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EN
The calcium-binding protein S100B is produced primarily by astrocytes and exerts concentration-dependent paracrine and autocrine effects on neurons and glia. The numerous findings of a correlation between S100B and traumatic brain injury (TBI) have resulted in the employment of this protein as a clinical biomarker for such injury. Our present aim was to determine whether cycling with (V) or without (NV) vibration alters serum concentrations of S100B. Twelve healthy, male non-smokers (age: 25.3±1.6 yrs, body mass: 74.2±5.9 kg, body height: 181.0±3.7 cm, VO2peak: 56.9±5.1 ml·min-1·kg-1 (means ± SD)) completed in random order two separate trials to exhaustion on a vibrating bicycle (amplitude 4 mm and frequency 20 Hz) connected to an ergometer. The initial workload of 100 W was elevated by 50 W every 5 min and the mean maximal period of exercise was 25:27±1:30 min. The S100B in venous blood taken at rest, immediately after the test, and 30, 60 and 240 min post-exercise exhibited no significant differences (p>0.05), suggesting that cycling with and without vibration does not influence this parameter.
EN
The hippocampus plays a role in new learning, memory and emotion and is a component of the neuroanatomical stress circuit. The structure is involved in terminating hypothalamic-pituitary-adrenocortical (HPA) axis responses to stress and attenuates stress responses by shutting off this axis. The immunoreactivity (-ir) of c-Fos, NGF and its receptor TrkA following acute and chronic open-field stress were studied in CA1-CA3 and the DG of the hippocampus. The material consisted of 21 male adult rats divided into three groups: nonstressed (control) animals and rats exposed to acute (15 min once) and chronic (15 min daily for 21 days) aversive stimulation (open-field exposure). The brains were stained with use of immunohistochemical methods for c-Fos, NGF or TrkA. In the animals exposed to acute open-field stress the number of c-Fos-, TrkAand NGF-ir cells was higher in all the structures studied than in the control animals. However they were differentiated only in c-Fos immunoreactivity. In the rats exposed to chronic open-field stress the number of c-Fos-ir cells in the structures of the hippocampal formation studied was smaller than in rats exposed to acute stress and was comparable to that in the control group. No differences were observed between the groups exposed to acute and chronic stress in the number of TrkA-ir cells in the structures under investigation. The number of NGF-ir neurons in CA1 and CA2 was lower after exposure to chronic than after exposure to acute stress but was still higher than that in the control group. Our findings indicate that neurons of CA1-CA3 and the DG are engaged in the stress response after acute as well as chronic open-field exposure. This is probably related to the important role of the hippocampus in processing new spatial information as well as in the habituation processes, although these appear to have different mechanisms.
EN
The amygdala is a critical component of the neuroanatomical stress circuit. It plays a role in the generation of responses to emotional stimuli. The central (CeA) and medial (MeA) amygdaloid nuclei are implicated in activation of the hypothalamic-pituitary-adrenocortical (HPA) axis. The immunoreactivity (-ir) of c-Fos, NGF and its receptor, TrkA, following acute and chronic open-field stress were studied in the CeA and MeA nuclei of the amygdala. The material consisted of 21 male adult rats divided into three groups: non-stressed (control) animals, rats exposed to acute (once only lasting 15 min) and chronic (15 min daily over 21 days) aversive stimulation (open-field exposure). The brains were stained with the use of immunohistochemical methods for c-Fos, NGF or TrkA. In the control rats c-Fos-, TrkA- and NGF-ir cells were observed in the nuclei studied, but the quantity varied, being moderate or high (immunoreactive to TrkA and NGF) or low (immunoreactive to c-Fos). In the animals exposed to acute open-field stress the number of c-Fos-ir, NGF-ir and TrkA-ir cells in the nuclei under examination was differentiated but higher than that in the control animals. In the animals exposed to chronic open-field stress the number of c-Fos-ir cells in the nuclei studied was similar and was smaller than those in animals exposed to acute stress. The number of TrkA-ir neurons was also lower in comparison to that in animals exposed to acute stress. However, no significant differences in the number of NGF-ir cells were observed between the groups exposed to acute and chronic stress. Diverse expression of c-Fos protein following both acute and chronic stress stimulation may prove the functional heterogeneity of the amygdaloid nuclei investigated. The decrease observed in both c-Fos- and TrkA-ir in MeA (only TrkA in CeA) of animals exposed to chronic stress may indicate the phenomenon of habituation.
EN
The neurotrophins are a family of small proteins that were first identified as survival factors for sympathetic and sensory neurons and have since been shown to control survival, development and function of neurons and myelin formation in the central and peripheral nervous systems. Prosurvival and plasticity-promoting effects of mammalian neurotrophins: NGF, BDNF, NT-3 and NT-4 are mediated through activation of the tropomyosin-related kinase family of receptor tyrosine kinases (TrkA, TrkB, TrkC). The spinal cord of the adult rat is rich in BDNF protein which exceeds brain levels and is expressed in neurons occupying all spinal laminae (Skup et al. 2002, Macias et al. 2007). Locomotor exercise of the uninjured rats, an approach used to improve motor functions after injury, increased perikaryonal levels of BDNF mRNA within the majority of cells and of BDNF protein in processes surrounding large neurons of the lumbar motor nuclei. Exercise increased also staining intensity and number of TrkB receptor immunoreactive small cells of the spinal grey matter, which were identified as oligodendrocytes. When applied to the rats with complete spinal cord transection, exercise caused BDNF up-regulation in distinct populations of neurons in motor nuclei and increased motoneuron innervation (Skup et al. 2009, 2012). Data strongly suggested that the spinal network is under BDNF control, targeting neurons but also oligodendrocytes, recruited to neurotrophin signaling by the activated network. Multifaceted functions of BDNF make this molecule a promising one in attempts to stimulate neuronal regeneration and remyelination, but until recently treatments directed to increase the BDNF supply to injury-affected spinal networks only moderately improved locomotor functions. We therefore attempted to deliver BDNF via neurons transduced with adeno-associated virus serotype 1/2 (AAV1/2) expressing BDNF under the control of the synapsin promoter in the lumbo-sacral network below the complete transection. Based on functional, histological and biochemical assessments, I shall show that BDNF secreted from BDNF-expressing neurons in lumbar segments improves locomotor functions and alters excitability of the spinal network. Searching for the mechanisms of these changes we revealed that the increased segmental BDNF concentrations led to an increase in GAP-43 expression, GAD67 mRNA and protein expression and GABA levels, reducing post-lesion GABA deficits in the thoracic/lumbar segments. BDNF did not compensate the deficit of the potassium-chloride co-transporter KCC2, responsible for GABAA receptor-mediated hyperpolarizing inhibition. We conclude that sustained delivery of BDNF to the isolated spinal cord network causes neuronal rearrangements and increases inhibitory transmission under conditions of lesion-induced altered neuronal excitability, leading to locomotor improvement in paraplegic rats. Since glia affect excitability and remyelination we study astroglial/ oligodendroglial responses to BDNF overexpression. Support: Polish-German grant S007/P-N/2007/01, EMBO ASTF211.00-2007, NCN3975/(P)1/2010/39 & 3247/2010/39.
EN
Neurotrophins promote survival and suppress apoptosis in many populations of neurons. Currently, phosphatidylinositol-3 kinase (PI-3K) is recognized as the main mediator of this protective effect. However, most of the data collected so far on the anti-apoptotic signaling of neurotrophins were obtained using trophic withdrawal paradigms. Recent data from our and other groups indicate that extracellular-signal-regulated kinase 1/2 (Erk1/2) may play a critical role in suppressing neuronal apoptosis triggered by cellular damage. Thus, it appears that either Erk1/2 or PI-3K, depending on the nature of the death-inducing stimulus, can mediate anti-apoptotic signaling of neurotrophins. In this review, we discuss the contribution of Erk1/2 and PI-3K to neuroprotection by neurotrophins. We also present data suggesting possible mechanisms by which these pathways might suppress neuronal death.
EN
The immunoreactivity (ir) for c-Fos, NGF and TrkA, following an acute and chronic open field stress, were studied in the periventricular zone of rat hypothalamus. Adult rats were divided into three groups: control, exposed to acute (single exposure -15 minutes) and chronic (multiple exposures - 15 minutes daily for 21 days) open field stress. In the control rats neurons immunoreactive to c-Fos, TrkA and NGF were found. The number of TrkA- and NGF-ir cells was high, whereas this of c-Fos-ir ones was low. In animals exposed to acute open field stress the number of c-Fos-ir cells in the examined nuclei varied, however it was much higher than that in the control animals. The number of TrkA-ir neurons in all the studied nuclei was also higher than that in the control animals, but the increase of the number of NGF-ir neurons was not observed in supraoptic nucleus. In the animals exposed to chronic open field stress the number of c-Fos-ir cells was increased in comparison to that in the control rats. After chronic stress exposure the number of TrkA-ir neurons in supraoptic nucleus remained high in comparison to that in animals exposed to acute stress, whereas it was decreased in other studied nuclei. No significant differences in the number of NGF-ir cells were observed between the groups exposed to the acute and chronic stress. Observed decrease of c-Fos- and TrkA-ir in the studied nuclei in the animals suffering from chronic stress in comparison with the acute one may indicate the occurrence of habituation phenomenon. This phenomenon does not concern NGF-ir.
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