Behavioural pharmacology
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Behavioural pharmacology · Oct 2010
Intrathecal injection of anti-CX3CR1 neutralizing antibody delayed and attenuated pain facilitation in rat tibial bone cancer pain model.
This study was designed to investigate the effect of intrathecal injection of anti-CX3CR1 neutralizing antibody on pain behaviors in the rat tibial bone cancer pain model. Syngeneic Walker 256 mammary gland carcinoma cells were injected into the tibia medullary cavity to establish the rat model of bone cancer pain. ⋯ Intrathecal injection of anti-CX3CR1 neutralizing antibody both delayed the development of ambulatory pain and hyperalgesia and attenuated established pain facilitation, but had no effects on destruction of bone. Our results suggest that intrathecal injection of anti-CX3CR1 neutralizing antibody delayed and attenuated pain facilitation in the rat tibial bone cancer pain model.
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Behavioural pharmacology · Oct 2010
Behavioral and neurochemical effects of chronic L-DOPA treatment on nonmotor sequelae in the hemiparkinsonian rat.
Depression and anxiety are the prevalent nonmotor symptoms that worsen quality of life for Parkinson's disease (PD) patients. Although dopamine (DA) cell loss is a commonly proposed mechanism, the reported efficacy of DA replacement therapy with L-DOPA on affective symptoms is inconsistent. To delineate the effects of DA denervation and chronic L-DOPA treatment on affective behaviors, male Sprague-Dawley rats received unilateral 6-hydroxydopamine or sham lesions and were treated daily with L-DOPA (12 mg/kg+benserazide, 15 mg/kg, subcutaneously) or vehicle (0.9% NaCl, 0.1% ascorbic acid) for 28 days before commencing investigations into anxiety (locomotor chambers, social interaction) and depression-like behaviors (forced swim test) during the OFF phase of L-DOPA. ⋯ Although DA lesion reduced climbing behaviors on day 2 of exposure to the forced swim test, chronic L-DOPA treatment did not reverse these effects. Neurochemically, L-DOPA treatment in hemiparkinsonian rats reduced norepinephrine levels in the prefrontal cortex, striatum, and hippocampus. Collectively, these data suggest that chronic L-DOPA therapy in severely DA-lesioned rats does not improve nonmotor symptoms and may impair nondopaminergic processes, indicating that long-term L-DOPA therapy does not exert necessary neuroplastic changes for improving affect.