| Abstrakt: |
Cell volume is continuously compromised by the generation of local and transient osmotic microgradients associated with uptake of nutrients, secretion, cytoskeletal remodeling and transynaptic ionic gradients. It is also disturbed in pathological conditions including those leading to hyponatremia or those associated with ion redistribution such as ischemia, trauma and epilepsy. Changes in cell volume, swelling or shrinkage, appear as key signals in directing the cell death type to necrosis or apoptosis and as signals for proliferation. Cell swelling in brain is critical since the limited expansion imposed by the rigid cranium results in vascular rupture and the consequent ischemic episodes and neuronal death. Besides, disturbing the extracellular/intracellular ionic equilibrium in the brain, as occurs in isosmotic swelling or during volume recovery after hyposmotic swelling results in hyperexcitability and hypersynchrony of neuronal activity. Therefore, the role for amino acids as osmolytes in volume regulation, particularly those being synaptically inhibitory or inert is of particular importance. However, others such as glutamate exacerbate neuronal excitability and lead ultimately to excitotoxicity and neuronal death. Understanding the implication of amino acids in cell volume control, and elucidating the signals and mechanisms underlying their participation is crucial to the design of strategies to prevent swelling and to protect brain cells, neurons particularly, from the deleterious effects of ionic disequilibrium and excitotoxicity. This is important also for avoiding the dangers of a rapid correction of the osmolarity of external fluids in hyponatremic conditions. This review presents an overview of the available information about the amino acid contribution to volume regulation after swelling in hyposmotic and isosmotic conditions, their role in volume recovery after cell shrinkage and their implication in cell volume changes during apoptosis and proliferation. [ABSTRACT FROM AUTHOR] |
