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The Journal of Neuroscience, May 1, 2003, 23(9):3572
BRIEF COMMUNICATION
 1 Receptor-Related Neuroactive Steroids Modulate
Cocaine-Induced Reward
Pascal
Romieu1,
Rémi
Martin-Fardon2,
Wayne D.
Bowen3, and
Tangui
Maurice1
1 Centre National de la Recherche Scientifique
Unité Mixte de Recherche 5102, University of Montpellier II,
34095 Montpellier cedex 5, France, 2 Department of
Neuropharmacology, The Scripps Research Institute, La Jolla, California
92307, and 3 Unit on Receptor Biochemistry and
Pharmacology, Laboratory of Medicinal Chemistry, National Institute of
Diabetes and Digestive and Kidney Diseases, National Institutes of
Health, Bethesda, Maryland 20892
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ABSTRACT |
The  1 receptor is critically involved in the
rewarding effect of cocaine, as measured using the conditioned place
preference (CPP) procedure in mice. Neuroactive steroids exert rapid
neuromodulatory effects in the brain by interacting with
GABAA, NMDA, and 1 receptors. At the
1 receptor level, 3 -hydroxy-5-androsten-17-one
[dehydroepiandrosterone (DHEA)] and 3-hydroxy-5-pregnen-20-one
(pregnenolone) act as agonists, whereas 4-pregnene-3,20-dione
(progesterone) is an efficient antagonist. The present study sought to
investigate the action of neuroactive steroids in acquisition of
cocaine-induced CPP in C57BL/6 mice. None of these steroids induced CPP
alone. However, pretreatment with DHEA or pregnenolone (5-20 mg/kg,
s.c.) during conditioning with cocaine (10 mg/kg, i.p.) increased the
conditioned score. On the contrary, pretreatment with either
progesterone (10 or 20 mg/kg, s.c.) or finasteride (25 mg/kg, twice a
day), a 5 -reductase inhibitor, blocked acquisition of cocaine (20 mg/kg)-induced CPP. A crossed pharmacology was observed between
steroids and 1 ligands. The 1 antagonist
N-[2-(3,4-dichlorophenyl)ethyl]-N-methyl-2-(dimethylamino)ethylamine blocked cocaine-induced CPP and its potentiation by DHEA or
pregnenolone. Progesterone blocked cocaine-induced CPP and its
potentiation by the 1 agonist igmesine. These results
showed that neuroactive steroids play a role in cocaine-induced
appetence, through their interaction with the 1
receptor. Therefore, neuroendocrine control of cocaine addiction may
not involve solely glucocorticoids. The importance of neuroactive
steroids as factors of individual vulnerability to drug addiction
should, thus, be considered.
Key words:
cocaine; neuroactive steroids; locomotor activity; reward; convulsions; 1 receptor
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Introduction |
Cocaine is a major drug of abuse
worldwide. It is a potent stimulant, exerting its effects primarily by
its dopaminergic agonist activity on the mesocorticolimbic pathways. It
is widely accepted that the addictive and reinforcing actions of
cocaine are the results of its ability to block the reuptake of
dopamine (DA) and thereby to increase DA neurotransmission (Ritz et
al., 1987 ). Acute administration of cocaine induces hyperlocomotion and
stereotypies, whereas repeated administrations provoke sensitization to
the drug effects, with reinforcement and dependence appearing within a
short time after the first administration (Koob and Nestler, 1997).
Besides its action on DA, cocaine is known to affect the hypothalamopituitary adrenal axis, leading to increased levels of
corticotropin-releasing hormone (Sarnyai et al., 1992),
adrenocorticotropin hormone, and glucocorticoids (Moldow and
Fischman, 1987). In turn, glucocorticoids play a particular role
in vulnerability to cocaine intake and drug effects in terms of
stress-induced regulation of dopaminergic neurons (Marinelli and
Piazza, 2002).
However, with the exception of the anticonvulsant potency of
4-pregnene-3,20-dione (progesterone) metabolites against
cocaine-induced seizures (Gasior et al., 1997), little is known
regarding the influence on cocaine addiction of steroids synthesized
upstream to glucocorticoids in adrenals, gonads, and the brain. Among
them are neurosteroids (i.e., steroids synthesized in the brain and acting locally to modulate neuronal cell activity) (Baulieu, 1981). Neurosteroids are known to exert their modulatory effects primarily via
nongenomic actions and are known to affect learning and memory processes, mood, and depression (Rupprecht and Holsboer, 1999). 3-Hydroxy-5-pregnen-20-one (pregnenolone),
3-hydroxy-5-androsten-17-one [dehydroepiandrosterone (DHEA)], and
their sulfate esters are considered as excitatory steroids because they
act as negative modulators of the GABAA receptor
(Majewska et al., 1988, 1990) and positive modulators of NMDA receptors
(Wu et al., 1991). Progesterone and its reduced metabolite
3-hydroxy-5-pregnan-20-one (allopregnanolone) act as positive
modulators of the GABAA receptor (Schumacher and McEwen, 1989) and negative modulators of NMDA receptors (Smith, 1991). In addition, neuroactive steroids interact with the
1 receptor, with in vitro
affinities for brain [3H](+)-SKF-10,047
(N-[3H]allyl-normetazocine)-labeled
sites of 300 nM, 1 µM,
and 3 µM for progesterone, DHEA, and
pregnenolone, respectively (Su et al., 1988; Maurice et al., 1996).
Moreover, pregnenolone, DHEA, and their sulfate esters also act as
1 receptor agonists, whereas progesterone is a
potent 1 antagonist (Monnet et al., 1995;
Bergeron et al., 1996; Maurice et al., 1999, 2001). The
1 receptor is an intracellular neuronal
protein associated with endoplasmic reticular, plasma, nuclear, and
mitochondrial membranes (Alonso et al., 2000). The
1 receptor ligands potently modulate
intracellular Ca2+ mobilizations and
extracellular Ca2+ influx (Hayashi et al.,
2000) in addition to numerous responses to neurotransmitters (Monnet et
al., 1992; Gonzalez-Alvear and Werling, 1994). This nonselective but
efficient neuromodulatory system plays a major role in memory processes
and response to stress or depression (for review, see Maurice et al.,
1999, 2001). Moreover, the 1 receptor is
involved in several aspects of cocaine action (for review, see Maurice
et al., 2002), including hyperlocomotion (Menkel et al., 1991),
sensitization (Ujike et al., 1996), rewarding effects (Romieu et al.,
2000, 2002), convulsions, and lethality (Matsumoto et al., 2001).
The present study examined the effects of neuroactive steroids, namely
pregnenolone, DHEA, and progesterone, on cocaine-induced appetitive
properties, using the conditioned place preference (CPP) paradigm in
C57BL/6 mice. The results show that pregnenolone and DHEA, devoid of
effect by themselves, markedly increased cocaine-induced CPP, whereas
progesterone blocked it. A crossed pharmacology was observed between
steroids and 1 ligands, because the
potentiating effects of pregnenolone and DHEA were blocked by
preadministration of the 1 antagonist
N-[2-(3,4-dichlorophenyl)ethyl]-N-methyl-2-(dimethylamino)ethylamine (BD1047), whereas the potentiating effect of the
1 agonist igmesine was blocked by
progesterone. Neuroactive steroids may, thus, act through the
1 receptor to modulate cocaine-induced reward.
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Materials and Methods |
Animals. Male C57BL/6 mice, 1 month of age and
weighing 24-26 gm, were purchased from Iffa-Credo
(Saint-Germain-sur-l'Arbresle, France). The animals were housed in
groups with ad libitum access to food and water in a
temperature- and humidity-controlled animal facility on a 12 hr
light/dark cycle (lights off at 8:00 P.M.). Experiments were performed
between 10:00 A.M. and 6:00 P.M. in a sound-attenuated and
air-regulated experimental room, to which mice were habituated at least
30 min before each experiment. All animal procedures were conducted in
strict adherence to the European Communities Council (EEC) Directive of
November 24, 1986 (86-609/EEC).
Drugs. Cocaine was purchased from Cooper (Brive, France).
Progesterone, pregnenolone, and DHEA were obtained from
Sigma-Aldrich (Saint-Quentin Fallavier, France).
(+)-N-cyclopropylmethyl-N-methyl-1,4-diphenyl-1-ethyl-but-3-en-1-ylamine (igmesine) was provided by Dr. F. J. Roman (Pfizer
GRD, Fresnes, France), and BD1047 was synthesized in the
Laboratory of Medicinal Chemistry as described previously (De
Costa et al., 1992). Cocaine was dissolved in physiological
saline, igmesine and BD1047 were dissolved in distilled water, and
steroids were suspended in pure sesame oil
(Sigma-Aldrich). They were injected intraperitoneally or
subcutaneously in a volume of 100 µl per 20 gm of body weight.
CPP procedure. The apparatus consisted of a
polyvinylchloride box divided into two compartments of equal
size (15 × 15 × 35 cm high) separated by a sliding door,
the first one with black walls and floor and the second one with white
walls and floor. Each compartment presented different floor textures
(smooth for the black one and covered by a wire mesh grid for the white
one). A 60 W lamp lit the white compartment during all experiments.
The procedure consisted of three phases (Romieu et al., 2000, 2002).
For preconditioning (day 1), each mouse was placed in the white
compartment and doors were raised after 5 sec. The mouse freely
explored the apparatus for 10 min. Preconditioning was repeated after 6 hr. The exploration was videotaped, and the amount of time spent in
each compartment was recorded to determine the unconditioned
preference. Animals showing a strong unconditioned preference (>570
sec) were discarded. Conditioning (days 2-5) was conducted using an
unbiased procedure. In each group, one-half of the animals received
drugs in the spontaneously preferred compartment and the other half in
the nonpreferred compartment. Each mouse was confined to the
drug-paired compartment for 30 min. In coadministration experiments,
mice received steroids and/or 1 ligands 10 min
before cocaine. After a 6 hr washout period, vehicle solutions were
injected and mice were confined in the other compartment for 30 min.
During the postconditioning test (day 6), each mouse freely explored the apparatus for 10 min, and the time spent in each compartment was
determined. The conditioned score (mean ± SEM) was calculated as
the difference of time spent in the drug-paired compartment between the
postconditioning and preconditioning. Data were analyzed using a
parametric ANOVA, followed by a Newman-Keuls' post hoc test. The criterion for statistical significance was p < 0.05.
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Results |
Effects of neuroactive steroids on cocaine-induced CPP
Cocaine conditioning during 4 d resulted in dose-dependent
acquisition of CPP. A dose of 10 mg/kg led to a conditioned score of
+60 sec (black columns; p < 0.05) (Fig.
1a,b), and a dose
of 20 mg/kg led to a conditioned score of +120 sec (black column; p < 0.01) (Fig.
2a,b). The steroids
DHEA (Fig. 1a) and pregnenolone (Fig. 1b), 5-20
mg/kg subcutaneously, failed to induce CPP alone. However, pretreatment
before a low dose of cocaine (10 mg/kg) resulted in the potentiation of
cocaine-induced CPP (F(7,107) = 7.41;
p < 0.0001 for DHEA) (Fig. 1a)
(F(5,61) = 3.70; p < 0.01 for pregnenolone) (Fig. 1b). In particular, DHEA at 10 and 20 mg/kg and pregnenolone at 10 mg/kg provoked significant
increases in the conditioned scores compared with cocaine-treated
animals (p < 0.05 each).
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Figure 1.
Effects of neuroactive steroids on acquisition of
cocaine-induced CPP: coadministration of DHEA (a)
or pregnenolone (b). Steroids were administered
subcutaneously 10 min before cocaine, which was given immediately
before placement in the compartment during conditioning. Conditioned
scores represent the difference in time spent in the drug-paired
compartment between the postconditioning and preconditioning sessions.
Mice per group: n = 12-16
(a) and n = 8-12
(b). V, Vehicle. *p < 0.05 and **p < 0.01 versus the V+V-treated group;
#p < 0.05 versus the cocaine+V-treated
group.
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Figure 2.
Effects of neuroactive steroids on acquisition of
cocaine-induced CPP: coadministration of progesterone
(a) or effect of the 5-reductase inhibitor
finasteride (b). Progesterone was administered
subcutaneously 10 min before cocaine, given immediately before
placement in the compartment during conditioning. Finasteride (25 mg/kg) was administered subcutaneously, every 12 hr during 6 d,
starting 1 d before preconditioning. Conditioned scores represent
the difference in time spent in the drug-paired compartment between the
postconditioning and preconditioning sessions. Mice per group:
n = 12-19 (a) and
n = 10-19 (b). V, Vehicle.
*p < 0.05 and **p < 0.01 versus the V+V-treated group; #p < 0.05 versus the cocaine+V-treated group.
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Progesterone (10-40 mg/kg, s.c.) administration failed to induce CPP
alone (Fig. 2a). However, preadministration of progesterone before cocaine (20 mg/kg) led to a U-shaped decrease in the conditioned score (F(7,115) = 3.56;
p < 0.01) (Fig. 2a). Progesterone (20 mg/kg) pretreatment prevented acquisition of cocaine-induced CPP, whereas a higher dose (40 mg/kg) failed to affect the conditioned score. Finasteride is a selective inhibitor of the 5-reductase enzyme that converts progesterone to 5-pregnane-3,20-dione, the precursor of allopregnanolone (Trapani et al., 2002). When mice were
repeatedly treated with finasteride (25 mg/kg, s.c., twice a day during
6 d), they failed to acquire cocaine-induced CPP (F(3,50) = 4.43; p < 0.01) (Fig. 2b). Finasteride treatment was, however, devoid
of effect alone. Finasteride administration resulted in a moderate
accumulation of progesterone and in depletion of both
5-pregnane-3,20-dione and allopregnanolone levels (Trapani et al.,
2002). The blockade of cocaine-induced CPP by finasteride suggested
that not only low levels of progesterone but also sustained levels of
allopregnanolone are important for the establishment of cocaine-induced
CPP. Indeed, at the highest dose tested, the progesterone treatment led
to increased allopregnanolone content, and consequently a U-shaped
effect of progesterone was observed.
Involvement of the 1 receptor in neuroactive
steroid effects
The 1 receptor has been shown to be
involved in the acquisition and expression of cocaine-induced CPP in
previous studies, although selective 1 ligands
failed to induce CPP by themselves (Romieu et al., 2000, 2002). Because
the 1 receptor is a critical target for
neuroactive steroids in the brain, crossed pharmacology studies were
performed between steroids and 1 ligands.
First, the effect of the selective 1
antagonist BD1047 (10 mg/kg, s.c.) was examined. BD1047 pretreatment
resulted not only in the significant prevention of the cocaine-induced
CPP but also in blockade of the potentiation by DHEA
(F(7,133) = 3.97; p < 0.001) (Fig. 3a). Similarly,
BD1047 prevented the potentiating effect of pregnenolone (F(5,97) = 3.62; p < 0.01) (Fig. 3b). However, BD1047 administration failed to
induce CPP alone and affected only the conditioned scores observed in
cocaine-, DHEA-, or pregnenolone-treated groups (Fig. 3a,b).
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Figure 3.
Involvement of the 1 receptor in
the modulation of cocaine-induced CPP by neuroactive steroids: blockade
by the 1 antagonist BD1047 of the potentiating effects
of DHEA (a) or pregnenolone
(b). BD1047 was administered intraperitoneally
simultaneously with the steroid, given subcutaneously 10 min before
cocaine, injected immediately before placement in the compartment
during conditioning. Mice per group: n = 12-25
(a) and n = 12-26
(b). V, Vehicle. *p < 0.05 and **p < 0.01 versus the V+V-treated group;
#p < 0.05 versus the cocaine+V-treated
group.
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The selective 1 agonist igmesine (10-30
mg/kg, i.p.) (Fig. 4a) failed
to induce CPP alone in the 10-30 mg/kg dose range. However,
pretreatment with the compound before cocaine (10 mg/kg, i.p.)
significantly potentiated cocaine-induced CPP
(F(5,92) = 5.48; p < 0.001) (Fig. 4a). At 10 mg/kg, igmesine significantly increased the cocaine-induced conditioned score
(p < 0.05). We thus tested the antagonizing
effect of progesterone (20 mg/kg, s.c.) on the facilitation of
cocaine-induced CPP induced by igmesine (Fig. 4b).
Progesterone not only significantly prevented cocaine-induced CPP but
also blocked the potentiation by igmesine
(F(7,125) = 2.83; p < 0.001) (Fig. 4b).
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Figure 4.
Involvement of the 1 receptor in
the modulation of cocaine-induced CPP by neuroactive steroids:
coadministration of the 1 agonist igmesine before
cocaine (a) and blockade of its effect by
progesterone (b). Progesterone was administered
subcutaneously simultaneously with igmesine, given intraperitoneally 10 min before cocaine, injected immediately before placement in the
compartment during conditioning. Mice per group: n = 11-19 (a) and n = 10-20
(b). V, Vehicle. *p < 0.05 and **p < 0.01 versus the V+V-treated group;
#p < 0.05 and
##p < 0.01 versus the
cocaine+V-treated group.
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Discussion |
The present study provides evidence showing that neuroactive
steroids, namely DHEA, pregnenolone, and progesterone, interfere with
cocaine-induced reward in mice. None of the steroids tested alone
induced CPP in mice, a behavioral response considered as a reliable
index of drug-induced reward. However, pretreatment before cocaine
significantly modulated the acquisition of cocaine-induced CPP. On the
one hand, DHEA and its precursor pregnenenolone facilitated acquisition
of cocaine-induced CPP. On the other hand, progesterone or its
endogenous accumulation by finasteride inhibition of 5-reductase activity blocked the cocaine-induced response.
These steroids, originating endogenously from either the adrenal or
gonadal glands or the brain, are known to exert rapid neuromodulatory
actions on nerve cells (Rupprecht and Holsboer, 1999). In particular,
the sulfate ester of pregnenolone has been demonstrated to act as a
positive allosteric modulator of the NMDA receptor and a negative
allosteric modulator of the GABAA receptor
(Majewska et al., 1988; Wu et al., 1991). DHEA sulfate also acts as a
negative allosteric modulator of the GABAA
receptor (Majewska et al., 1990). On the contrary, progesterone
potentiates GABA-induced chloride currents and attenuates some neuronal
responses to NMDA (Wu et al., 1990; Smith, 1991). These effects through either GABAA or NMDA receptor modulation may
contribute to the present observations. Indeed, mesolimbic DA neurons
in the nucleus accumbens are under the control of inhibitory GABA
neurons and excitatory glutamatergic neurons originating from the
frontal cortex and hippocampus. For example, diazepam, a benzodiazepine acting as a positive GABAA receptor
modulator, reduced DA release in the nucleus accumbens measured by
in vivo microdialysis (Invernizzi et al., 1991) and as a
consequence attenuated cocaine-induced CPP (Meririnne et al., 1999). In
addition, presynaptic NMDA receptors facilitate central DA release
(Ault et al., 1998). In turn, competitive or noncompetitive NMDA
receptor antagonists decreased cocaine-induced locomotor stimulation
and sensitization (Karler et al., 1989) as well as CPP (Cervo and
Samanin, 1995). Because the respective pharmacological profile of DHEA,
pregnenolone, and progesterone on GABAA or NMDA
receptors is highly consistent, these interactions could be involved in
their effects on cocaine-induced CPP. However, most of the
GABAA or NMDA receptor modulators produced CPP or conditioned place aversion (CPA) by themselves. For instance, CPP was
observed with the direct GABAA agonist
meprobamate, the GABA metabolite  -hydroxybutyric acid, and several
benzodiazepine compounds, whereas benzodiazepine antagonists or inverse
agonists produced CPA (for review, see Tzschentke, 1998). Notably,
allopregnanolone, a neuroactive steroid devoid of affinity for the
1 receptor but acting as a highly efficient
GABAA receptor-positive modulator, induced CPP
after exogenous administration (Finn et al., 1996). Whereas NMDA
receptor competitive antagonists have also been reported to induce CPP,
inconsistent results were reported with noncompetitive antagonists. As
a particular example, dizocilpine has been described to induce either
CPP or CPA (Tzschentke, 1998). In the present study, the neuroactive
steroids failed to induce CPP or CPA alone, which seemed to indicate
that at the dose range tested they did not efficiently or selectively
interact with either GABAA or NMDA receptors.
The findings of the present study bring evidence that the
1 receptor, another molecular target mediating
some of the nongenomic effects of neuroactive steroids, is involved in
steroidal effects on cocaine-induced reward. First, the involvement of
the 1 receptor in several cocaine-induced
behavioral effects has been described previously (for review, see
Maurice et al., 2002). Selective 1 antagonists
blocked the locomotor stimulant effect of cocaine after acute
administration (Menkel et al., 1991; Witkin et al., 1993; McCracken et
al., 1999) and the development of behavioral sensitization after
repeated cocaine injections and withdrawal (Ujike et al., 1996).
Selective 1 antagonists or antisense
oligodeoxynucleotide probes targeting the 1
receptor also blocked acquisition or expression of cocaine-induced CPP
in mice (Romieu et al., 2000, 2002). Second, a crossed pharmacology
could be observed in the present study between neuroactive steroids and
1 ligands on this behavioral response.
Cocaine-induced CPP, and its stimulation by pretreatment with either
DHEA or pregnenolone, could be fully blocked using the
1 antagonist BD1047. Reciprocally,
progesterone blocked not only cocaine-induced CPP but also its
stimulation by the selective 1 agonist
igmesine. Such crossed pharmacology was previously observed on
physiological responses involving the 1
receptor, such as the potentiation of several NMDA-evoked responses
in vitro or in vivo (Monnet et al., 1995;
Bergeron et al., 1996). At the behavioral level, the antiamnesic
effects induced by DHEA, pregnenolone, and their sulfate esters on
several pharmacological models of amnesia involved an interaction with
the 1 receptor (Urani et al., 1998; Zou et
al., 2000; Maurice et al., 2001). The antistress effects of neuroactive
steroids in the conditioned fear stress or forced swim tests similarly
involved the 1 receptor (Noda et al., 2000;
Urani et al., 2001). In these different behavioral consequences of the
rapid nongenomic neuromodulation exerted by neuroactive steroids, a
clear crossed pharmacology with 1 receptors was described, suggesting a common mode of action and direct
interaction (Maurice et al., 1999, 2001). Therefore, the present
observations suggest that neuroactive steroids may influence
cocaine-induced reward through their interaction with the
1 receptor. Notably, both the
1 antagonist BD1047 and progesterone
completely blocked the potentiation of the cocaine-induced CPP by
either igmesine or neuroactive steroids. As mentioned previously,
neuroactive steroids may modulate dopaminergic neurons through their
effects on glutamatergic or GABAergic systems, either at the
presynaptic or postsynaptic level. However, activation of the
1 receptor may be a common pathway, putatively
downstream to these excitatory or inhibitory regulations, because its
inhibition results in a complete blockade of the behavioral response.
At the physiological level, the role of peripheral steroid hormones,
notably glucocorticoids, as endogenous modulators of the physiological
response to natural reinforcers and drugs of abuse has been documented
(Marinelli and Piazza, 2002). Other steroids and particularly centrally
synthesized steroids (i.e., neurosteroids) were known to be important
modulators of mood, depression, and affective disorders. Interestingly,
a recent report by Barrot et al. (1999) showed that
intracerebroventricular injection of pregnenolone sulfate increased DA
efflux measured in the rat nucleus accumbens by in vivo
microdialysis and potentiated the morphine-induced release.
Consequently, the authors suggested that this potentiation of
mesolimbic DA concentration may suggest an involvement of neuroactive
steroids in mood and motivation. The present observations brought
behavioral evidence for such an effect by showing that neuroactive
steroids could modulate responses to drug reward. DHEA, its precursor
pregnenolone, and their sulfate esters may indeed serve as endogenous
amplifiers of the rewarding effects of cocaine, whereas progesterone
may act as an inhibitor/stabilizer. It should be noted that although no
direct measure of brain steroid levels after cocaine has yet been
performed, circulating levels of both DHEA and progesterone are
affected by cocaine administration (Buydens-Branchey et al., 2002).
Therefore, individual levels of these steroids and evolution of the
DHEA/progesterone ratio after cocaine administration may putatively
constitute a reliable marker of vulnerability. Additional studies must
now be conducted to examine the involvement of DHEA and progesterone in
other manifestations of cocaine addiction, notably self-administration,
to validate their value as individual vulnerability markers.
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FOOTNOTES |
Received Nov. 12, 2002; revised Feb. 12, 2003; accepted Feb. 20, 2003.
This work was supported by Centre National de la Recherche
Scientifique. We thank Dr. F. J. Roman for the gift of igmesine and Dr. R. R. Matsumoto (Oklahoma University, Oklahoma City, OK) for helpful discussions.
Correspondence should be addressed to Dr. Tangui Maurice, Centre
National de la Recherche Scientifique Unité Mixte de Recherche 5102, University of Montpellier II, c.c. 090, place Eugène
Bataillon, 34095 Montpellier cedex 5, France. E-mail:
maurice{at}univ-montp2.fr.
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ABSTRACT
Introduction
