Journal of neurophysiology
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The basolateral amygdala (BLA) is the major amygdaloid nucleus distributed with mu opioid receptors. The afferent input from the BLA to the central nucleus of the amygdala (CeA) is considered important for opioid analgesia. However, little is known about the effect of mu opioids on synaptic transmission in the BLA. ⋯ Bath application of the Kv channel blockers, 4-AP (Kv1.1, 1.2, 1.3, 1.5, 1.6, 3.1, 3.2), alpha-dendrotoxin (Kv1.1, 1.2, 1.6), dendrotoxin-K (Kv1.1), or tityustoxin-Kalpha (Kv1.2) each blocked the inhibitory effect of DAMGO on mIPSCs. Double immunofluorescence labeling showed that some of the immunoreactivities of Kv1.1 and Kv1.2 were colocalized with synaptophysin in the BLA. This study provides new information that activation of presynaptic mu opioid receptors primarily attenuates GABAergic synaptic inputs to CeA-projecting neurons in the BLA through a signaling mechanism involving Kv1.1 and Kv1.2 channels.
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The group I metabotropic glutamate receptor (mGluR) subtype, mGluR1, is highly expressed on the apical dendrites of olfactory bulb mitral cells and thus may be activated by glutamate released from olfactory nerve (ON) terminals. Previous studies have shown that mGluR1 agonists directly excite mitral cells. In the present study, we investigated the involvement of mGluR1 in ON-evoked responses in mitral cells in rat olfactory bulb slices using patch-clamp electrophysiology. ⋯ ON-evoked responses elicited in the presence of THA-TBOA were significantly reduced or completely blocked by LY341495 or LY367385 (100 microM). These results demonstrate that glutamate transporters tightly regulate access of synaptically evoked glutamate from ON terminals to postsynaptic mGluR1s on mitral cell apical dendrites. Taken together with other findings, the present results suggest that mGluR1s may not play a major role in phasic responses to ON input, but instead may play an important role in shaping slow oscillatory activity in mitral cells and/or activity-dependent regulation of plasticity at ON-mitral cell synapses.
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Peripherally delivered opiates attenuate mechanical and thermal hyperalgesia in experimental models of inflammation, suggesting that activation of peripheral opioid receptors decreases the excitability of nociceptors in inflamed tissues. The current study examines the effects of peripheral morphine sulfate on response properties of sensory neurons in healthy and inflamed skin. Afferent units (185) were isolated from tibial nerve of rats using an in vitro glabrous skin-nerve teased-fiber preparation. ⋯ All morphine-sensitive units were nociceptors from inflamed skin with conduction velocities <1.3 m/s. Morphine effects were concentration-dependent and naloxone-sensitive, indicating that the effects were receptor-mediated. These findings provide direct evidence that morphine acts through peripheral opioid receptors to inhibit the activity of cutaneous nociceptors under conditions of inflammation.
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In a previous study, we hypothesized that the approach of presenting information-bearing stimuli to one ear and noise to the other ear may be a general strategy to determine hemispheric specialization in auditory cortex (AC). In that study, we confirmed the dominant role of the right AC in directional categorization of frequency modulations by showing that fMRI activation of right but not left AC was sharply emphasized when masking noise was presented to the contralateral ear. Here, we tested this hypothesis using a lexical decision task supposed to be mainly processed in the left hemisphere. ⋯ Additional presentation of contralateral noise did not significantly change activation in right AC, whereas it led to a significant increase of activation in left AC compared with the condition without noise. This is consistent with a left hemispheric specialization for lexical decisions. Thus our results support the hypothesis that activation by ipsilateral information-bearing stimuli is upregulated mainly in the hemisphere specialized for a given task when noise is presented to the more influential contralateral ear.
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A laterally herniated disk, spinal stenosis, and various degenerative or traumatic diseases of the spine can sometimes lead to a chronic compression and inflammation of the dorsal root ganglion and chronic abnormal sensations including pain. After a chronic compression of the dorsal root ganglion (CCD) in rats, the somata in the dorsal root ganglion (DRG) become hyperexcitable, and some exhibit ectopic, spontaneous activity (SA). Inflammatory mediators have a potential role in modulating the excitability of DRG neurons and therefore may contribute to the neuronal hyperexcitability after CCD. ⋯ IS slightly depolarized the resting membrane potential and decreased the current and voltage thresholds of action potential in both intact and dissociated neurons, although the magnitude of depolarization or decrease in action potential threshold was not significantly different between CCD and control. IS-evoked responses were found in a proportion of neurons in each size category including those with and without nociceptive properties. Inflammatory mediators, by increasing the excitability of DRG somata, may contribute to CCD-induced neuronal hyperexcitability and to hyperalgesia and tactile allodynia.