Suppression of the tail flick response to noxious heat and paw withdrawal response to noxious pressure were produced by electrical stimulation of arcuate nucleus of the hypothalamus (ARH) in pentobarbital anesthetized rats. Systemic administration of naloxone (2 mg/kg) greatly antagonized the ARH stimulation-produced inhibition of both algesic reflexes. The thresholds of stimulation for inhibition of two spinal nociceptive reflexes in the lightly anesthetized state were not significantly different from the thresholds of stimulation at the same ARH sites in the awake state in the same animals. These findings provide evidence establishing the (1) usefulness of the anesthetized rat model for investigation of antinociceptive mechanisms; (2) the involvement of endogenous opioid mechanisms in mediating ARH stimulation-produced analgesia.
We evaluated the effect of puerarin on spatial learning and memory ability of mice
with chronic alcohol poisoning. A total of 30 male C57BL/6 mice were randomly divided
into model, puerarin, and control groups (n=10 each). The model group received 60%
(v/v) ethanol by intragastric administration followed by intraperitoneal injection of
normal saline 30 min later. The puerarin group received intragastric 60% ethanol
followed by intraperitoneal puerarin 30 min later, and the control group received
intragastric saline followed by intraperitoneal saline. Six weeks after treatment,
the Morris water maze and Tru Scan behavioral tests and immunofluorescence staining
of cerebral cortex and hippocampal neurons (by Neu-N) and microglia (by Ib1) were
conducted. Glutamic acid (Glu) and gamma amino butyric acid (GABA) in the cortex and
hippocampus were assayed by high-performance liquid chromatography (HPLC), and tumor
necrosis factor (TNF)-α and interleukin (IL)-1β were determined by ELISA. Compared
with mice in the control group, escape latency and distance were prolonged, and
spontaneous movement distance was shortened (P<0.05) by puerarin. The number of
microglia was increased in both the cortex and hippocampal dentate gyrus (P<0.01),
and neurons were reduced only in the hippocampal dentate gyrus (P<0.01) in
puerarin-treated mice. In the model group, Glu and GABA levels decreased (P<0.05),
and Glu/GABA, TNF-α, and IL-1β increased (P<0.01) with puerarin treatment,
returning to near normal levels. In conclusion, puerarin protected against the
effects of chronic alcohol poisoning on spatial learning and memory ability primarily
because of anti-inflammatory activity and regulation of the balance of Glu and
GABA.
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