Recent reports demonstrate that repeated cocaine exposure generate silent
glutamatergic synapses which contribute to metaplasticity (Huang et al, 2009) and the
development of cocaine-induced locomotor sensitization (Brown et al, 2011). Silent
synapses are glutamatergic synapses which express NMDAR-mediated currents in the
absence of AMPAR-mediated currents (Isaac et al, 1995; Liao et al, 1995). Interestingly,
in vitro evidence supports the idea that silent glutamatergic synapses contain higher
levels of NR2B-containing NMDARs compared to neighboring active synapses.
Moreover, the authors showed that elevated levels of NR2B at silenced synapses
increased calcium entry into neurons and lowered the threshold for LTP induction (Lee et
al, 2010). This suggests that silent synapses are capable of undergoing rapid
metaplasticity to strengthen synaptic connections. Given these observations, it is
reasonable to assume that my cocaine administration schedules generated silent synapses
illustrated by the increases in NR2B protein. Furthermore, it is plausible that the extent to
which silent synapses were generated contributed to the differential salience of cocaine
reward elicited by Fix-C and Esc-C. Thus, increased numbers of silent synapses through
enhanced expression of NR2B provide greater potential for metaplasticity and subsequent
memory strengthening. Further research should use electrophysiological tools to
investigate the extent to which silent synapses were generated and how they may have
contributed to the observed behavioral effects.
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