<p class="first" id="d3191976e63">The effects on tramadol state-dependent memory of
bilateral intradorsal hippocampal
(intra-CA1) injections of physostigmine, an acetylcholinesterase inhibitor, and atropine,
a muscarinic acetylcholine receptor antagonist, were examined in adult male NMRI mice.
A single-trial step-down passive avoidance task was used for the assessment of memory
retention. Post-training intra-CA1 administration of an atypical μ-opioid receptor
agonist, tramadol (0.5 and 1 μg/mouse), dose dependently impaired memory retention.
Pretest injection of tramadol (0.5 and 1 μg/mouse, intra-CA1) induced state-dependent
retrieval of the memory acquired under the influence of post-training tramadol (1 μg/mouse,
intra-CA1). A pretest intra-CA1 injection of physostigmine (1 μg/mouse) reversed the
memory impairment induced by post-training administration of tramadol (1 μg/mouse,
intra-CA1). Moreover, pretest administration of physostigmine (0.5 and 1 μg/mouse,
intra-CA1) with an ineffective dose of tramadol (0.25 μg/mouse, intra-CA1) also significantly
restored retrieval. Pretest administration of physostigmine (0.25, 0.5, and 1 μg/mouse,
intra-CA1) by itself did not affect memory retention. A pretest intra-CA1 injection
of the atropine (1 and 2 μg/mouse) 5 min before the administration of tramadol (1 μg/mouse,
intra-CA1) dose dependently inhibited tramadol state-dependent memory. Pretest administration
of atropine (0.5, 1, and 2 μg/mouse, intra-CA1) by itself did not affect memory retention.
It can be concluded that dorsal hippocampal muscarinic acetylcholine receptor mechanisms
play an important role in the modulation of tramadol state-dependent memory.
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