Sb. Colling et al., LIMBIC GAMMA-RHYTHMS - I - PHASE-LOCKED OSCILLATIONS IN HIPPOCAMPAL CA1 AND SUBICULUM, Journal of neurophysiology, 80(1), 1998, pp. 155-161
Gamma oscillations (similar to 40 Hz) were induced in transverse hippo
campal slices by tetanic stimulation of CA1 and/or subiculum. Tetanic
stimulation of each site elicited population gamma oscillations in the
surrounding tissue <400 mu m away. Stimulation of CA1 alone could evo
ke activity at both CA1 and subiculum. Subicular stimulation, however,
did not transmit to CA1. When the rostral end of CAI was stimulated,
gamma oscillations transmitted across <1.5 mm of silent CA1 before rea
ppearing in the subiculum. Tetanic stimulation of CA1 increased [K+](o
), to 8.2 +/- 1.5 mM (mean +/- SE). The location of the peak increase
corresponded to the site of local gamma generation. Silent areas of CA
1 experienced smaller [K+](o) increases, to 4.9 +/- 0.7 mM. The subicu
lum, which generated gamma, remained at the baseline 3.0 mM. Although
fluctuations in [K+](o) may have an impact on the generation of gamma
rhythms, they are not necessary for them. Gamma oscillations had simil
ar frequencies in CA1 and subiculum (40.4 +/- 2.9 and 43.9 +/- 3.1 Hz,
respectively). When present in both, the oscillations typically were
phase locked with the subiculum lagging by 5.4 +/- 1.8 ms. When both C
A1 and subiculum were stimulated the lag decreased by 28%. These delay
s approximate those expected for the conduction velocity of axone betw
een the two regions, here estimated at 0.52 +/- 0.07 m/s. Transmission
of gamma oscillations from CA1 to subiculum was blocked by the focal
addition of the lpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic aci
d-receptor antagonist, 6-nitro-7-sulfamoylbenzo [f] quinoxaline-2,3-di
one, to the subiculum. Oscillations induced in CA1 by local tetanic st
imulation were blocked by focal application of the gamma-aminobutyric
acid-A (GABA(A)) receptor antagonist, bicuculline, to CA1. Focal appli
cation of bicuculline to the subiculum blocked gamma due to subicular
stimulation but not that due to CA1 stimulation. Bath-applied bicucull
ine disrupted subicular gamma evoked by subicular stimulation and led
to a transient period of epileptiform responses before completely bloc
king responses. The further addition of the GABA(B) receptor antagonis
t, CGP 55845A, reversed this block, restoring the epileptic discharges
evoked by tetanic stimulation. This suggests that the subiculum diffe
rs from hippocampal CA3 and neocortex, in having a powerful GABA(B) re
ceptor-dependent mechanism to prevent epileptic discharges. The subicu
lum generates gamma rhythms both in response to local stimulation and
to gamma rhythms evoked in CA1. Subicular gamma differs from that in C
A1 in the presence of population spike doublets rather than singlets o
n many cycles. In both areas, generation of gamma by local stimulation
depends on GABA(A) receptors, suggesting that the subiculum shares th
e interneuronal network mechanism we proposed for CA1.