Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of PFC stimulation on spontaneous and evoked discharges of neurons of parafascicular nucleus of thalamus were observed in rats. The results show that after PFC stimulation spontaneous of 78.7% PEN (48/61) and evoked discharges on noxious stimulation of 76.6% PEN (46/60) were decreased; spontaneous discharges of 72% PIN (18/25) were increased; inhibition response on noxious stimulation of 70.8% PIN (17/24) were decreased; and spontaneous discharges of 66.7% CON (6/9) and evoked discharges on noxious stimulation of 55.6% CON (5/9) were decreased. The results suggest that PFC might have analgesia action which was accomplished by modulating electric activities of pain-related neurons of parafascicular nucleus in thalamus.
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PMID:[Effect of prefrontal cortex stimulation on the activity of pain-related neurons in parafascicular nucleus of thalamus in rats]. 187 98

The influence of intraventricular injection of GABA on electrical activities of PEN and PIN in nucleus parafascicularis of the thalamus of rats was studied. The results showed that GABA could significantly inhibit the electrical discharges of PEN and increase the electrical discharges of PIN. So it was believed that intraventricularly injected GABA could antagonize or partly antagonize the excitatory action of noxious stimuli and might thus produce analgesia.
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PMID:[The influence of GABA injected into cerebral ventricle on electrical activities of pain-excitation neurons and pain-inhibition neurons in nucleus parafascicularis of the thalamus of rats]. 251 22

Two varieties of neurons were found in nucleus parafascicularis (pf) of the rat: one responds to noxious stimuli with an increase in firing (pain-excited neuron, PEN), the other with a decrease in firing (pain-inhibited neuron, PIN). Electroacupuncture (EA) has been shown to suppress PEN and excite PIN, which can be taken as an electrophysiological index for EA analgesia. This effect of EA subsided after prolonged (6 h) EA stimulation, suggesting the development of tolerance to EA. Intracerebroventricular (icv) injection of CCK-8 antiserum aiming at neutralizing endogenously released CCK-8 resulted in a complete restoration of the EA effect. Normal rabbit serum was not effective. CCK-8 antiserum per se did not affect the firing pattern of the PEN or PIN in nontolerant rat. The results obtained from single neuron recording in anesthetized animals thus confirmed those obtained in intact animals using the tail flick as the end point, implying that an excess of endogenously released CCK-8 may constitute one of the mechanisms for the development of EA tolerance.
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PMID:Reversal of electroacupuncture tolerance by CCK-8 antiserum: an electrophysiological study on pain-related neurons in nucleus parafascicularis of the rat. 822 97