Effect of food deprivation on formalin-induced nociceptive behaviors and ß-endorphin and sex hormone concentration in rats.

BACKGROUND: The present study examined the possible role of endogenous opioidergic system in effect of food deprivation on formalin-induced nociceptive behaviors in male and female rats. Also, we investigated the effect of food deprivation on the plasma level of beta-endorphin and sex hormones. METHODS: Food was withdrawn 48 h prior to performing the formalin test, but water continued to be available ad libitum. The formalin was injected into hind plantar paw. RESULTS: There is significant difference between male and female control rats during phase 2B. Following 48-h food deprivation, both male and female rats exhibited enhanced nociceptive behavior in response to formalin. Food deprivation for 12 and 24 h increased and for 48 h decreased beta-endorphin level in male and female rats. Food deprivation for 24 h decreased testosterone level in male, while it had no significant effect on female rats and food deprivation for 48 h decreased testosterone level in both sexes. Food deprivation for 24 h increased estradiol level in female and that for 48 h had no significant effect on male and female rats. CONCLUSIONS: The present study demonstrates the existence of food deprivation for 48 h causes enhancement of nociception in the formalin test in male and female rats that has correlation with decrease in plasma beta-endorphin and testosterone levels.

Long term exposure to norharman exacerbates 6-hydroxydopamine-induced parkinsonism: possible involvement of L-type Ca2+ channels.

beta-Carbolines (BCs) are considered as endogenous neurotoxins that may contribute to the pathogenesis of Parkinson's disease (PD). However, several lines of evidences show that these compounds have neuroprotective effect. This study was designed to assess effect of long term exposure to norharman, a BC compound which in mammalian brain occurs at high levels in the substantia nigra, on the progress of parkinsonism induced by 6-hydroxydopamine (6-OHDA). Animals were daily treated by norharman at doses 100, 200 and 1000microg/kg (i.p.) just before to four weeks after the intrastriatal injection of 6-OHDA. Statistical analysis of apomorphine-induced rotation tests demonstrates that treatment by norharman at doses 200 and 1000microg/kg for four weeks exacerbates significantly behavioral symptoms of the parkinsonism. To explore mechanisms by which norharman affects nigral dopaminergic cells, we studied the role of L-type Ca2+ channels. For this purpose, animals were daily treated with either L-type Ca2+ channel blocker of nifedipine at doses 2 and 5mg/kg (i.p.) or nifedipine together with norharman before to four weeks after the 6-OHDA injection. While treatment with nifedipine improved behavioral symptoms of the parkinsonism, treatment with both nifedipine and norharman had no affect on these symptoms. This data indicates that long term exposure to BCs promote nigral dopaminergic cell death possibly through L-type Ca2+ channels.

Effects of morphine on rat behaviour in the elevated plus maze: the role of central amygdala dopamine receptors.

The objective of the present study was to evaluate the possible role of dopamine D(1)/D(2) receptors of the central amygdala (CeA) on morphine-induced anxiolytic-like behaviour in adult male Wistar rats. The animals were bilaterally implanted with chronic cannulas the CeA and tested in an elevated plus maze (EPM) task. Intraperitoneal (i.p.) administration of morphine (5 and 6 mg/kg) increased the percentage of open arm time (%OAT) and open arm entries (%OAE), indicating an anxiolytic-like response. Intra-CeA administration of different doses of the dopaminergic agonist apomorphine (0.1-0.3 microg/rat) significantly increased %OAE, but not %OAT. Furthermore, co-administration of the same doses of apomorphine with an ineffective dose of morphine (4 mg/kg; i.p.) significantly increased %OAT and %OAE by the opioid. Single microinjection of the D(1) dopaminergic antagonist SCH23390 (0.5-1.5 microg/rat) or sulpiride (0.5-1.5 microg/rat) into the CeA caused no significant change for %OAT and %OAE. The obtained results also show that intra-CeA microinjection of the same doses of SCH23390 or sulpiride inhibits the anxiolytic-like effect of morphine (6 mg/kg; i.p.). Pre-treatment of animals with SCH23390 (intra-CeA) or sulpiride (intra-CeA) reversed the response induced by apomorphine (0.3 microg/rat) plus morphine (4 mg/kg; i.p.). It should be considered that the drugs also did not show any effect on locomotor activity in all experiments. In conclusion, these findings suggest that the central amygdala dopaminergic mechanisms, probably via D(1)/D(2) receptors, may be involved in the modulation of morphine-induced anxiolytic-like behaviour in rat.