Saenz CM, Borowski T, De Lacalle S (2008) Contrasting effects of estrogen on memory tasks in young female rats. Neuroscience 2008 Abstracts 794.17/UU7. Society for Neuroscience, Washington, DC.
Summary: Sleep deprivation may lead to behavioral alterations and it has been associated with a hyperalgesic state in human beings and animal models. The tricyclic antidepressant amitriptyline can be used as an analgesic drug in patients and in chronic pain animal models that are not improved with classical analgesics, such as spinal nerve injury induced model of peripheral neuropathy. The pain hypersensitivity following both paradoxical sleep deprivation (PSD) and peripheral nerve injury shares common spinal mechanisms, which involve at least the glutamate receptors and nitric oxide. In this way, we evaluated the effects of amitriptyline pretreatment in the thermal hyperalgesia observed in paradoxical sleep deprived rats. Amitriptyline (10 and 30 mg/Kg) or saline were administered i.p. during 11 days to male Wistar rats (n = 7/group, 250 – 350 g). In the last 3 or 4 days of treatment the animals were submitted to 72 or 96 hours of PSD, respectively, or remained in home cages, being subsequently evaluated for their thermal sensitivity on a hot plate test (52oC or 46oC), 1 or 24 hours after the last drug administration. In order to verify if the results observed in the highest withdrawal latencies were due to a reduction on the locomotor activity rather than an analgesic effect, the number of squares crossed in an open field arena during 5 minutes, subsequently to the hot plate test was counted. The results demonstrated that paw withdrawal latency response to 52oC was significantly lower in paradoxical sleep deprived rats than controls (-37%, p<0.05). This hyperalgesic effect was also detected in animals pre-treated with 10 mg/kg (-41%, p<0.05) or 30 mg/Kg (-53%, p<0.05) of amitriptyline. At the highest dose, both groups presented a higher withdrawal threshold when compared to their respective saline groups (+185%, p<0.05 and +112%, p<0.05; control and sleep deprived rats, respectively). However, in the open field test a decrease in the number of squares crossed in control animals was observed (-52%, p<0.05), but not in sleep deprived rats (-3%, p>0.05). When the animals were allowed to recover for 24h from sleep deprivation, the pre-treatment with amitriptyline (10 mg/Kg) was not able to prevent the hyperalgesic state (-60%, p<0.05). Even with lower thermal stimulus (46oC) and sleep deprivation period (72h), the difference between control and sleep deprived animals could still be detected (-40%, p<0.05), with no changes after an amitriptyline 10 mg/Kg pre-treatment (-43%, p<0.05). Overall, these findings highlight that thermal pain hypersensitivity induced by PSD was not prevented by amitriptyline pre-treatment, as observed in other models of inductive pain.
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