Respiratory syncytial virus (RSV) is the major cause of respiratory illness in infants worldwide. Neurologic alterations, such as seizures and ataxia, have been associated with RSV infection. We demonstrate the presence of RSV proteins and RNA in zones of the brainsuch as the hippocampus, ventromedial hypothalamic nucleus, and brainstem-of infected mice. One month after disease resolution, rodents showed behavioral and cognitive impairment in marble burying (MB) and Morris water maze (MWM) tests. Our data indicate that the learning impairment caused by RSV is a result of a deficient induction of long-term potentiation in the hippocampus of infected animals. In addition, immunization with recombinant bacillus Calmette-Guérin (BCG) expressing RSV nucleoprotein prevented behavioral disorders, corroborating the specific effect of RSV infection over the central nervous system. Our findings provide evidence that RSV can spread from the airways to the central nervous system and cause functional alterations to the brain, both of which can be prevented by proper immunization against RSV.espiratory syncytial virus (RSV) is an enveloped virus with a negative-sensed, single-stranded RNA genome that encodes 11 proteins (1, 2). RSV is the most prevalent pathogen of the Paramyxoviridae family and is the leading cause of lower respiratory tract infection in infants worldwide. RSV infects more than 70% of children in the first year of life, and 100% of children by age 2 years (3, 4). Although most symptoms of RSV infection, such as bronchiolitis and pneumonia, are related to airway inflammation, several central nervous system (CNS) manifestations have been reported in ∼2% of patients with RSVassociated bronchiolitis (5), including seizures, central apnea, lethargy, feeding or swallowing difficulties, muscular tone or strabismus abnormalities, cerebrospinal fluid (CSF) abnormalities, and encephalopathy (6-8). Recently, there has been an increase in the number of case reports on RSV-caused encephalopathy, highlighting the importance of these symptoms (9).Previous clinical studies have suggested an association between neurological symptoms and RSV infection (6,8,10), and other studies have documented the presence of RSV and RSV-specific antibodies in the CSF of patients suffering from severe bronchiolitis (11, 12). However, the pathophysiological mechanism responsible for RSV-caused encephalopathy remains undefined.Despite evidence demonstrating the presence of RSV in the CSF of infected children and CNS alterations resulting from severe respiratory infection by this virus, several aspects of RSV biology regarding the CNS, such as the entrance mechanism, localization, and spreading of RSV in the CNS and its associated tissues, remain obscure. Here, we evaluated whether RSV was able to access the CNS and cause cognitive sequelae using BALB/c mice and Sprague-Dawley rats. Immunofluorescence and quantitative real-time RT-PCR assays revealed the presence of both RSV nucleoprotein (N) and genetic material in the brains of infected anima...

These results suggest that early transvenous phrenic nerve pacing may mitigate ventilator-induced diaphragm dysfunction.

Antidepressant drugs are usually administered for several weeks for the treatment of major depressive disorder. However, they are also prescribed in several additional psychiatric conditions as well as during long-term maintenance treatments. Antidepressants induce adaptive changes in several forebrain structures which include modifications at glutamatergic synapses. We recently found that repetitive administration of the selective serotonin reuptake inhibitor (SSRI) fluoxetine to naïve adult male rats induced an increase of mature, mushroom-type dendritic spines in several forebrain regions. This was associated with an increase of GluA2-containing α-amino-3-hydroxy-5-methylisoxazole-4-propionate receptors (AMPA-Rs) in telencephalic postsynaptic densities. To unravel the functional significance of such a synaptic re-arrangement, we focused on glutamate neurotransmission in the hippocampus. We evaluated the effect of four weeks of 0.7 mg/kg fluoxetine on long-term potentiation (LTP) and long-term depression (LTD) in the CA1 hippocampal subfield. Recordings in hippocampal slices revealed profound deficits in LTP and LTD at Schaffer collateral-CA1 synapses associated to increased spine density and enhanced presence of mushroom-type spines, as revealed by Golgi staining. However, the same treatment had neither an effect on spine morphology, nor on LTP and LTD at perforant path-CA1 synapses. Cobalt staining and immunohistochemical experiments revealed decreased AMPA-R Ca2+ permeability in the stratum radiatum (s.r.) together with increased GluA2-containing Ca2+ impermeable AMPA-Rs. Therefore, 4 weeks of fluoxetine treatment promoted structural and functional adaptations in CA1 neurons in a pathway-specific manner that were selectively associated with impairment of activity-dependent plasticity at Schaffer collateral-CA1 synapses.

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