Neuronal-glial interactions and behaviour

@article{citeulike:2483816, abstract = {Both neurons and glia interact dynamically to enable information processing and behaviour. They have had increasingly intimate, numerous and differentiated associations during brain evolution. Radial glia form a scaffold for neuronal developmental migration and astrocytes enable later synapse elimination. Functionally syncytial glial cells are depolarised by elevated potassium to generate slow potential shifts that are quantitatively related to arousal, levels of motivation and accompany learning. Potassium stimulates astrocytic glycogenolysis and neuronal oxidative metabolism, the former of which is necessary for passive avoidance learning in chicks. Neurons oxidatively metabolise lactate/pyruvate derived from astrocytic glycolysis as their major energy source, stimulated by elevated glutamate. In astrocytes, noradrenaline activates both glycogenolysis and oxidative metabolism. Neuronal glutamate depends crucially on the supply of astrocytically derived glutamine. Released glutamate depolarises astrocytes and their handling of potassium and induces waves of elevated intracellular calcium. Serotonin causes astrocytic hyperpolarisation. Astrocytes alter their physical relationships with neurons to regulate neuronal communication in the hypothalamus during lactation, parturition and dehydration and in response to steroid hormones. There is also structural plasticity of astrocytes during learning in cortex and cerebellum.}, author = {Laming, P. R. and Kimelberg, H. and Robinson, S. and Salm, A. and Hawrylak, N. and Muller, C. and Roots, B. and Ng, K. }, citeulike-article-id = {2483816}, doi = {10.1016/S0149-7634(99)00080-9}, journal = {Neuroscience \& Biobehavioral Reviews}, keywords = {glia, review}, month = {May}, number = {3}, pages = {295--340}, posted-at = {2008-03-07 12:28:11}, priority = {0}, title = {Neuronal-glial interactions and behaviour}, url = {http://dx.doi.org/10.1016/S0149-7634(99)00080-9}, volume = {24}, year = {2000} }

TY - JOUR ID - citeulike:2483816 L3 - citeulike-article-id:2483816 TI - Neuronal-glial interactions and behaviour JF - Neuroscience & Biobehavioral Reviews VL - 24 IS - 3 SP - 295 EP - 340 N2 - Both neurons and glia interact dynamically to enable information processing and behaviour. They have had increasingly intimate, numerous and differentiated associations during brain evolution. Radial glia form a scaffold for neuronal developmental migration and astrocytes enable later synapse elimination. Functionally syncytial glial cells are depolarised by elevated potassium to generate slow potential shifts that are quantitatively related to arousal, levels of motivation and accompany learning. Potassium stimulates astrocytic glycogenolysis and neuronal oxidative metabolism, the former of which is necessary for passive avoidance learning in chicks. Neurons oxidatively metabolise lactate/pyruvate derived from astrocytic glycolysis as their major energy source, stimulated by elevated glutamate. In astrocytes, noradrenaline activates both glycogenolysis and oxidative metabolism. Neuronal glutamate depends crucially on the supply of astrocytically derived glutamine. Released glutamate depolarises astrocytes and their handling of potassium and induces waves of elevated intracellular calcium. Serotonin causes astrocytic hyperpolarisation. Astrocytes alter their physical relationships with neurons to regulate neuronal communication in the hypothalamus during lactation, parturition and dehydration and in response to steroid hormones. There is also structural plasticity of astrocytes during learning in cortex and cerebellum. KW - glia KW - review AU - Laming, PR AU - Kimelberg, H AU - Robinson, S AU - Salm, A AU - Hawrylak, N AU - Muller, C AU - Roots, B AU - Ng, K PY - 2000/05// UR - http://dx.doi.org/10.1016/S0149-7634(99)00080-9 ER -