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Abstract
The ability of a synapse to be modulated both positively and negatively may be considered
as a plausible model for the formation of learning and memory. The CA1 to perirhinal
cortex projection is one of the multiple hippocampal-neocortical projections considered
to be crucially involved in memory consolidation. We and others have previously demonstrated
the ability of this projection to undergo long-term potentiation (LTP), however it
is currently unknown whether the CA1-perirhinal projection can also be modified negatively
(i.e. demonstrate long-term depression (LTD)). Here we investigate whether the CA1
to perirhinal projection in vivo in the anaesthetised animal shows a frequency-dependent
pattern of synaptic plasticity that is coupled with brain-derived neurotrophic factor
(BDNF) expression. Five groups of animals were used and each group underwent one of
five different stimulation protocols (1 Hz, 5 Hz, 10 Hz, 50 Hz or 100 Hz) followed
by post-stimulation recordings at baseline stimulation intensity (0.05 Hz) for 1h.
Paired-pulse facilitation (PPF) recordings were taken both during baseline and 1h
post-stimulation across six inter-pulse intervals (IPIs). Following all experiments,
tissue samples were taken from area CA1 and perirhinal cortex from both the unstimulated
and stimulated hemispheres of each brain and analysed for BDNF. Results indicated
that LTP was observed following 50 Hz and 100 Hz HFS but LTD was not observed following
any low-frequency stimulation. Pre- and post-stimulation PPF recordings revealed no
difference for any of the stimulation frequencies, suggesting that the plasticity
observed may involve a post- rather than a presynaptic mechanism. Finally, changes
in BDNF were positively correlated with stimulation frequency in the area CA1 but
the same pattern was not observed in the perirhinal cortex. These findings suggest
that the CA1 to perirhinal cortex projection is electrophysiologically excitatory
in nature and that changes in BDNF levels in this projection may not be predictive
of changes in synaptic plasticity.