Neuroscience
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Perinatal exposure to nicotine produces ventilatory and chemoreflex deficits in neonatal mammals. Medullary 5-HT neurons are putative central chemoreceptors that innervate respiratory nuclei and promote ventilation, receive cholinergic input and express nicotinic acetylcholine receptors (nAChRs). Perforated patch clamp recordings were made from cultured 5-HT neurons dissociated from the medullary raphé of 0-3 day old mice expressing enhanced yellow fluorescent protein driven by the enhancer region for PET1 (ePet-EYFP). ⋯ Nicotine exposed neurons exhibited ∼67% of the response to acidosis recorded in neurons given vehicle (p = 0.005), with older neurons exposed to high dose prenatal and postnatal nicotine, exhibiting only 28% of that recorded in the vehicle neurons (p < 0.01). In neurons exposed to low or high dose prenatal and postnatal nicotine, acute nicotine exposure led to a smaller increase in FR (∼+51% vs +168%, p = 0.026) and response to acidosis (+6% vs +67%, p = 0.014) compared to vehicle. These data show that exposure to nicotine during development reduces chemosensitivity of 5-HT neurons as they mature, an effect that may be related to the abnormal chemoreflexes reported in rodents exposed to nicotine in utero, and may cause a greater risk for sudden infant death syndrome (SIDS).
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Normal sleep-wake behavior is extremely important for humans to maintain basic physiological and cognitive activities. However, the neural mechanisms underlying sleep-wake regulation are not fully understood. The paraventricular nucleus (PVN) of the hypothalamus has been classically defined as a region for the regulation of the hypothalamoneurohypophysial system and autonomic nervous system. ⋯ The calcium activities of PVN glutamatergic neurons began to increase before non-rapid-eye movement (NREM) sleep to wake transitions and NREM sleep to rapid-eye-movement (REM) sleep transitions and began to decrease before wake to NREM sleep transitions. Then we used chemogenetic manipulations together with polysomnographic recordings, activation of PVN neurons increased wakefulness and decreased NREM sleep, while inhibition of PVN neurons caused a reduction in wakefulness and an increase in NREM sleep. Altogether, our findings revealed an important role for PVN glutamatergic neurons in the regulation of wake state.
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The pulvinar, the largest thalamic nucleus in the primate brain, has connections with a variety of cortical areas and is involved in many aspects of higher brain functions. Among cortico-pulvino-cortical systems, the connection between the middle temporal area (MT) and the pulvinar has been thought to contribute significantly to complex motion recognition. Recently, the common marmoset (Callithrix jacchus), has become a valuable model for a variety of neuroscience studies, including visual neuroscience and translational research of neurological and psychiatric disorders. ⋯ Most labeled terminals were small but these comingled with a few large terminals, distributed mainly in the dorsomedial part of the PIm. Our results further delineate the organization of projections from MT to the pulvinar in the marmoset as forming parallel complex networks, which may differentially contribute to motion processing. It is interesting that the densest projections from MT target the PIm, the subnucleus recently reported to preferentially receive direct retinal projections.
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Glutamine is an astroglia-derived precursor of the neurotransmitter glutamate, and its astroglia-to-neuron transfer is controlled by distinct glutamine transporters on the astrocytic and neuronal sites. In this study, we focused on the role of astrocytic glutamine efflux-mediating system N transporter SN1 in the maintenance of glutamatergic neurotransmission by analyzing the electrophysiological parameters ex vivo in the brain slices from control mice and mice in which vivo-morpholino technique was used to diminish SN1 protein. The glutamatergic transmission was characterized by electrophysiological recordings, ultrastructure of neuron terminals, and determination of proteins related to glutamate synaptic transmission: synaptophysin, synaptotagmin, and vit1A. ⋯ SN1 depletion resulted in a reduction of field potentials (FPs), unaltered frequency of spontaneous and miniature excitatory postsynaptic currents (sEPSCs/mEPSCs), and presented a tendency towards a decrease of long-term potentiation (LTP). Ultrastructurally, preserved number of synaptic vesicles, primarily localized centrally of the cell body, correlates with unchanged levels of synaptic proteins. Collectively, the study indicates that glutamatergic transmission proceeds relatively independently of the SN1 - mediated glutamine transfer to the synapse.
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Maternal separation in ABA rats promotes cell proliferation in the dentate gyrus of the hippocampus.
Anorexia nervosa (AN) is a serious eating disorder characterized by self-starvation and excessive weight loss. Several studies support the idea that life stressors during the postnatal period could play a pivotal role in the pathogenesis of AN, underlying the multifactorial etiology of this disease. The activity-based anorexia (ABA) animal model mimics core features of the mental disorder, including severe food restriction, weight loss, and hyperactivity. ⋯ We focused our attention on the adult hippocampal neurogenesis, a process involved in the response to environmental stimuli and stressful condition. We analyzed the volume of the whole hippocampus and the proliferation rate in the dentate gyrus (DG) by quantifying Ki67-cells density and characterizing neuronal phenotype (DCX) and glial cells (GFAP) with double-fluorescence technique. The results obtained showed that only in maternally separated anorexic rats there is an increase of proliferation in DG, underlying the presence of a synergic effect of MS and ABA that boost the proliferation of new neurons and glia progenitors in a more evident way in females in comparison to males.