Neuroscience
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Although selective serotonin reuptake inhibitors are commonly prescribed for prenatal depression, there exists controversy over adverse effects of SSRI use on fetal development. Few studies have adequately isolated outcomes due to SSRI exposure and those due to maternal psychiatric conditions. Here, we directly investigated outcomes of exposure to widely-used SSRIs Fluoxetine and Citalopram on the developing nervous system of Xenopus laevis tadpoles, using an integrative experimental approach. ⋯ Both behavioral and electrophysiological findings indicate that cells and circuits in the Fluoxetine treated optic tecta are hyperexcitable, while the Citalopram group exhibits decreased excitability. Taken together, these results show that early developmental exposure to SSRIs is sufficient to induce neurodevelopmental effects, however these effects can be complex and vary depending on the SSRI. This may explain some discrepancies across human studies, and further underscores the importance of serotonergic signaling for the developing nervous system.
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At the vertebrate neuromuscular junction (NMJ), presynaptic homeostatic potentiation (PHP) refers to the upregulation of neurotransmitter release via an increase in quantal content (QC) when the postsynaptic nicotinic acetylcholine receptors (nAChRs) are partially blocked. The mechanism of PHP has not been completely worked out. In particular, the identity of the presumed retrograde signal is still a mystery. ⋯ Using immunofluorescence we observed ASIC2a and ASIC1 subunits at the NMJ. Our results indicate that protons and ASIC channels are involved in activating PHP at the mouse NMJ. We speculate that the partial blockade of nAChRs leads to a modest decrease in the pH of the synaptic cleft (∼0.2 pH units) and this activates ASIC channels on the presynaptic nerve terminal.
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Emerging evidence supports an increased role for NG2/CSPG4-expressing cells in the process of neuroregeneration and synaptic plasticity, due to the increased production of multifunctional chondroitin sulfate proteoglycan (NG2/CSPG4). However, the response of NG2/CSPG4-expressing cells in spinal cord injury (SCI) remains to be elcudiated. Expression and distribution of NG2/CSPG4-expressing cells were studied by immunoelectron microscopy in the ventral horns (VH) of an intact and injured rat spinal cord. ⋯ At 7 days after SCI at the Th8 level in the reactive glial zone of VH, the expression of NG2/CSPG4 sharply increased in NG2 glia at a distance of 3-5 mm and in reactive astrocytes were observed at all investigated distances caudally from the epicenter of injury. The obtained results indicate the presence of NG2/CSPG4-positive astrocytes in the intact spinal cord, and in the case of damage, an increase in the ability of reactive astrocytes to produce NG2/CSPG4. SCI leads to increased expression of NG2/CSPG4 by NG2 glia in the early stages after injury, which decreases with distance from the epicenter of the injury, as well as at later stages.
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Sensory cortical neurons can nonlinearly integrate a wide range of inputs. The outcome of this nonlinear process can be approximated by more than one receptive field component or filter to characterize the ensuing stimulus preference. The functional properties of multidimensional filters are, however, not well understood. ⋯ The interaction between the two STRFs was reduced by noise exposure in A1 but not in VAF. The results reveal new functional distinctions between A1 and VAF indicating that (i) A1 has stronger interactions of the two STRFs than VAF, (ii) noise exposure diminishes modulation parameter representation contained in the noise more strongly for the first STRF in both fields, and (iii) plasticity induced by noise exposure can affect the strength of filter interactions in A1. Taken together, ascertaining two STRFs per neuron enhances the understanding of cortical information processing and plasticity effects in core auditory cortex.
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Dopamine influences food intake behavior. Reciprocally, food intake, especially of palatable dietary items, can modulate dopamine-related brain circuitries. Among these reciprocal impacts, it has been observed that an increased intake of dietary fat results in blunted dopamine signaling and, to compensate this lowered dopamine function, caloric intake may subsequently increase. ⋯ To determine which of the midbrain dopamine projections may contribute to this effect, we next compared the impact of 6-OHDA lesions of terminal fields, targeting the dorsal striatum, the lateral nucleus accumbens and the medial nucleus accumbens. We found that 6-OHDA lesion of the lateral nucleus accumbens, but not of the dorsal striatum or the medial nucleus accumbens, led to increased fat intake. These findings indicate a role for lateral nucleus accumbens dopamine in regulating food preference, in particular the intake of fat.