Neuroscience
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The unique, unmyelinated perikarya of spiral ganglion cells (SGCs) in the human cochlea are often arranged in functional units covered by common satellite glial cells. This micro anatomical peculiarity presents a crucial barrier for an action potential (AP) travelling from the sensory receptors to the brain. Confocal microscopy was used to acquire systematically volumetric data on perikarya and corresponding nuclei in their full dimension along the cochlea of two individuals. ⋯ Results show that temporal parameters of the spiking pattern are affected by the size of the cell body. Cathodic stimulation was found to induce stronger variations of spikes while also leading to the lowest thresholds and longest latencies. Therefore, anodic stimulation leads to a more uniform excitation profile among SGCs with different cell body size.
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The effect of brain-derived neurotrophic factor (BDNF) on depressive-like behavior and serotonin (5-HT) system in the brain of antidepressant sensitive cataleptics (ASC)/Icg mouse strain, characterized by depressive-like behavior, in comparison with the parental nondepressive CBA/Lac mouse strain was examined. Significant decrease of catalepsy and tail suspension test (TST) immobility was shown 17days after acute central BDNF administration (300ng i.c.v.) in ASC mice. In CBA mouse strain, BDNF moderately decreased catalepsy without any effect on TST immobility time. ⋯ Increased tryptophan hydroxylase-2 (Tph-2) and 5-HT(2A) receptor genes expression accompanied by 5-HT(2A) receptor sensitization was shown in BDNF-treated ASC but not in CBA mouse strain, suggesting BDNF-induced increase of the brain 5-HT system functional activity and activation of neurogenesis in "depressive" ASC mice. There were no changes found in the 5-HT transporter mRNA level in BDNF-treated ASC and CBA mice. In conclusion, central administration of BDNF produced prolonged ameliorative effect on depressive-like behavior accompanied by increase of the Tph-2, 5-HT(1A) and 5-HT(2A) genes expression and 5-HT(2A) receptor functional activity in animal model of hereditary behavior disorders.
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Tuning of cortical neurons is often measured as a static property, or during a steady-state regime, despite a number of studies suggesting that tuning depends on when it is measured during a neuron's response (e.g., onset vs. sustained vs. offset). We have previously shown that phase-locked tuning to feature transients evolves as a dynamic quantity from the onset of the sound. In this follow-up study, we examined the phase-independent tuning during feature transients. ⋯ For 95% of neurons, tuning changed significantly from the onset, over the course of the response. For a majority of these cells, the change occurred within the first 40ms following a feature onset, often even around 10-20ms. This solidifies the idea that tuning can change rapidly from onset tuning to the sustained, steady-state tuning.
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Inhibition of substance P (SP) activity through the use of NK1 receptor antagonists has been shown to be a promising neuroprotective therapy following traumatic brain injury (TBI). Conversely, recent research has implicated SP in the stimulation of neurogenesis, suggesting that the neuropeptide has the potential to promote recovery following TBI. This study characterised the effects of SP and the NK1 antagonist, n-acetyl tryptophan (NAT), on cell proliferation following diffuse TBI. ⋯ Infusion of SP (±NAT) promoted cellular proliferation in the subventricular zone and dentate gyrus following TBI. This increase was largely associated with microglial proliferation and did not correspond with functional improvements. These results suggest that NAT treatment results in neuroprotection following TBI, mediated in part via inhibition of microglia.
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Parkinson's disease (PD) is a progressive neurodegenerative disorder whose etiology is thought to have environmental (toxin) and genetic contributions. The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyrimidine (MPTP) induces pathological features of PD including loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and striatal dopamine (DA) depletion. We previously described the striatal transcriptional response following acute MPTP administration in MPTP-sensitive C57BL/6J mice. ⋯ However neither paraquat nor MPTP elicits cross-attenuation. Thus exposure to specific toxins triggers distinct transcriptional responses in striatum that are influenced by prior exposure to the same toxin. The prolonged refractory period described here for MPTP could explain at the molecular level the reported discrepancies between different MPTP administration regimens and may have implications for our understanding of the relationship between environmental toxin exposure and PD.