Processing of information from the parafascicular nucleus of the thalamus through the basal ganglia.

Accumulating evidence implicates the parafascicular nucleus of the thalamus (Pf) in basal ganglia (BG)-related functions and pathologies. Despite Pf connectivity with all BG components, most attention is focused on the thalamostriatal system and an integrated view of thalamic information processing in this network is still lacking. Here, we addressed this question by recording the responses elicited by Pf activation in single neurons of the substantia nigra pars reticulata (SNr), the main BG output structure in rodents, in anesthetized mice. We performed optogenetic activation of Pf neurons innervating the striatum, the subthalamic nucleus (STN), or the SNr using virally mediated transcellular delivery of Cre from injection in either target in Rosa26-LoxP-stop-ChR2-EYFP mice to drive channelrhodopsin expression. Photoactivation of Pf neurons connecting the striatum evoked an inhibition often followed by an excitation, likely resulting from the activation of the trans-striatal direct and indirect pathways, respectively. Photoactivation of Pf neurons connecting the SNr or the STN triggered one or two early excitations, suggesting partial functional overlap of trans-subthalamic and direct thalamonigral projections. Excitations were followed in about half of the cases by an inhibition that might reflect recruitment of intranigral inhibitory loops. Finally, global Pf stimulation, electrical or optogenetic, elicited similar complex responses comprising up to four components: one or two short-latency excitations, an inhibition, and a late excitation. These data provide evidence for functional connections between the Pf and different BG components and for convergence of the information processed through these pathways in single SNr neurons, stressing their importance in regulating BG outflow.

[Assessment of psycho-trauma caused by the aggressions committed by patients with psychosis against their family caregivers: across-sectional survey]. / Évaluation du psycho-traumatisme lié aux agressions commises par les patients psychotiques sur leurs aidants familiaux: enquête transversale dans la région de Sfax, Tunisie.

INTRODUCTION: the management of patients with psychosis is associated with a risk of exposure to violence which can affect all the stakeholders, in particular the family entourage. Caregiving role generates violence and this can have a psychological impact on the caregivers. The purpose of this study is to evaluate the prevalence of aggressions perpetrated by patients with psychosis on their family caregivers as well as to assess the psychological and traumatic impact on family caregivers and to identify factors associated with it. METHODS: family caregivers of patient with psychosis were interviewed. We used two psychometric scales: the perception of prevalence of aggression scale (POPAS) and the impact of event scale-revised. RESULTS: the whole number of participants was 95. Three out of four caregivers (75.8%) reported having been subjected to moderate to severe aggressions by their sick relatives during the past year. Moderate to severe aggressions were significantly more common among older male caregivers, parents of patients with psychosis living in a different home. Fifty-four point seven percent of caregivers had possible posttraumatic stress disorder (PTSD) and the risk of developing this disorder increased significantly as the perceived severity of aggressions increased. The same sociodemographic profile of the caregivers, related to the severity of the aggressions, was associated with a risk of developing PTSD in the caregivers. CONCLUSION: the aggressions committed by patients with psychosis against their family caregivers appear to have a significant psychological and traumatic impact. Interventions targeting violence committed by patients with psychosis in their family environment should also be integrated into patient management.

S100ß-mediated astroglial control of firing and input processing in layer 5 pyramidal neurons of the mouse visual cortex.

KEY POINTS: Inputs impinging on layer 5 pyramidal neurons perform essential operations as these cells represent one of the most important output carriers of the cerebral cortex. However, the contribution of astrocytes, a type of glial cell, to these operations is poorly documented. Here we found that optogenetic activation of astrocytes in the vicinity of layer 5 in the mouse primary visual cortex induces spiking in local pyramidal neurons through Nav1.6 ion channels and prolongs the responses elicited in these neurons by stimulation of their distal inputs in cortical layer 1. This effect partially involved glutamatergic signalling but relied mostly on the astrocytic calcium-binding protein S100ß, which regulates the concentration of calcium in the extracellular space around neurons. These findings show that astrocytes contribute to the fundamental computational operations of the cortex by acting on the ionic environment of neurons. ABSTRACT: The most complex cerebral functions are performed by the cortex, whose most important output is carried out by its layer 5 pyramidal neurons. Their firing reflects integration of the sensory and contextual information that they receive. There is evidence that astrocytes influence cortical neuron firing through the release of gliotransmitters such as ATP, glutamate or GABA. These effects have been described at the network and at the synaptic levels, but it is still unclear how astrocytes influence neuron input-output transfer function at the cellular level. Here, we used optogenetic tools coupled with electrophysiological, imaging and anatomical approaches to test whether and how astrocytic activation affected processing of distal inputs to layer 5 pyramidal neurons (L5PNs). We show that optogenetic activation of astrocytes near L5PN cell body prolonged firing induced by distal inputs to L5PNs and potentiated their ability to trigger spikes. The observed astrocytic effects on L5PN firing involved glutamatergic transmission to some extent but relied mostly on release of S100ß, an astrocytic Ca2+ -binding protein that decreases extracellular Ca2+ once released. This astrocyte-evoked decrease in extracellular Ca2+ elicited firing mediated by activation of Nav1.6 channels. Our findings suggest that astrocytes contribute to the cortical fundamental computational operations by controlling the extracellular ionic environment.