Rewarding properties of β-endorphin as measured by conditioned place preference

Abstract

The role of beta-endorphin as a possible mediator in the reinforcing properties of opiates was investigated using a conditioned place preference paradigm. Heroin, a synthetic opiate known to have reinforcing properties, produced a strong preference for an environment previously paired with heroin injection at all doses tested (0.25, 0.5, 1.0, 2.0 mg/kg SC). No such place preference was observed following saline injections. Rats also showed dose-dependent place preference for the environment paired with beta-endorphin when injected intracerebroventricularly (significant dose was 2.5 micrograms). At higher doses (5.0 and 10.0 micrograms) rats showed no preference for the paired environment, but were catatonic. Pretreatment with naloxone (0.04, 0.2, 1.0 mg/kg SC) attenuated the rewarding effect of beta-endorphin (2.5 micrograms) at all doses tested. The lowest dose of naloxone which had no aversive effect when tested alone could also significantly block the positive effect of beta-endorphin. The reinforcing dose of beta-endorphin (2.5 micrograms) also produced an increase in locomotor activity, when tested in photocell cages. This suggests that the hyperactivity induced by beta-endorphin may contribute to the preference for an environment previously paired with the same drug. The reinforcing effect of beta-endorphin is most probably mediated by the mu and/or delta opioid subtype receptor, since beta-endorphin has a high affinity for these receptors. These results demonstrate positive reinforcing properties of beta-endorphin in the central nervous system.

Association of the κ-opioid system with alcohol dependence

“…In neither case did [1][2][3] 0.015 CAG TGA SNP [2][3][4] 0.010 AGG GAA SNP [3][4][5] 0.044 GGG AAA SNP [4][5][6] 0.005 GGA AAG SNP [5][6][7] 0.065 GAA AGA* SNP [6][7][8] 0.027 AAC -SNP [7][8][9] 0.062 ACA* -SNP [8][9][10] 0.09 CAT** -SNP [9][10][11] 0.08 --SNP [10][11][12] 0.28 --SNP [11][12][13] 0.37 --SNP [12][13][14] 0.60 --SNP [13][14][15] 0.031 TGC TGT SNP [14][15][16] 0.057 GCA GTA SNP [15][16][17] 0.074 CCT** TAA SNP [16][17][18] 0.30 --Individual overtransmitted haplotypes for alcohol dependence are indicated in bold when P < 0.05; *P = 0.06, and **P < 0.10.…”

“…[1][2][3][4][5] The opioid system appears to play an important role in the reward system by influencing dopamine release in the nucleus accumbens. 6 There are three major groups of endogenous opioid peptides (dynorphins, endorphins and enkephalins) and three corresponding opioid receptors, k-opioid receptor (KOR), m-opioid receptor (MOR) and d-opioid receptor (DOR).…”

The role of beta-endorphin in the acute motor stimulatory and rewarding actions of cocaine in mice

“…As central administration of beta-endorphin induces CPP (Amalric et al 1987) and cocaine causes the release of beta-endorphin in the nucleus accumbens (Olive et al 2001), a brain region where local administration of opiates induces reward (Kelsey et al 1989;Wise 1989;Wise and Hoffman 1992), we then tested the possibility that the endogenous opioid peptide beta-endorphin could also be important in the cocaine-induced reward. A single conditioning with cocaine (15 mg/kg) failed to induce CPP (Fig.…”

“…Intracerebroventricular beta-endorphin administration has been shown to increase motor activity and to induce conditioned place preference (CPP) in rats (Amalric et al 1987). Furthermore, cocaine has been shown to cause the release of beta-endorphin in the nucleus accumbens (Olive et al 2001), raising the possibility that this neuropeptide may be important in these actions of cocaine.…”

AgRP(83–132) and SHU9119 differently affect activity-based anorexia

“…These data urge for further investigations on the involvement of other POMC-derived neuropeptides in the development of ABA, like B-endorphin. B-Endorphin stimulates food intake as well as rewarding processes and nociception (Amalric et al, 1987;Glass et al, 1999;Kalra and Horvath, 1998;Mucha and Herz, 1985;Przewlocki and Przewlocka, 2001). Yet a possible anorexic potency of B-endorphin was discovered by generating (male) B-endorphin-deficient mice, which are obese and hyperphagic (Appleyard et al, 2003).…”