, an effect that could contribute to the reduction of L-LTP in the IL-6 tg slices. These results indicate that persistently increased levels of IL-6 can lead to alterations in mTOR regulation of L-LTP, possibly affecting learning and memory.
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Ubiquitin-proteasome system (UPS) has emerged as major molecular mechanism which modulates synaptic plasticity. However, very little is known about what happens if this system fails during postnatal brain development. In the present study, MG132 was administered intracerebroventricularly in BALB/c mice pups at postnatal day one (P1), a very crucial period for synaptogenesis. ⋯ Real-Time PCR analyses showed significant increase in hippocampal expression of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunit glutamate A1 (GluA1), but no change in the brain-derived neurotrophic factor (Bdnf) expression in MG132 mice. Western blot analyses showed decreased levels of pThr286-CaMKIIα:CaMKIIα and pSer133-CREB:CREB ratio but increased pro:mature BDNF ratio in the hippocampus of MG132 mice. Taken together, postnatal proteasome inhibition could lead to accumulation of intracellular amyloid-β protein aggregates, which mediate hippocampus-dependent spatial memory impairments in adult mice.
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Pseudorabies virus (PRV), a neurovirulent α-herpesvirus, spreads between neurons at synaptic connections. PRV-infected neurons have been shown to exhibit functional deficits with the attenuated PRV152 Bartha strain negatively influencing neuronal functioning in in vitro model systems. However, the impact of this attenuated PRV152 Bartha strain on the native central nervous system has not been fully explored. ⋯ The minor changes in the approximated passive membrane parameters induced by the infection cannot explain the full loss in excitability, indicating that channel densities and properties have changed. This impact on neuronal functioning might contribute to the lethal neurovirulent effects of PRV viruses as vital neuronal circuits might cease activity. Since the detrimental effects of the attenuated PRV152 Bartha strain are reduced compared to wild-type strains, it comprises an excellent tool to study the neuropathological mechanisms of viral infections.