الفهرس 
Literature ReviewOnly 14 pages are availabe for public view
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Abstract
In summary, the results of the present study indicated that GBP had
antinociceptive effects in hot plate and late phase of formalin test.
Similarly, LTG had antinociceptive effects in hot plate and both phases of
formalin test. However, LEV possessed antinociceptive effects only
against thermal stimuli in the hot plate test.
The antinociceptive mechanism of GBP was mediated, at least in
part, by CB1 and opioid receptors in hot plate and formalin tests.
However, 5-HT3 receptors were involved in the antinociceptive
mechanism of GBP in formalin test only. Furthermore, the antinociceptive
mechanism of LEV against thermal stimuli using hot plate test was
mediated by 5-HT3 and opioid receptors not CB1 receptors. However,
these receptors were not involved in the antinociceptive mechanism of
LTG in both tests of pain. GBP did not induce any motor deficits in the
tested mice. In contrast, LEV and LTG caused motor impairment in the
rotarod test. This effect was not mediated by CB1, 5-HT3 and opioid
receptors in all drugs.
Treatment with 10 doses of GBP, LEV or LTG for 20 days after the
development of peripheral diabetic neuropathy induced antihyperalgesic
effect using hot plate test. However, treatment with GBP and LEV, but
not LTG had antiallodynic effects.
Since peripheral diabetic neuropathy caused histopathological
changes in large (e.g. spinal cord) and peripheral nerves (e.g. sciatic
nerve), repeated treatment with both GBP and LEV produced some
neurogenerative effects on spinal cord and sciatic nerve. However, LTG
possessed neurogenerative effects on sciatic nerve only.
Spinal glia are activated in the peripheral diabetic neuropathy.
Treatment with LEV decreased the expression of spinal microglia.
Furthermore, GBP and LEV suppressed the expression of astrocytes.