Abstract：
:Despite significant progress, many uncertainties remain regarding molecular and cellular mechanisms governing opiate tolerance. We report that loss of EphB2 receptor reverse signaling results in a marked acceleration of morphine tolerance in vivo. EphB2 null mice exhibited no significant difference in brain or blood morphine metabolism, mu opiate receptor affinity or binding capacity. Motor and sensory performance for EphB2 null mice was also comparable to controls for both morphine naïve or tolerized states. Regional distributions of mu opioid receptor, CGRP and substance P were also unaltered in EphB2 null mice. However EphB2 null mice, but not animals homozygous for kinase dead version of EphB2, exhibited significant modification of context-dependent anti-nociceptive responses following chronic morphine treatment. To verify the changes seen in EphB2 null mice arise from impairment of hippocampal learning, discreet bilateral lesions of the dorsal hippocampus were produced in wildtype mice demonstrating striking similarities to that seen in EphB2 null mice for opiate-dependent behavior. The results demonstrate that EphB2 reverse signaling plays a unique and requisite role in inhibiting the development of opiate-dependent tolerance in vivo.
journal_name
Behav Brain Resjournal_title
Behavioural brain researchauthors
Huroy S,Kanawaty A,Magomedova L,Cummins CL,George SR,van der Kooy D,Henderson JTdoi
10.1016/j.bbr.2015.09.023subject
Has Abstractpub_date
2016-03-01 00:00:00pages
85-96eissn
0166-4328issn
1872-7549pii
S0166-4328(15)30196-0journal_volume
300pub_type
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