The slow waves of NREM-sleep reflect experience-dependent plasticity and play a direct role in the restorative functions of sleep. Importantly, slow waves behave as traveling waves and their propagation is assumed to occur through cortico-cortical white matter connections. In this light, the corpus callosum (CC) may represent the main responsible for cross-hemispheric slow wave propagation. To verify this hypothesis, we performed overnight hd-EEG recordings in five patients who underwent total callosotomy due to drug-resistant epilepsy (CP; 2 females), in three non-callosotomized neurological patients (NP; 2 females), and in sample of 24 healthy adult subjects (HS; 13 females). In all CP slow waves displayed a significantly reduced probability of cross-hemispheric propagation and a stronger inter-hemispheric asymmetry. PCO371 purchase In both CP and HS, the incidence of large slow waves within individual NREM epochs tended to differ across hemispheres, with a relative overall predominance of the right over the left hemispherding of NREM slow waves through the study of a rare population of totally callosotomized patients. Our results demonstrate a causal role of the corpus callosum in the cross-hemispheric traveling of sleep slow waves. Additionally, we found that callosotomy does not affect the relative tendency of each hemisphere at generating slow waves. Incidentally, we also found that slow waves tend to originate more often in the right than in the left hemisphere in both callosotomized and healthy adult individuals.Despite extensive research into understanding synaptic mechanisms of striatal plasticity, the functional role played by astrocytes in this region remains to be fully elucidated. It was recently demonstrated that high-frequency stimulation (HFS) of cortical inputs induced long-term depression (LTD) mediated by adenosine A1 receptor (A1R) activation at corticostriatal synapses of the direct pathway (cortico-dSPN) in the dorsolateral striatum (DLS). Because astrocyte-derived adenosine has been shown to regulate synaptic transmission in several brain areas, we investigated whether this form of neuron-astrocyte signaling contributes to synaptic plasticity in the DLS of male and female mice. We found that cortical HFS increases calcium (Ca2+) levels in striatal astrocytes through activation of metabotropic glutamate receptor type 5 signaling (mGluR5) and that this astrocyte-mediated response is necessary for A1R-mediated LTD. Consistent with this, astrocyte activation with Gq DREADDs induced A1R-mediated synaptic depression at cortico-dSPN synapses. Together, these results indicate that astrocytes are integral elements of striatal A1R-mediated LTD.Significance statementAbnormal striatal circuit function is implicated in several disorders such as Parkinson’s Disease and Huntington’s Disease. Thus, there is a need to better understand the mechanisms supporting proper striatal activity. While extensive work has revealed the many important contributions from neurons in striatal function, far less is known about the role of astrocytes in this brain area. We show that long-term depression (LTD) at corticostriatal synapses of the direct pathway is not strictly a neuronal phenomenon; astrocytes respond to corticostriatal stimulation and this astrocyte response is necessary for LTD. This research adds to the accumulating evidence that astrocytes are active and integral players in synaptic communication, and that neuron-astrocyte interactions are key cellular processes involved brain function.Presence of novel or degraded communication sounds likely results in activation of basal forebrain cholinergic neurons increasing release of acetylcholine (ACh) onto pre- and post-synaptic nicotinic acetylcholine receptors (nAChRs) in primary auditory cortex (A1). nAChR subtypes include high-affinity heteromeric nAChRs commonly composed of α4 and β2 subunits and low-affinity homomeric nAChRs composed of α7 subunits. In young male FBN rats, we detail 1) the distribution/expression of nAChR subunit transcripts in excitatory (VGluT1) and inhibitory (VGAT) neurons across A1 layers; 2) heteromeric nAChR binding across A1 layers and 3) nAChR excitability in A1 layer (L) 5 cells. In aged rats, we detailed the impact of aging on A1 nAChR subunit expression across layers, heteromeric nAChR receptor binding, and nAChR excitability of A1 L5 cells.A majority of A1 cells co-expressed transcripts for β2 and α4 with or without α7, while dispersed sub-populations expressed β2 and α7 or α7 alone. nAChR subunit transcripts were ways in which A1 neurons respond to release of ACh in challenging acoustic environments. This study detailed the distribution and expression of nAChR subunit transcript and protein across A1 layers in young and aged rats. Results showed a differential distribution of nAChR subunits across A1 layers. Age-related decreases in transcript/protein expression were reflected in age-related subunit specific functional loss of nAChR signaling to ACh application in A1 layer 5. Together these findings could reflect the age-related decline in selective attention observed in the elderly.Rad3 is the orthologue of ATR and the sensor kinase of the DNA replication checkpoint in Schizosaccharomyces pombe Under replication stress, it initiates checkpoint signaling at the forks necessary for maintaining genome stability and cell survival. To better understand the checkpoint initiation process, we have carried out a genetic screen in fission yeast by random mutation of the genome looking for mutants defective in response to the replication stress induced by hydroxyurea. In addition to the previously reported tel2-C307Y mutant (1), this screen has identified six mutations in rqh1 encoding a RecQ DNA helicase. Surprisingly, these rqh1 mutations except a start codon mutation are all in the helicase domain, indicating that the helicase activity of Rqh1 plays an important role in the replication checkpoint. In support of this notion, integration of two helicase-inactive mutations or deletion of rqh1 generated a similar Rad3 signaling defect and heterologous expression of human RECQ1, BLM and RECQ4 restored the Rad3 signaling and partially rescued a rqh1 helicase mutant.