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Osmolality and nonsynaptic epileptiform bursts in rat CA1 and dentate gyrus
Author(s) -
Roper Steven N.,
Obenaus Andre,
Dudek F. Edward
Publication year - 1992
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410310115
Subject(s) - dentate gyrus , bursting , hippocampal formation , extracellular , neuroscience , excitatory postsynaptic potential , convulsion , chemistry , hippocampus , biophysics , biology , epilepsy , biochemistry , inhibitory postsynaptic potential
In several clinical situations, such as hyposmolar states and hypoxia‐ischemia, reductions in the size of the extracellular space are associated with increased seizure susceptibility. Nonsynaptic interactions provide a likely means of mediating the effect of extracellular space on seizure susceptibility. Synchronous bursting of CA1 hippocampal neurons occurs via nonsynaptic mechanisms in solutions containing very low {Ca 2+ } and excitatory amino acid antagonists. We tested the hypothesis that lowering the osmolality of the extracellular medium could induce nonsynaptic bursting in the dentate gyrus, even though it is normally resistant to this treatment. Extracellular field potentials were recorded in the dentate gyrus and CA1 area of rat hippocampal slices. In the low‐{Ca 2+ } solution with normal osmolality, bursts of population spikes were recorded from the dentate gyrus in only 7% of the slices, but solutions with decreased osmolality induced bursting in 63%. Corresponding values for the CA1 area were 60 and 73%, respectively. Mannitol, which reversed the hyposmolar state, abolished bursting in both regions. This study demonstrates that reducing the size of the extracellular space by lowering extracellular osmolality can transform a seizure‐resistant area into one that exhibits robust epileptiform activity.