Neuroreport
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The age effect on classical eyeblink conditioning in unrestrained mice (C57BL/6J strain) was evaluated. Mice were trained at one of three age periods (8, 45-50 or 85-90 weeks). ⋯ On the other hand, in the trace paradigm with a stimulus-free trace interval of 500 ms, significant deficits became apparent at the age of 45-50 weeks. These results indicate that trace eyeblink conditioning is more susceptible to age-related deterioration of memory in mice than delay eyeblink conditioning.
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Our previous work has shown that PSD-95/SAP90 is required for NMDA receptor-mediated thermal hyperalgesia. To address the role of PSD-95/SAP90 in chronic pain, the present study investigated the effect of the deficiency of PSD-95/SAP90 on nerve injury-induced neuropathic pain. ⋯ The intrathecal administration of antisense oligodeoxynucleotide specifically against PSD-95/SAP90, but not sense or missense oligodeoxynucleotide, dose-dependently delayed the onset of tactile allodynia and thermal hyperalgesia. These results suggest that PSD-95/SAP90 might be involved in the central mechanisms of the development of chronic neuropathic pain.
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The tetrodotoxin-resistant voltage-gated sodium channel Nav 1.8 is expressed only in nociceptive sensory neurons. This channel has been proposed to contribute significantly to the sensitization of primary sensory neurons after injury. ⋯ The results from the present studies reveal that Nav 1.8 is a necessary mediator of NGF-induced thermal hyperalgesia but is not essential for PGE2-evoked hypersensitivity. Neuropathic pain behaviours were unchanged in Nav 1.8 -/- mice indicating that this channel is not involved in the alteration of sensory thresholds following peripheral nerve injury.