title: CA3 neuron excitation and epileptiform discharge are sensitive to osmolality.
abstract: 1. The clinical signs of rapidly developing overhydration commonly include generalized tonic-clonic seizure, which can be combatted by raising plasma osmolality. How cortical neurons respond to osmotic imbalance has been addressed only recently. In the CA3 cell region of hippocampal slices, lowered osmolality (-40 mOsm) rapidly swelled cells, increasing field potential amplitude over a period of 8 min and thereby elevating field effects and associated neuronal synchronization. 2. Over a longer time course (10-30 min), spontaneous excitatory postsynaptic potential (EPSP) amplitude gradually increased in 7 of 10 CA3 neurons recorded intracellularly. In nine additional CA3 cells, hyposmolality gradually induced combinations of action potential discharge, endogenous bursting, and increased synchronized synaptic input. All of these effects reversed in normosmotic ACSF. 3. Hyperosmotic artificial cerebrospinal fluid (ACSF) using mannitol reduced field potentials and dramatically lowered CA3 excitability by reducing spontaneous EPSP amplitude and associated bursting. Again, the gradual onset (10-30 min) of changes in spontaneous EPSP amplitude appeared independent of field potential changes, which were already maximal by 8 min. 4. Cutting mossy fibers did not affect the excitability changes induced by osmotic stress noted above. The EPSP/inhibitory postsynaptic potential (IPSP) sequence evoked from mossy fibers or stratum oriens was unaltered by osmotic change and so did not represent osmosensitive afferent input to CA3 neurons. Furthermore, as measured at the soma, resting membrane potential, cell input resistance, and the action potential threshold were unchanged in all cells. It followed that, because the CA3 neurons themselves were not responsive, a recurrent excitatory pathway could not represent the osmosensitive input.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Anatomy and Cell Biology, Queen's University, Kingston, Ontario, Canada.
authors.forename: V
authors.initials: V
authors.lastname: Saly
authors.forename: R D
authors.initials: RD
authors.lastname: Andrew
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000818:Animals; D004558:Electric Stimulation; D004594:Electrophysiology; D004827:Epilepsy / Q000503:physiopathology*; D006624:Hippocampus / Q000166:cytology / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials / Q000502:physiology; D009412:Nerve Fibers / Q000502:physiology; D009431:Neural Conduction / Q000502:physiology; D009434:Neural Pathways / Q000166:cytology / Q000502:physiology; D009457:Neuroglia / Q000502:physiology; D009474:Neurons / Q000502:physiology*; D009994:Osmolar Concentration; D011712:Pyramidal Tracts / Q000166:cytology / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013569:Synapses / Q000502:physiology