Brain research bulletin
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Brain research bulletin · Apr 2006
Comparative StudyDifferential expression of NK1 and GABAB receptors in spinal neurones projecting to antinociceptive or pronociceptive medullary centres.
The balance between excitatory and inhibitory input exerted upon spinal cord neurones that belong to spinofugal pathways determines the ultimate type of information transmitted to the brain. We compared the relative expression of NK1 and GABAB receptors in two spinomedullary pathways targeting an antinociceptive area and a pronociceptive centre, respectively, the lateral part of the caudal ventrolateral medulla (VLMlat) and the dorsal reticular nucleus (DRt). Spinal cord sections of rats injected in the VLMlat or DRt with the retrograde tracer cholera toxin subunit B were triple-immunoreacted for the tracer, NK1 receptors and GABAB receptors. ⋯ As to lamina I neurones projecting to the DRt, multipolar neurones mainly expressed GABAB receptors while the majority of flattened and pyramidal neurones co-localized NK1 and GABAB receptors. The present results suggest that the expression of NK1 and GABAB receptors varies in neurones participating to different spinofugal pathways. The importance of the present findings in the knowledge of the endogenous supraspinal pain control system is discussed.
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Brain research bulletin · Mar 2006
The effect of sevoflurane on intracellular calcium concentration from cholinergic cells.
The mechanism of action of volatile anesthetics is not completely understood. Calcium release from internal stores may alter signaling pathways that influence neurotransmission. Abnormalities of the regulation of intracellular calcium concentration ([Ca2+]i) from patients with malignant hyperthermia is a hallmark of this syndrome indicating the potential of these agents to interact with proteins involved in Ca2+ signaling. ⋯ Carbachol, a drug that releases Ca2+ from the IP3 pool, abolished the effect of sevoflurane. In addition, xestospongin D, a cell-permeant IP3 receptor antagonist, decreased significantly the sevoflurane increase on [Ca2+]i. Our data suggest that the sevoflurane-induced increase on [Ca2+]i from SN56 cells occurs through the release of calcium from IP3-sensitive calcium stores.
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Brain research bulletin · Mar 2006
Comparative StudySubthalamic oscillatory activities at beta or higher frequency do not change after high-frequency DBS in Parkinson's disease.
This study aimed to assess whether changes in the patterns of local field potential (LFP) oscillations of the subthalamic nucleus (STN) underlie to the clinical improvement within 60 s after turning off subthalamic DBS. We studied by spectral analysis the STN LFPs recorded in 13 nuclei from 7 patients with Parkinson's disease before and immediately after unilateral high-frequency (130 Hz) stimulation of the same nucleus, when the clinical benefit of DBS was unchanged. The results were compared with LFP data previously reported [A. ⋯ After DBS (10-15 min) of the STN, the recorded nuclei significantly differed from the control, failing to show significant changes either in the beta bands or at higher frequencies (60-90 and 250-350 Hz). The patterns of subthalamic LFP oscillations after DBS therefore differ from those after dopaminergic medication. These results suggest (1) that subthalamic LFP modulations are not the epiphenomenon of peripheral motor improvement and (2) that the transitory clinical efficacy maintained after discontinuation of subthalamic DBS is not associated with local modulation of LFP activity at beta or higher frequencies within the STN.
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Brain research bulletin · Mar 2006
Chronic buspirone treatment normalizes regional serotonin synthesis in the olfactory bulbectomized rat brain: an autoradiographic study.
The effects of chronic buspirone treatments, administered by minipump at doses of 10 and 20 mg/(kg day) for 14 days, on brain 5-HT synthesis in olfactory bulbectomized (OBX) rats were evaluated. The alpha-[14C]methyl-L-tryptophan autoradiographic method was used. We compared the synthesis in the buspirone treated OBX rats (administered either 10 mg/(kg day) (OBX-10) or 20 mg/(kg day) (OBX-20)) to that of the saline treated OBX rats (OBX-SAL), and the sham operated rats (SHX) treated with saline. ⋯ These results suggest that normalization (reduction to the level found in the SHX-SAL rats) of 5-HT synthesis in the OBX requires a greater dose of buspirone (20 mg/(kg day)) than that needed to produce a desensitization of the 5-HT1A receptors in the sham operated rats (10 mg/(kg day)). This probably indicates that 5-HT1A receptors have different functionality in the OBX rats than that found in the intact or sham operated rats. Furthermore, our results support the hypothesis that 5-HT1A receptors mediate the antidepressant-like effect of 5-HT1A agonists, as the chronic 5-HT1A agonist treatment in the depression model known to be sensitive to antidepressants resulted in the normalization of 5-HT synthesis.
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Brain research bulletin · Mar 2006
Down-regulation of GFRalpha-1 expression by antisense oligodeoxynucleotide attenuates electroacupuncture analgesia on heat hyperalgesia in a rat model of neuropathic pain.
Glial cell line-derived neurotrophic factor (GDNF) has been proved to play an important role in the modulation of nociceptive transmission especially during neuropathic pain. It was reported that electroacupuncture (EA) had potent analgesic effect on neuropathic pain and our previous studies indicated that EA could activate endogenous GDNF signaling system (GDNF and its receptor GFRalpha-1) in dorsal root ganglions (DRGs) of neuropathic pain rats. ⋯ The results showed that: (1) cumulative EA had potent analgesic effect on neuropathic pain in rats; (2) the expression of GFRalpha-1 in DRGs was down-regulated by intrathecal delivery of antisense ODN, but not by normal saline (NS) or mismatch ODN; (3) EA analgesia was significantly attenuated by antisense ODN treatment. The present study demonstrated that endogenous GDNF signaling system was involved in EA analgesia on neuropathic pain in rats, which would deepen our realization of the mechanism of EA analgesia.