Long-term administration of paroxetine increases cortical EEG beta and gamma band activities in healthy awake rats.

Understanding the electrophysiological properties of antidepressant medications is important to resolve the response heterogeneity of these drugs in clinical practice. Administration of paroxetine, a selective serotonin reuptake inhibitor, has been shown to increase serotonin levels that affect cortical activities in healthy subjects. However, the extent to which cortical oscillations can be altered by ongoing administration of paroxetine is not known.

Neutralization of Interleukin 1-beta is associated with preservation of thalamic capillaries after experimental traumatic brain injury.

Introduction: Traumatic brain injury to thalamo-cortical pathways is associated with posttraumatic morbidity. Diffuse mechanical forces to white matter tracts and deep grey matter regions induce an inflammatory response and vascular damage resulting in progressive neurodegeneration. Pro-inflammatory cytokines, including interleukin-1β (IL-1β), may contribute to the link between inflammation and the injured capillary network after TBI.

Impaired oligodendrogenesis in the white matter of aged mice following diffuse traumatic brain injury.

Senescence is a negative prognostic factor for outcome and recovery following traumatic brain injury (TBI). TBI-induced white matter injury may be partially due to oligodendrocyte demise. We hypothesized that the regenerative capacity of oligodendrocyte precursor cells (OPCs) declines with age.

RGS5: a novel role as a hypoxia-responsive protein that suppresses chemokinetic and chemotactic migration in brain pericytes.

Adaptive biological mechanisms to hypoxia are crucial to maintain oxygen homeostasis, especially in the brain. Pericytes, cells uniquely positioned at the blood-brain interface, respond fast to hypoxia by expressing regulator of G-protein signalling 5 (RGS5), a negative regulator of G-protein-coupled receptors. RGS5 expression in pericytes is observed in pathological hypoxic environments (e.

Diffuse Traumatic Injury in the Mouse Disrupts Axon-Myelin Integrity in the Cerebellum.

Cerebellar dysfunction after traumatic brain injury (TBI) is commonly suspected based on clinical symptoms, although cerebellar pathology has rarely been investigated. To address the hypothesis that the cerebellar axon-myelin unit is altered by diffuse TBI, we used the central fluid percussion injury (cFPI) model in adult mice to create widespread axonal injury by delivering the impact to the forebrain. We specifically focused on changes in myelin components (myelin basic protein [MBP], 2',3'-cyclic nucleotide 3'-phosphodiesterase [CNPase], nodal/paranodal domains [neurofascin (Nfasc), ankyrin-G], and phosphorylated neurofilaments [SMI-31, SMI-312]) in the cerebellum, remote from the impact, at two, seven, and 30 days post-injury (dpi).

Beta secretase 1-dependent amyloid precursor protein processing promotes excessive vascular sprouting through NOTCH3 signalling.

Amyloid beta peptides (Aβ) proteins play a key role in vascular pathology in Alzheimer's Disease (AD) including impairment of the blood-brain barrier and aberrant angiogenesis. Although previous work has demonstrated a pro-angiogenic role of Aβ, the exact mechanisms by which amyloid precursor protein (APP) processing and endothelial angiogenic signalling cascades interact in AD remain a largely unsolved problem. Here, we report that increased endothelial sprouting in human-APP transgenic mouse (TgCRND8) tissue is dependent on β-secretase (BACE1) processing of APP.

Interleukin-1 Beta Neutralization Attenuates Traumatic Brain Injury-Induced Microglia Activation and Neuronal Changes in the Globus Pallidus.

Traumatic brain injury (TBI) increases the risk of delayed neurodegenerative processes, including Parkinson's disease (PD). Interleukin-1beta (IL-1β), a key pro-inflammatory cytokine, may promote secondary injury development after TBI. Conversely, neutralizing IL-1β was found to improve functional recovery following experimental TBI.

Regulator of G-protein signaling 5 regulates the shift from perivascular to parenchymal pericytes in the chronic phase after stroke.

Poststroke recovery requires multiple repair mechanisms, including vascular remodeling and blood-brain barrier (BBB) restoration. Brain pericytes are essential for BBB repair and angiogenesis after stroke, but they also give rise to scar-forming platelet-derived growth factor receptor β (PDGFR-β)-expressing cells. However, many of the molecular mechanisms underlying this pericyte response after stroke still remain unknown.

Loss of Regulator of G-Protein Signaling 5 Leads to Neurovascular Protection in Stroke.

Background and Purpose- In ischemic stroke, breakdown of the blood-brain barrier (BBB) aggravates brain damage. Pericyte detachment contributes to BBB disruption and neurovascular dysfunction, but little is known about its regulation in stroke. Here, we investigated how loss of RGS5 (regulator of G protein signaling 5) in pericytes affects BBB breakdown in stroke and its consequences.

The pericyte secretome: Potential impact on regeneration.

Personalized and regenerative medicine is an emerging therapeutic strategy that is based on cell biology and biomedical engineering used to develop biological substitutes to maintain normal function or restore damaged tissues and organs. The secretory capacities of different cell types are now explored as such possible therapeutic regenerative agents in a variety of diseases. A secretome can comprise chemokines, cytokines, growth factors, but also extracellular matrix components, microvesicles and exosomes as well as genetic material and may differ depending on the tissue and the stimulus applied to the cell.

STAT3 precedes HIF1α transcriptional responses to oxygen and oxygen and glucose deprivation in human brain pericytes.

Brain pericytes are important to maintain vascular integrity of the neurovascular unit under both physiological and ischemic conditions. Ischemic stroke is known to induce an inflammatory and hypoxic response due to the lack of oxygen and glucose in the brain tissue. How this early response to ischemia is molecularly regulated in pericytes is largely unknown and may be of importance for future therapeutic targets.

Pericytes secrete pro-regenerative molecules in response to platelet-derived growth factor-BB.

Brain pericytes not only maintain the anatomical, biochemical and immune blood-brain barrier, but display features of mesenchymal stem cells (MSCs) in vitro. MSCs have pro-regenerative properties attributed to their secretome. However, whether also brain pericytes possess such pro-regenerative capacities is largely unknown.

Platelet-derived growth factor-BB has neurorestorative effects and modulates the pericyte response in a partial 6-hydroxydopamine lesion mouse model of Parkinson's disease.

Parkinson's disease (PD) is a neurodegenerative disease where the degeneration of the nigrostriatal pathway leads to specific motor deficits. There is an unmet medical need for regenerative treatments that stop or reverse disease progression. Several growth factors have been investigated in clinical trials to restore the dopaminergic nigrostriatal pathway damaged in PD.

Endogenous brain pericytes are widely activated and contribute to mouse glioma microvasculature.

Glioblastoma multiforme (GBM) is the most common brain tumor in adults. It presents an extremely challenging clinical problem, and treatment very frequently fails due to the infiltrative growth, facilitated by extensive angiogenesis and neovascularization. Pericytes constitute an important part of the GBM microvasculature.

Brain pericytes acquire a microglial phenotype after stroke.

Pericytes are located on the abluminal side of endothelial cells lining the microvasculature in all organs. They have been identified as multipotent progenitor cells in several tissues of the body including the human brain. New evidence suggests that pericytes contribute to tissue repair, but their role in the injured brain is largely unknown.

Perivascular mesenchymal stem cells in the adult human brain: a future target for neuroregeneration?

Perivascular adult stem cells have been isolated from several tissues, including the adult human brain. They have unique signatures resembling both pericytes and mesenchymal stem cells. Understanding the nature of these cells in their specific vascular niches is important to determine their clinical potential as a new adult stem cell source.

The adult human brain harbors multipotent perivascular mesenchymal stem cells.

Blood vessels and adjacent cells form perivascular stem cell niches in adult tissues. In this perivascular niche, a stem cell with mesenchymal characteristics was recently identified in some adult somatic tissues. These cells are pericytes that line the microvasculature, express mesenchymal markers and differentiate into mesodermal lineages but might even have the capacity to generate tissue-specific cell types.

Ischemia/reperfusion in rat: antioxidative effects of enoant on EEG, oxidative stress and inflammation.

Primary Objective: The present study was undertaken to evaluate whether enoant, which is rich in polyphenols, has any effect on electroencephalogram (EEG), oxidative stress and inflammation in ischemia/reperfusion (I/R) injury.

Methods: Ischemia was induced by 2-hour occlusion of bilateral common carotid artery. Animals orally received enoant.

Adult generation of glutamatergic olfactory bulb interneurons.

The adult mouse subependymal zone (SEZ) harbors neural stem cells that are thought to exclusively generate GABAergic interneurons of the olfactory bulb. We examined the adult generation of glutamatergic juxtaglomerular neurons, which had dendritic arborizations that projected into adjacent glomeruli, identifying them as short-axon cells. Fate mapping revealed that these originate from Neurog2- and Tbr2-expressing progenitors located in the dorsal region of the SEZ.

The role of solid food intake in antimuscarinic-induced convulsions in fasted mice.

Animals treated with scopolamine after fasting develop convulsions after they are allowed to eat ad libitum. This study was aimed at investigating the effect on these convulsions of liquid food intake, feeding by gavage, and placebo. Fasted mice treated with saline or scopolamine were allowed to eat solid food, slurry food or liquid food ad libitum, given placebo, or given liquid food by gavage.

Proliferating neuronal progenitors in the postnatal hippocampus transiently express the proneural gene Ngn2.

Little is known of the transcription factors expressed by adult neural progenitors produced in the hippocampal neurogenic niche. Here, we study the expression of the proneural basic helix-loop-helix (bHLH) transcription factor Neurogenin-2 (Ngn2) in the adult hippocampus. We have characterized the pattern of expression of Ngn2 in the adult hippocampus using immunostaining for Ngn2 protein and a Ngn2-green fluorescent protein (GFP) reporter mouse strain.

Electroencephalographic characterization of scopolamine-induced convulsions in fasted mice after food intake.

The present study was conducted to evaluate scopolamine-induced convulsions in fasted mice after food intake effects on the cortical electroencephalogram (EEG). Continuous EEG recordings were taken with Neuroscan for 10 min in freely moving mice with six chronic cortical electrode implants. Animals were weighed and deprived of food for 48 h.

Conditional labeling of newborn granule cells to visualize their integration into established circuits in hippocampal slice cultures.

The dentate gyrus continues to produce new granule cells throughout life. Understanding the mechanisms underlying their integration into the pre-existing hippocampal circuitry is of crucial importance. In the present study, we developed an approach allowing visual tracking of newborn granule cells in hippocampal organotypic slices.