Administration of monosodium glutamate (MSG) to neonatal rats has been reported to destroy aspartatergic (ASPergic) and glutamatergic (GLUergic) neurons. Ageing has been shown to induce cell loss, a rather general CNS atrophy, and slowness in the CNS functions. On the other hand, it has been hypothesized that two of the main reasons for opiate dependence development are the blockade by opiates of the NMDA receptors and their associated upregulation and supersensitivity. Accordingly, the abstinence syndrome precipitating effect of naloxone (NL) has been assumed to be the consequences of the removal by NL of opiate from NMDA receptors without being able to prevent upregulated and supersensitive NMDA receptors from being stimulated stronger than normal. To investigate the role of the decrease in the number of NMDA receptors in the development of morphine (M) physical dependence, 4 g/kg MSG was SC injected into neonatal rats on days 2,4,6,8 and 10 after birth. Their littermate controls SC received equimolar NaCl solution. Three or 14 months later, three pellets containing 75 mg base M were SC implanted into male rats treated neonatally with MSG or equimolar NaCl solution. Seventy-two hours after pellet implantation, all rats were injected with 2 mg/kg NL intraperitoneally. Some abstinence syndrome signs were counted or rated for 15 min immediately after NL injection and then statistically evaluated. The NL-precipitated abstinence syndrome was less intense in 3-month-old MSG-treated rats than in controls, most probably due to the decrease in the number of NMDA receptors in MSG-treated rats. The intensity of the NL-induced abstinence syndrome was found stronger in 14-month-old MSG-treated rats than in controls. The more intense development of physical dependence in 14-month-old MSG-treated rats was attributed to the upregulation and supersensitivity developed before pellet implantation to compensate for the destruction of NMDA receptors by MSG administered in the neonatal period. The attenuation of the M physical dependence intensity in 14-month-old control rats was explained by cell loss, CNS atrophy, and slowness in the CNS function.