Characterization of β-endorphin-immunoreactivity in limbic brain structures of rats self-administering heroin or cocaine

Abstract

Abstract-The effects of intravenous self-administration of 3Opg infusions of either heroin or cocaine, or saline on the concentrations of f3-endorphin-immunoreactivity (BE-IR) in the anterior part of the rat brain limbic system were studied. Self-administration of heroin and cocaine for 5 daily sessions resulted in a marked reduction of the concentrations of BE-IF? in the nucleus accumbens, rostra1 striatum, septum and hippocampus at the time of the scheduled next session on day 6. In pooled extracts of these regions from rats receiving saline, combined application of high-pressure liquid chromatography (HPLC) fractionation and specific radioimmunoassays revealed the presence of a number of pE-related peptides co-chromatographing with synthetic non-acetylated and acetylated a, p-and y-type endorphins. Similar profiles were found after HPLC fractionation of extracts of these regions from rats self-administering heroin and cocaine. Rats self-administering heroin or cocaine, however, showed decreased amounts of all detected forms of g-endorphin as compared to saline rats. These findings indicate that both self-administration of an opiate that induces psychic as well as physical dependence and of a non-opiate stimulant inducing psychic but not physical dependence, results in a significant decrease of PE and related peptides in limbic brain regions of the rat. All forms of 6E detected after HPLC were equally affected, suggesting an overall effect of the drugs on peptide turnover. These results suggest that BE and related peptides may be involved in the neurochemical mechanisms underlying psychic dependence to drugs.

Strain and cocaine-induced differential opioid gene expression may predispose Lewis but not Fischer rats to escalate cocaine self-administration

“…Indeed, we found a Pomc mRNA downregulation both in the dorsal and ventral striatum in cocaine-exposed compared to yoked-saline rats, irrespective of Strain. Similar evidence was reported by Sweep et al (1988) showing that rats self-administering heroin or cocaine have decreased amounts of beta-endorphin in DS and NAcc, measured by high-pressure liquid chromatography, compared to saline rats. However, another report showed higher release of the peptide in the NAcc of rats exposed to cocaine self-administration compared to saline-control rats using microdialysis and ELISA assays (Roth-Deri et al, 2003).…”

The effects of piracetam on heroin-induced CPP and neuronal apoptosis in rats

“…β-EP, one of the most important endogenous opioid peptides, is distributed widely in the central nervous system and is responsible for a wide range of biological activities in the body (He et , 2011;Maslov et al, 2013;Wang et al, 2006). Our results demonstrated that chronic heroin resulted in a significant reduction of β-EP in the mPFC and AcbC within the corticolimbic system, which is consistent with the previous studies (Sweep et al, 1988(Sweep et al, , 1989. Interestingly, heroin-induced neuronal apoptosis were also detected in the mPFC and AcbC, and HP treatment normalized the β-EP levels and neuronal morphologies in the same areas.…”

Basolateral amygdala inactivation abolishes conditioned stimulus- and heroin-induced reinstatement of extinguished heroin-seeking behavior in rats

“…In rats engaging in morphine-seeking behavior (prior to any infusion of morphine), changes occur in monoamine and amino acid neurotransmitter turnover rates in the NAc, hippocampal formation, septum, amygdala, and the brainstem, relative to those seen in morphine-yoked controls (Smith et al 1984). Furthermore, at the regularly scheduled time of self-administration, decreases are observed in β-endorphin immunoreactivity in limbic structures, including the NAc, septum, hippocampus, and rostral striatum, that are suggestive of a conditioned decrease in β-endorphin turnover (Sweep et al 1988;Sweep et al 1989). Based on these findings, it can be postulated that the BLA may mediate incentive motivational effects of heroin and heroin-paired conditioned stimuli through its interaction with selective cortical structures and the mesocorticolimbic dopamine system.…”