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.