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Synaptic Level (synaptic + level)
Selected AbstractsElectrophysiological Identification of the Functional Presynaptic Nerve Terminals on an Isolated Single Vasopressin Neurone of the Rat Supraoptic NucleusJOURNAL OF NEUROENDOCRINOLOGY, Issue 5 2010T. Ohbuchi Release of arginine vasopressin (AVP) and oxytocin from magnocellular neurosecretory cells (MNCs) of the supraoptic nucleus (SON) is under the control of glutamate-dependent excitation and GABA-dependent inhibition. The possible role of the synaptic terminals attached to SON neurones has been investigated using whole-cell patch-clamp recording in in vitro rat brain slice preparations. Recent evidence has provided new insights into the repercussions of glial environment modifications on the physiology of MNCs at the synaptic level in the SON. In the present study, excitatory glutamatergic and inhibitory GABAergic synaptic inputs were recorded from an isolated single SON neurone cultured for 12 h, using the whole-cell patch clamp technique. Neurones expressed an AVP-enhanced green fluorescent protein (eGFP) fusion gene in MNCs. In addition, native synaptic terminals attached to a dissociated AVP-eGFP neurone were visualised with synaptic vesicle markers. These results suggest that the function of presynaptic nerve terminals may be evaluated directly in a single AVP-eGFP neurone. These preparations would be helpful in future studies aiming to electrophysiologically distinguish between the functions of synaptic terminals and glial modifications in the SON neurones. [source] Oestrogen Regulates the Expression and Function of Dopamine Transporters in Astrocytes of the Nigrostriatal SystemJOURNAL OF NEUROENDOCRINOLOGY, Issue 9 2007S. Karakaya Dopamine is actively and specifically eliminated from the extracellular space by astrocytes and neurones through dopamine transporters (DAT) and, afterwards, either recycled into vesicles or metabolised. The availability of dopamine reflects a critical point in the regulation of dopamine activity within the nigrostriatal circuit under normal and pathological conditions. From previous studies, we know that oestrogen regulates the efficacy of dopaminergic neurones at the synaptic level and improves dopamine function during Parkinson's disease. Accordingly, we investigated the contribution of local astroglial for extracellular dopamine elimination and the impact of oestrogen on DAT expression and activity. Using neonatal striatal and midbrain astrocyte cultures, we could demonstrate that astrocytes possess a specific dopamine uptake machinery and express DAT at considerable levels. The application of 17,-oestradiol decreased the expression of DAT by 80% and 60% in midbrain and striatal astroglia cultures, respectively. The unspecific dopamine transporters (OCT3, VMAT2) were not detected in astroglia. Functionally, oestrogen exposure inhibited the clearance of dopamine from the extracellular space by 45% and 35% compared to controls in midbrain and striatal astroglia, respectively. The effect on DAT expression and activity was completely antagonised by the oestrogen receptor antagonist ICI 182 780. In conclusion, our data suggest that the positive reinforcement of dopamine transmission under physiological conditions and the alleviative impact of oestrogen under pathological conditions may be the result of a decline in DAT expression and therefore delayed dopamine uptake by astroglia. [source] Mechanisms underlying human motor system plasticity,MUSCLE AND NERVE, Issue 5 2001Babak Boroojerdi MD Abstract There has been increased interest in the ability of the adult human nervous system to reorganize and adapt to environmental changes throughout life. This ability has been termed "plasticity." Plastic changes in the cerebral cortex have been studied: (a) as modifications of sensory or motor cortical representation of specific body parts (cortical maps, body representation level); and (b) as changes in the efficacy of existing synapses or generation of new synapses (neuronal or synaptic level). In this review, we describe paradigms used to study mechanisms of plasticity in the intact human motor system, the functional relevance of such plasticity, and possible ways to modulate it. © 2001 John Wiley & Sons, Inc. Muscle Nerve 24: 602,613, 2001 [source] The Role of Glia and the Immune System in the Development and Maintenance of Neuropathic PainPAIN PRACTICE, Issue 3 2010Ricardo Vallejo MD Abstract Neuropathic pain refers to a variety of chronic pain conditions with differing underlying pathophysiologic mechanisms and origins. Recent studies indicate a communication between the immune system and the nervous system. A common underlying mechanism of neuropathic pain is the presence of inflammation at the site of the damaged or affected nerve(s). This inflammatory response initiates a cascade of events resulting in the concentration and activation of innate immune cells at the site of tissue injury. The release of immunoactive substances such as cytokines, neurotrophic factors, and chemokines initiate local actions and can result in a more generalized immune response. The resultant neuroinflammatory environment can cause activation of glial cells located in the spinal cord and the brain, which appear to play a prominent role in nociception. Glial cells, also known as neuroglia, are nonconducting cells that modulate neurotransmission at the synaptic level. Glial cells can be subdivided into two primary categories: microglia and macroglia, which include astrocytes and oligodendrocytes. Astrocytes and microglia are known to play a role in the development, spread, and potentiation of neuropathic pain. Following peripheral nociceptive activation via nerve injury, microglia become activated and release pro-inflammatory cytokines such as tumor necrosis factor-,, interleukin-1,, and interleukin-6, thereby initiating the pain process. Microglia propagate the neuroinflammation by recruiting other microglia and eventually activating nearby astrocytes, which prolongs the inflammatory state and leads to a chronic neuropathic pain condition. Our review focuses on the role of glia and the immune system in the development and maintenance of neuropathic pain. [source] Receptive fields and functional architecture in the retinaTHE JOURNAL OF PHYSIOLOGY, Issue 12 2009Vijay Balasubramanian Functional architecture of the striate cortex is known mostly at the tissue level , how neurons of different function distribute across its depth and surface on a scale of millimetres. But explanations for its design , why it is just so , need to be addressed at the synaptic level, a much finer scale where the basic description is still lacking. Functional architecture of the retina is known from the scale of millimetres down to nanometres, so we have sought explanations for various aspects of its design. Here we review several aspects of the retina's functional architecture and find that all seem governed by a single principle: represent the most information for the least cost in space and energy. Specifically: (i) why are OFF ganglion cells more numerous than ON cells? Because natural scenes contain more negative than positive contrasts, and the retina matches its neural resources to represent them equally well; (ii) why do ganglion cells of a given type overlap their dendrites to achieve 3-fold coverage? Because this maximizes total information represented by the array , balancing signal-to-noise improvement against increased redundancy; (iii) why do ganglion cells form multiple arrays? Because this allows most information to be sent at lower rates, decreasing the space and energy costs for sending a given amount of information. This broad principle, operating at higher levels, probably contributes to the brain's immense computational efficiency. [source] Brain metabolism in rett syndrome: Age, clinical, and genotype correlations,ANNALS OF NEUROLOGY, Issue 1 2009Alena Horská PhD Objective Brain metabolism, as studied by magnetic resonance spectroscopy (MRS), has been previously shown to be abnormal in Rett syndrome (RTT). This study reports the relation of MRS findings to age, disease severity, and genotype. Methods Forty RTT girls (1,14 years old) and 12 age-matched control subjects were examined. Single-voxel proton MRS of left frontal white matter was performed. Results NAA/Cr ratios decreased and myoinositol/Cr ratios increased with age in RTT patients (both p < 0.03), whereas these ratios were stable in control. The mean glutamate and glutamine/Cr ratio was 36% greater in RTT patients than in control (p = 0.043). The mean NAA/Cr ratio was 12.6% lower in RTT patients with seizures compared with those without seizures (p = 0.017). NAA/Cr ratios decreased with increasing clinical severity score (p = 0.031). Compared with patients with T158X, R255X, and R294X mutations, and C-terminal deletions, patients with the R168X mutation tended to have the greatest severity score (0.01 , p , 0.11) and the lowest NAA/Cr ratio (0.029 , p < 0.14). Interpretation Decreasing NAA/Cr and increasing myoinositol/Cr with age are suggestive of progressive axonal damage and astrocytosis in RTT, respectively, whereas increased glutamate and glutamine/Cr ratio may be secondary to increasing glutamate/glutamine cycling at the synaptic level. The relations between NAA/Cr, presence or absence of seizures, and disease severity suggest that MRS provides a noninvasive measure of cerebral involvement in RTT. Ann Neurol 2009;65:90,97 [source] REVIEW: Norepinephrine and stimulant addictionADDICTION BIOLOGY, Issue 2 2009Mehmet Sofuoglu ABSTRACT No pharmacotherapies are approved for stimulant use disorders, which are an important public health problem. Stimulants increase synaptic levels of the monoamines dopamine (DA), serotonin and norepinephrine (NE). Stimulant reward is attributable mostly to increased DA in the reward circuitry, although DA stimulation alone cannot explain the rewarding effects of stimulants. The noradrenergic system, which uses NE as the main chemical messenger, serves multiple brain functions including arousal, attention, mood, learning, memory and stress response. In pre-clinical models of addiction, NE is critically involved in mediating stimulant effects including sensitization, drug discrimination and reinstatement of drug seeking. In clinical studies, adrenergic blockers have shown promise as treatments for cocaine abuse and dependence, especially in patients experiencing severe withdrawal symptoms. Disulfiram, which blocks NE synthesis, increased the number of cocaine-negative urines in five randomized clinical trials. Lofexidine, an ,2 -adrenergic agonist, reduces the craving induced by stress and drug cues in drug users. In addition, the NE transporter (NET) inhibitor atomoxetine attenuates some of d-amphetamine's subjective and physiological effects in humans. These findings warrant further studies evaluating noradrenergic medications as treatments for stimulant addiction. [source] Diacylglycerol kinases in the regulation of dendritic spinesJOURNAL OF NEUROCHEMISTRY, Issue 3 2010Karam Kim J. Neurochem. (2010) 112, 577,587. Abstract Diacylglycerol (DAG) is an important lipid-signaling molecule that binds and activates various downstream effectors. Tight control over the production and removal of DAG is important in maintaining the dynamic responses of the DAG signaling system to a changing environment. Diacylglycerol kinases (DGKs) are enzymes that convert DAG to phosphatidic acid (PA). This conversion terminates DAG signaling and, at the same time, initiates additional signaling events downstream of PA, which also acts as a lipid-signaling molecule. However, little is known about how (or if) DGKs are targeted to specific subcellular sites or how DGKs tightly regulate local DAG and PA signaling. Dendritic spines are tiny protrusions on neuronal dendrites that receive the majority of excitatory synaptic inputs. They are also the sites where DAG molecules are produced through activation of postsynaptic receptors, including metabotropic glutamate receptors and NMDA receptors. Accumulating evidence indicates that synaptic levels of DAG and PA are important determinants of dendritic spine stability and that the DGK, isoform at excitatory postsynaptic sites is critically involved in spine maintenance. In addition, DGK, appears to form a multi-protein complex with functionally related proteins to organize efficient DAG and PA signaling pathways at excitatory synapses. [source] | |||||||||||||