Establishing an animal model for National Acupuncture Detoxification Association (NADA) auricular acupuncture protocol.

The use of opioids in the treatment of chronic pain has increased dramatically in the past few decades making them one of the most commonly prescribed medications in the US. However, long-term use of opioids is limited by development of tolerance (decreased antinociceptive efficacy) and opioid-induced hyperalgesia - paradoxical sensitization to noxious (hyperalgesia) and non-noxious (allodynia) stimuli. Novel adjunctive therapies are needed to increase the efficacy and prolong the duration of action of opioids in chronic pain treatment.

In vivo activation of the SK channel in the spinal cord reduces the NMDA receptor antagonist dose needed to produce antinociception in an inflammatory pain model.

N-methyl-D-aspartate receptor (NMDAR) antagonists have been shown to reduce mechanical hypersensitivity in animal models of inflammatory pain. However, their clinical use is associated with significant dose-limiting side effects. Small-conductance Ca-activated K channels (SK) have been shown to modulate NMDAR activity in the brain.

Pain after discontinuation of morphine treatment is associated with synaptic increase of GluA4-containing AMPAR in the dorsal horn of the spinal cord.

Withdrawal from prescribed opioids results in increased pain sensitivity, which prolongs the treatment. This pain sensitivity is attributed to neuroplastic changes that converge at the spinal cord dorsal horn. We have recently reported that repeated morphine administration triggers an insertion of GluA2-lacking (Ca(2+)-permeable) α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors (AMPAR) in the hippocampus.

Hippocampal GluA1-containing AMPA receptors mediate context-dependent sensitization to morphine.

Glutamatergic systems, including AMPA receptors (AMPARs), are involved in opiate-induced neuronal and behavioral plasticity, although the mechanisms underlying these effects are not fully understood. In the present study, we investigated the effects of repeated morphine administration on AMPAR expression, synaptic plasticity, and context-dependent behavioral sensitization to morphine. We found that morphine treatment produced changes of synaptic AMPAR expression in the hippocampus, a brain area that is critically involved in learning and memory.

Metabotropic actions of kainate receptors in the regulation of I(sAHP) and excitability in CA1 pyramidal cells.

Kainate receptors (KARs) mediate postsynaptic responses in CA3 pyramidal cells and CA1 interneurones in the hippocampus. In CA1 pyramidal cells knockout studies have inidcated the presence of functional GluR6-containing KARs, however in this region they made no ionotropic contribution to the synaptic responses. In the meantime, a metabotropic function was reported for presynaptic KARs modulating transmitter release in CA1.

Evolution of melanopsin photoreceptors: discovery and characterization of a new melanopsin in nonmammalian vertebrates.

In mammals, the melanopsin gene (Opn4) encodes a sensory photopigment that underpins newly discovered inner retinal photoreceptors. Since its first discovery in Xenopus laevis and subsequent description in humans and mice, melanopsin genes have been described in all vertebrate classes. Until now, all of these sequences have been considered representatives of a single orthologous gene (albeit with duplications in the teleost fish).