جستجوی مقالات مرتبط با کلیدواژه « هسته لوکوس سرولئوس » در نشریات گروه « پزشکی »

Repetitive administration of opioid agonists induced dependency to these substances and thus limits their clinical usage. The locus coeruleus (LC) is a key brain structure implicated in dependency tolerance and the expression of somatic signs of morphine withdrawal syndrome. Orexin is a neuropeptide that involve in morphine tolerance and dependence, as well. OX1R has been detected in LC nucleus. In this study we examined the expression of OX1R during dependency and also in the withdrawal syndrome in neurons of LC nucleus in rats.

To incite dependency, morphine sulfate (10 mg/kg) was injected intraperitoneally twice a day for 10 days in male Wistar rats. For induction of withdrawal syndrome, naloxone was injected (2 mg/kg) subcutaneously in day 10, two hours after the last injection of morphine. In order to measure the expression of OX1R, RT-PCR was used.

This study shows that morphine dependency leads to increase expression of OX1R in neurons of LC nucleus. We also observed that morphine withdrawal syndrome with naloxone induced decreasing of OX1R expression in this region. In another word, amounts of this receptors back to normal level before dependency.

Due to results obtained from this study, we observed an increase in the expression of OX1R in neurons of LC nucleus and also return in the level of this receptors to baseline after exposure to naloxone and withdrawal syndrome. Hence we could suggest that OX1Rs in LC nucleus are involved in dependency and withdrawal syndrome.

Estradiol is a neuroactive steroid, which is found in several brain areas such as locus coeruleus (LC). Estradiol modulates nociception by binding to its receptors and also by allosteric interaction with other membranebound receptors like glutamate and GABAA receptors. LC is involved in noradrenergic descending pain modulation.

In order to study the effect of 17β-estradiol on both acute and persistent pain modulation and its mechanisms, formalin was injected into the hind paw of male rats. Formalin-induced responses including licking and flexing duration and paw jerking frequency were recorded for 60 min after injection of 50 μl of 2% formalin. Also, the expression of α2 and γ1 subunits of GABAA receptor genes were examined by RT-PCR technique.

The results of the current study showed that intra-locus coeruleus injection of 17β-estradiol attenuated the second phase, but not the acute phase of formalin induced pain (P< 0.05). GABAA receptor antagonist (bicuculline) reversed the antinociceptive effect of 17β-estradiol, but the expression level of α2 and γ1 subunits of GABAA receptor genes were not significantly changed.

It may be concluded that the analgesic effect of 17β-estradiol in formalin induced inflammatory pain is possibly mediated through the interaction with membrane-bound GABAA receptors, however this effect is not exerted at the gene expression level.

Barrel cortex of rodents is responsible for sensory information processing via facial whiskers. Locus coeruleus (LC), main source of cortical norepinephrine (NE), influences tactile sensory processing. In this study, the effect of phasic electrical stimulation of LC and sensory deprivation following the deflection of adjacent whisker on response properties of principal whisker related-neurons in layer IV of rat barrel cortex was investigated. Response properties of 18 neurons in controls and 22 neurons in sensory deprivation group (P4) were evaluated using extracellular single unit recording following the controlled deflection of adjacent whisker or before a combined deflection of principal and adjacent whiskers. All whiskers on the left muzzle, except for D2, were plucked every other day for two mounts in P4 group. In both groups, LC was stimulated at 0, 50, 100, 200, 400 and 800 ms before adjacent whisker deflection and its effect on response latency, response magnitude and CTR (Condition Test Ratio) index was assessed. The mechanical deflection of adjacent whisker with no electrical stimulation of LC in P4 group caused significant decrease and increase in neuronal response magnitude and CTR index, respectively. Almost in all times of LC stimulation and following combinations of whisker deflection, LC electrical stimulation before adjacent whisker deflection in P4 group caused a decrease in neuronal response magnitude and an increase in CTR index. LC electrical stimulation following sensory deprivation modulates neuronal response properties and changes the response patterns.