Pharmacology, biochemistry, and behavior
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Pharmacol. Biochem. Behav. · Oct 2006
Corticotropin-releasing factor receptor type 1, but not type 2, in the ventromedial hypothalamus modulates dopamine release in female rats.
Corticotropin-releasing factor (CRF) plays an important role in stress responses and is mediated through two subtypes of receptors, CRF receptor type 1 (CRFR1) and CRF receptor type 2 (CRFR2). Each CRF receptor might have a different function through several neurotransmitter systems; however, the mechanism remains unclear. ⋯ On the other hand, this change did not always occur after Ucn II administration. These results suggest that the activation of CRFR1, but not CRFR2, modulates the release of DA in VMH.
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Pharmacol. Biochem. Behav. · Sep 2006
Antinociceptive tolerance revealed by cumulative intracranial microinjections of morphine into the periaqueductal gray in the rat.
The periaqueductal gray (PAG) appears to play a key role in morphine antinociception and tolerance. The objective of this manuscript is to develop a cumulative dose microinjection procedure so the hypothesized role of the PAG in morphine antinociceptive tolerance can be assessed using dose-response analysis. Rats were implanted with a guide cannula into the ventrolateral PAG. ⋯ Repeated microinjections of saline into the PAG had no effect on nociception. Pretreatment with twice daily injections of morphine, either systemically (5 mg/kg, s.c.) or into the PAG (5 micro g/0.4 micro l), for 2 days produced a two-fold increase in the ED(50) for morphine antinociception. These data validate the use of an intracranial cumulative dose procedure to assess morphine potency and demonstrate that microinjection of morphine into the PAG is sufficient to produce tolerance.
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Pharmacol. Biochem. Behav. · Sep 2006
Gabapentin enhances the analgesic response to morphine in acute model of pain in male rats.
Whenever opioids as drug of choice result in inadequate analgesia, the combinational therapy would be the solution. In this study the co-administration of gabapentin with morphine is evaluated in acute model of pain. Therefore the antinociceptive effect of gabapentin (30 or 90 mg/kg, s.c.) and morphine (0.5, 1 or 3 mg/kg, s.c.) alone or in combination were measured by tail-flick test in intact adult male rats. ⋯ The co-administration of gabapentin with analgesic doses of 1 and 3 mg/kg morphine had also increased significantly AUC. Therefore gabapentin enhanced the antinociceptive effect of both analgesic and subanalgesic doses of morphine in a dose dependent manner. In conclusion co-administration of gabapentin with low doses of morphine produced therapeutic analgesia which could have important clinical application.
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Pharmacol. Biochem. Behav. · Jul 2006
Slow-release and injected progesterone treatments enhance acute recovery after traumatic brain injury.
The benefits of continuous progesterone release via subcutaneous silastic capsule implants were compared to daily subcutaneous injections in a rat model of traumatic brain injury (TBI). Adult male Sprague-Dawley rats received either bilateral frontal cortex contusions or sham surgery. Rats were injected with progesterone or vehicle at 1 and 6 h post-injury, then once every 24 h for six days with tapering of the dose over the final two treatments. ⋯ All groups with implanted capsules increased locomotor activity compared to those given progesterone injections. In conclusion, steady-state progesterone treatment after TBI decreases edema and anxiety and increases activity, thus enhancing behavioral recovery. A continuous mode of pharmacological administration may prove to be more beneficial in translational and clinical testing than bolus injections over the same period of time.
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Pharmacol. Biochem. Behav. · Apr 2006
Role of TRPV1 and cannabinoid CB1 receptors in AM 404-evoked hypothermia in rats.
AM 404 inhibits endocannabinoid uptake and enhances the cannabinoid CB(1)-mediated effects of endogenous cannabinoids. Accumulating evidence also suggests that AM 404 acts at sites other than the endocannabinoid system. One site is the transient receptor potential vanilloid 1 cation channel (TRPV1). ⋯ Pre-treatment with SB 366791 (2 mg/kg, i.p.), a new TRPV1 antagonist, also abolished the hypothermia evoked by AM 404 (20 mg/kg, i.p.). In contrast, pre-treatment with SR 141716A (Rimonabant), a CB(1) antagonist, or AA-5-HT, a fatty acid amide hydrolase (FAAH) blocker, did not affect AM 404-evoked hypothermia. The present data demonstrate that AM 404 evokes a significant hypothermia in rats that is dependent on TRPV1 receptor activation.