Abstract
The role of corticosterone in the initiation and expression phases of sensitization to cocaine was examined. To determine the effect of corticosterone on the initiation of sensitization, male Sprague-Dawley rats were given a sham adrenalectomy (ADX), or ADX surgery. Approximately 1 week later, rats were given a cocaine (15 mg/kg, IP) injection on day 1. On days 2–6, rats were given cocaine (30 mg/kg, IP), and the next day, a cocaine challenge (15 mg/kg) was administered (= early withdrawal). Four days later, 50% of the ADX rats were given corticosterone pellets and corticosterone in the evening drinking water to mimic the circadian variation in corticosterone levels. After 1 week, rats were given a final saline challenge followed by a cocaine challenge (15 mg/kg) the next day (= late withdrawal). Locomotor activity was monitored after cocaine treatment on day 1 and after challenge at early and late withdrawal. Sham controls demonstrated a sensitized locomotor response to the cocaine challenge at early withdrawal, with a slight increase in this behavioral sensitization at the late withdrawal time. In contrast, sensitization was not observed in ADX rats after early withdrawal from cocaine, but this attenuation was not permanent, since ADX animals demonstrated control levels of sensitization by the late withdrawal time 12 days later. Animals given corticosterone replacement 1 week prior to the late cocaine challenge also demonstrated a sensitized response similar to control levels. The effect of corticosterone on the expression of sensitization was examined by administering daily cocaine as before followed by surgery a few days later. The treatment groups were sham, ADX and ADX+corticosterone replacement as described. Fourteen days later, a saline injection was given followed by a cocaine challenge the next day. Behavioral sensitization to a cocaine challenge was found in all three treatment groups. These data suggest that adrenal hormones are necessary during the initiation phase of sensitization when observed after early withdrawal (1 day), but not when sensitization is examined at a later withdrawal time (12 days). In addition, corticosterone levels do not significantly affect the expression phase of behavioral sensitization to cocaine.
Similar content being viewed by others
References
Abercrombie ED, Keefe KA, DiFrischia DS, Zigmond MJ (1989) Differential effect of stress on in vivo dopamine release in striatum, nucleus accumbens, and medial frontal cortex. J Neurochem 52:1655–1658
Ackerman JM, White FJ (1992) Decreased activity of rat A10 dopamine neurons following withdrawal from repeated cocaine. Eur J Pharmacol 218:171–173
Antelman SM, Eichler AJ, Black CA, Kocan D (1980) Interchangeability of stress and amphetamine in sensitization. Science 207:329–331
Badiani A, Morano MI, Akil H, Robinson TE (1995) Circulating adrenal hormones are not necessary for the development of sensitization to the psychomotor activating effects of amphetamine. Brain Res 673:13–24
Barrot M, Rouge-Pont F, Maccari S, Marinelli M, le Moal M, Simon H, Piazza PV (1994) Glucocorticoids and drug abuse (III): influences of basal corticosterone secretion on the effects of cocaine and morphine on accumbens dopamine. Soc Neurosci Abstr 20:1633
Cador M, Cole BJ, Koob GF, Stinus L, le Moal M (1993a) Central administration of corticotropin releasing factor induces long-term sensitization tod-amphetamine. Brain Res 606:181–186
Cador M, Dulluc J, Mormede P (1993b) Modulation of the locomotor response to amphetamine by corticosterone. Neuroscience 56:981–988
Cole BJ, Cador M, Stinus L, Rivier C, Rivier J, Vale W, le Moal M, Koob GF (1990a) Critical role of the hypothalamic pituitary adrenal axis in amphetamine-induced sensitization of behavior. Life Sci 47:1715–1720
Cole BJ, Cador M, Stinus L, Rivier J, Vale W, Koob GF, le Moal M (1990b) Central administration of a CRF antagonist blocks the development of stress-induced behavioral sensitization. Brain Res 512:343–346
Cools AR (1991) Differential role of mineralocorticoid and glucocorticoid receptors in the genesis of dexamphetamine-induced sensitization of mesolimbic, alphal adrenergic receptors in the ventral striatum. Neuroscience 43:419–428
Deroche V, Piazza PV, Casolini P, Maccari S, le Moal M, Simon H (1992a) Stress-induced sensitization to amphetamine and morphine psychomotor effects depend on stress-induced corticosterone secretion. Brain Res 598:343–348
Deroche V, Piazza PV, Maccari S, le Moal M, Simon H (1992b) Repeated corticosterone administration sensitizes the locomotor response to amphetamine. Brain Res 584:309–313
Deroche V, Piazza PV, Casolini P, le Moal M, Simon H (1993) Sensitization to the psychomotor effects of amphetamine and morphine induced by food restriction depends on corticosterone secretion. Brain Res 611:352–356
Ffrench-Mullen JMH (1995) Cortisol inhibition of calcium currents in guinea pig hippocampal CA1 neurons via G-protein-coupled activation of protein kinase C. J Neurosci 15:903–911
Francis D, Meaney MJ, Gratton A (1994) Stress-induced sensitization to the locomotor stimulant effect of amphetamine is modulated by corticosterone. Soc Neurosci Abstr 20:822
Harfstrand A, Fuxe K, Cintra A, Agnati LF, Zini I, Wikstrom A-C, Okret S, Zhao-Ying Y, Goldstein M, Steinbusch H, Verhofstad A, Gustafsson J-A (1986) Glucocorticoid receptor immunoreactivity in monoaminergic neurons of rat brain. Proc Natl Acad Sci USA 83:9779–9783
Joels M, De Kloet De (1992) Control of neuronal excitability by corticosteroid hormones. Trends Neurosci 15:25–30
Kalivas PW, Duffy P (1989) Similar effects of daily cocaine and stress on mesocorticolimbic dopamine neurotransmission in the rat. Biol Psychiatry 25:913–928
Kalivas PW, Duffy P (1990) The effect of acute and daily cocaine treatment on extracellular dopamine in the nucleus accumbens. Synapse 5:48–58
Kalivas PW, Duffy P (1993) Time course of extracellular dopamine and behavioral sensitization to cocaine. I. Dopamine axon terminals. J Neurosci 13:266–275
Kalivas PW, Stewart J (1991) Dopamine transmission in the initiation and expression of drug- and stress-induced sensitization of motor activity. Brain Res Rev 16:223–224
Kalivas PW, Sorg BA, Hooks MS (1993) The pharmacology and neural circuitry of sensitization to psychostimulants. Behav Pharmacol 4:315–334
Knich ET, Eisenberg RM (1979) Effect of amphetamine on plasma corticosterone in the conscious rat. Neuroendocrinology 29:110–118
Koe BK (1976) Molecular geometry of inhibitors of the uptake of catecholamines and serotonin in synaptosomal preparations of rat brain. J Pharmacol Exp Ther 199:649–661
Marinelli M, Piazza PV, Deroche V, Maccari S, le Moal M, Simon H (1994) Corticosterone circadian secretion differently facilitates dopamine-mediated psychomotor effect of cocaine and morphine. J Neurosci 14:2724–2731
Meyer JS, Micco DJ, Stephenson BS, Krey LC, McEwen BS (1979) Subcutaneous implantation method for chronic glucocorticoid replacement therapy. Physiol Behav 22:867–870
Milliken GA, Johnson DE (1984) Analysis of messy data, volume I: designed experiments. Lifetime Learning Publications, Belmont, Calif.
Moghaddam B, Bunney BS (1989) Differential effect of cocaine on extracellular dopamine levels in rat medial prefrontal cortex and nucleus accumbens: comparison to amphetamine. Synapse 4:156–161
Munck A, Guyre PM (1986) Glucocorticoid physiology, pharmacology and stress. Adv Exp Med Biol 196:81–96
Ortiz J, Kosten TA, DeCaprio J, Nestler EJ (1994) Differential effects of corticosterone on locomotor sensitization to cocaine in Fischer and Lewis rats: possible biochemical mechanisms. Soc Neurosci Abstr 20:1633
Pauly JR, Robinson SF, Collins AC (1993) Chronic corticosterone administration enhances behavioral sensitization to amphetamine in mice. Brain Res 620:195–202
Pettit HO, Pan H-T, Parsons LH, Justice JB, Jr (1990) Extracellular concentrations of cocaine and dopamine are enhanced during chronic cocaine administration. J Neurochem 55:798–804
Piazza PV, Maccari S, Deminiere J-M, le Moal M, Mormede P, Simon H (1991) Corticosterone levels determine individual vulnerability to amphetamine self-administration. Proc Natl Acad Sci USA 88:2088–2092
Rivet JM, Stinus L, le Moal M, Mormede P (1989) Behavioral sensitization to amphetamine is dependent on corticosteroid receptor activation. Brain Res 498:149–153
Rivier C, Vale W (1987) Cocaine stimulates adrenocorticotropin (ACTH) secretion through a corticotropin-releasing factor (CRF)-mediated mechanism. Brain Res 422:403–406
Robinson TE, Becker JB (1986) Enduring changes in brain and behavior produced by chronic amphetamine administration: a review and evaluation of animal models of amphetamine psychosis. Brain Res Rev 11:157–198
Robinson TE, Jurson PA, Bennett JA, Bentgen KM (1988) Persistent sensitization of dopamine neurotransmission in ventral striatum (nucleus accumbens) produced by prior experience with (+)-amphetamine: a microdialysis study in freely moving rats. Brain Res 462:211–222
Segal DS, Kuczenski R (1992a) Repeated cocaine administration induces behavioral sensitization and corresponding decreased extracellular dopamine responses in caudate and accumbens. Brain Res 577:351–355
Segal DS, Kuczenski R (1992b) In vivo microdialysis reveals a diminished amphetamine-induced dopamine reponse corresponding to behavioral sensitization produced by repeated amphetamine pretreatment. Brain Res 521:303–332
Sorg BA, Kalivas PW (1993) Effects of cocaine and footshock stress on extracellular dopamine levels in the medial prefrontal cortex. Neuroscience 53:695–703
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Prasad, B.M., Ulibarri, C., Kalivas, P.W. et al. Effect of adrenalectomy on the initiation and expression of cocaine-induced sensitization. Psychopharmacology 125, 265–273 (1996). https://doi.org/10.1007/BF02247338
Received:
Revised:
Issue Date:
DOI: https://doi.org/10.1007/BF02247338