On the synchronizing mechanisms of tetanically induced hippocampal oscillations

gamma (30-100 Hz) and beta (10-30 Hz) oscillations follow tetanic stimulati on in the CA1 region of the rat hippocampal slice. Pyramidal neurons underg o a slow depolarization after the tetanus and generate synchronous action p otentials. The slow depolarization was previously attributed to metabotropi c glutamate receptor (mGluR) activation. However, we found that this event was mediated by GABA(A) receptors, being blocked by bicuculline (50 mu M) a nd accompanied by a dramatic drop in input resistance. Experiments with NMD A and non-NMDA glutamate receptor antagonists revealed that fast synaptic e xcitation was not necessary for oscillations. IPSPs were strongly depressed during the oscillations. Instead, synchronization was caused by field effe cts, as shown by: (1) Action potentials of pyramidal neurons proximal (<200 mu m) to the stimulation site were often preceded by negative deflections of the intracellular potential that masked a net transmembrane depolarizati on caused by the population spike. (2) Pyramidal neurons located on the sur face of the slice, where field effects are weak, fired repetitively but wer e not synchronized to the network activity. (3) A moderate decrease (50 mOs m) in artificial CSF (ACSF) osmolality did not affect the slow depolarizati on but increased oscillation amplitude and duration and recruited previousl y silent neurons into oscillations. (4) 50 mOsm increase in ACSF osmolality dramatically reduced, or abolished, post-tetanic oscillations. Phasic IPSP s, not detectable in proximal neurons, were present, late in the oscillatio n, in cells located 200-400 mm from the stimulation site and possibly contr ibuted to slowing the rhythm during the gamma to beta transition.