Transient cerebral ischemia induces the neuroglial proliferative activity and the potential to redirect neuroglial differentiation.

Brain injury triggers a complex response involving morphological changes, cellular proliferation, and differentiation of newly formed neuroglial subpopulations. These processes have been extensively studied in animal stroke models with permanent large vessel occlusion. However, less is known about neuroglial response after transient cerebral ischemia.

Neuroplasticity and Multilevel System of Connections Determine the Integrative Role of Nucleus Accumbens in the Brain Reward System.

A growing body of evidence suggests that nucleus accumbens (NAc) plays a significant role not only in the physiological processes associated with reward and satisfaction but also in many diseases of the central nervous system. Summary of the current state of knowledge on the morphological and functional basis of such a diverse function of this structure may be a good starting point for further basic and clinical research. The NAc is a part of the brain reward system (BRS) characterized by multilevel organization, extensive connections, and several neurotransmitter systems.

Neurovascular Unit as a Source of Ischemic Stroke Biomarkers-Limitations of Experimental Studies and Perspectives for Clinical Application.

Cerebral stroke, which is one of the most frequent causes of mortality and leading cause of disability in developed countries, often leads to devastating and irreversible brain damage. Neurological and neuroradiological diagnosis of stroke, especially in its acute phase, is frequently uncertain or inconclusive. This results in difficulties in identification of patients with poor prognosis or being at high risk for complications.

Nicotine-induced CREB and DeltaFosB activity is modified by caffeine in the brain reward system of the rat.

Coffee and nicotine consumption are frequently combined, indicating possible intensifying effect of caffeine on smoking behavior, although neurobiological background of this phenomenon remains unknown. We aimed at determining the effect of caffeine and nicotine, applied separately or simultaneously, on activation of six structures of the brain reward system: nucleus accumbens (NAc), ventral tegmental area (VTA), amygdala (Amg), hippocampus (Hip), medial prefrontal cortex (mPfr) and dorsal striatum (CdP) in the adult male Wistar rats. Activation of two transcription factors, the phosphorylated form of cyclic AMP-response element binding protein (pCREB) and DeltaFosB (ΔFosB) was assessed by immunohistochemistry after multiple-dose five-days psychostimulants administration followed by 20min and 24h survival, respectively.

BDNF: A Key Factor with Multipotent Impact on Brain Signaling and Synaptic Plasticity.

Brain-derived neurotrophic factor (BDNF) is one of the most widely distributed and extensively studied neurotrophins in the mammalian brain. Among its prominent functions, one can mention control of neuronal and glial development, neuroprotection, and modulation of both short- and long-lasting synaptic interactions, which are critical for cognition and memory. A wide spectrum of processes are controlled by BDNF, and the sometimes contradictory effects of its action can be explained based on its specific pattern of synthesis, comprising several intermediate biologically active isoforms that bind to different types of receptor, triggering several signaling pathways.

Cholesterol as a modifying agent of the neurovascular unit structure and function under physiological and pathological conditions.

The brain, demanding constant level of cholesterol, precisely controls its synthesis and homeostasis. The brain cholesterol pool is almost completely separated from the rest of the body by the functional blood-brain barrier (BBB). Only a part of cholesterol pool can be exchanged with the blood circulation in the form of the oxysterol metabolites such, as 27-hydroxycholesterol (27-OHC) and 24S-hydroxycholesterol (24S-OHC).

Transcription factor Pax6 is expressed by astroglia after transient brain ischemia in the rat model.

Reactive astrogliosis is regarded as an universal astrocytic response to different kinds of lesions, concerned with glial fibrillary acidic protein (GFAP) up-regulation, cellular hypertrophy and proliferation. The origin of reactive and proliferating cells in the adult brain is still disputable. Persistent progenitors as well as de-differentiating adult cells of various glial lineages are regarded as possible candidates.

The astrocytic contribution to neurovascular coupling--still more questions than answers?

Cerebral blood flow adequate for brain activity and metabolic demand is maintained through the processes of autoregulation and neurovascular coupling. Astrocytes undoubtedly make an important contribution to these processes. The critical factors that determine the polarity of astrocytic response include: metabolites (e.