| HETEROSYNAPTIC POTENTIATION OF INHIBITORY TRANSMISSION
IN THE LATERAL AMYGDALA |
| E.P. Bauer*; J.E. LeDoux |
| Center for Neural Science, NYU, NY, NY, USA |
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LTP of excitatory synapses is a candidate
mechanism for the plasticity seen in the lateral amygdala (LA) during
fear conditioning. Plasticity of inhibitory transmission within the
LA would have important implications for the processing of incoming
signals. Inhibitory neurons receive convergent input from the thalamus
and cortex (Szinyei et al., 2000), and LTP of cortical synapses to
inhibitory cells has been described (Mahanty and Sah, 1998). We used
in vitro whole-cell recordings to examine potentiation of the IPSP
component of the synaptic response in excitatory LA cells. We stimulated
thalamic and cortical inputs by placing stimulating electrodes in
the internal and external capsules respectively. Tetanization of either
pathway (30 Hz, 100 stimuli, given twice) resulted in LTP of the EPSP
in the tetanized pathway only, but LTP of the IPSP in both pathways.
The IPSP in the tetanized path was potentiated immediately, but LTP
of the IPSP in the untetanized path did not occur until 10-15min after
the tetanus. Bath application of ifenprodil (an antagonist of the
NR2B subunit of the NMDA receptor; 10 M)
and nifedipine (an L-type voltage-gated calcium channel blocker; 30M),
did not block LTP of the IPSP in either path after tetanization of
thalamo-LA inputs. Both antagonists have been shown to impair LTP
at thalamic input synapses to excitatory neurons (Bauer et al., 2002).
Moreover, loading the recorded cell with the calcium chelator BAPTA
did not prevent LTP of the IPSP in either path. Further recordings
from the inhibitory neurons themselves will elucidate the mechanisms
of this heterosynaptic LTP. Supported by NIMH grants: 46516, 38774,
00956.
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