The long-term effects of repeated amphetamine treatment in vivo on amphetamine, KCl and electrical stimulation evoked striatal dopamine release in vitro

doi:10.1016/0024-3205(88)90343-8

Life Sciences

Volume 42, Issue 24, 1988, Pages 2447-2456

https://doi.org/10.1016/0024-3205(88)90343-8 Get rights and content

Abstract

Exposure to amphetamine (AMPH) in vivo produces an enduring enhancement (‘sensitization’) in AMPH-stimulated striatal DA release in vitro. Experiments were conducted to determine whether striatal DA release evoked by neuronal depolarization is altered by AMPH pretreatment in a similar manner. It was found that AMPH pretreatment produced a long-lasting (at least one week) enhancement in striatal DA release evoked by AMPH, KCl or electrical field stimulation. In contrast, the basal rate of DA efflux was not altered by pretreatment condition. A mechanism by which a single change in the intracellular distribution of DA could enhance both AMPH- and depolarization-induced DA release is proposed.

References (56)

T.E. Robinson et al.
Brain Res. Rev.
(1986)
M.G. Kolta et al.
Neuropharmacology
(1985)
T.E. Robinson et al.
Eur. J. Pharmacol.
(1982)
T.E. Robinson et al.
Brain Res.
(1982)
J. Peris et al.
Pharmacol. Biochem. Behav.
(1987)
G.V. Rebec et al.
Pharmacol. Biochem. Behav.
(1980)
T.G. Heffner et al.
Pharmacol. Biochem. Behav.
(1980)
J.B. Becker et al.
J. Neurosci. Meth.
(1984)
T.E. Robinson et al.
Neuropharmacology
(1987)
R.A. Wilcox et al.
Eur. J. Pharmacol.
(1986)

F. Orrego

Neuroscience

(1979)

J. Aceves et al.

Neuroscience

(1981)

D.S. Segal et al.

Pharmacol. Biochem. Behav.

(1974)

L. Magos

Eur. J. Pharmacol.

(1969)

N. Rowland et al.

Appetite

(1981)

P. Muller et al.

Eur. J. Pharmacol.

(1979)

J.M. Roberts-Lewis et al.

Brain Res.

(1986)

S.M. Antelman et al.

T.E. Robinson et al.

Life Sci.

(1985)

T.E. Robinson et al.

Brain Res.

(1985)

R. Kuczenski et al.

Pharmacol. Biochem. Behav.

(1981)

T. Nishikawa et al.

Eur. J. Pharmacol.

(1983)

T.E. Robinson et al.

Pharmacol. Biochem. Behav.

(1987)

J.B. Justice et al.

J. Neurosci. Meth.

(1988)

B.A. McMillen et al.

Biochem. Pharmacol.

(1980)

A.H. Mulder

P.H. Connell

Amphetamine Psychosis

(1958)

E.H. Ellinwood et al.

Am. J. Psychiatry

(1973)

Cited by (97)

Reciprocal cross-sensitization between cocaine and RU 24969 in male and female preweanling rats
2021, Pharmacology Biochemistry and Behavior
Citation Excerpt :
That RU 24969 cross-sensitizes with cocaine, but not methamphetamine, suggests that differences in monoamine transporter affinity or mechanism of action might be the critical factor determining whether cross-sensitization occurs. Although mechanism of action can play an important role in behavioral sensitization (Castañeda et al., 1988), it is more likely that cocaine's affinity for the 5-HT transporter is crucial. Specifically, cocaine dramatically increases synaptic levels of both DA and 5-HT; whereas, methamphetamine preferentially increases DA and norepinephrine levels, while having little affinity for the 5-HT transporter (Andrews and Lucki, 2001; Reith et al., 1997; Zhang et al., 2001; for a review, see Howell and Kimmel, 2008).
Neuronal adaptations involving dopaminergic, glutamatergic, and serotonergic neurotransmitter systems are responsible for behavioral sensitization. Because of common underlying mechanisms, cross-sensitization between compounds of different drug classes can be observed. The purpose of the present study was to determine whether a one- or four-day pretreatment regimen of RU 24969 (a 5-HT_1A/1B receptor agonist) would reciprocally cross-sensitize with cocaine or methamphetamine in male and female preweanling rats. Rats were pretreated with RU 24969 (0 or 5 mg/kg) for 4 days (PD 17–20) and then challenged with cocaine (10 or 20 mg/kg) or methamphetamine (1 or 2 mg/kg) on PD 22. Reciprocal cross-sensitization was also assessed (i.e., rats were pretreated with psychostimulants and tested with RU 24969). In a follow-up experiment, the ability of RU 24969 and cocaine to reciprocally cross-sensitize was assessed using a one-day pretreatment regimen. Reciprocal cross-sensitization between cocaine and RU 24969 was evident in preweanling rats, whereas methamphetamine and RU 24969 did not cross-sensitize. When a one-trial pretreatment regimen was used, cross-sensitization was only detected when rats were pretreated with RU 24969 and tested with cocaine, but not the reverse. In sum, the present results show that the nonselective 5-HT_1A/1B receptor agonist RU 24969 cross-sensitizes with cocaine, but not methamphetamine, in preweanling rats. This dichotomy may be a function of cocaine having a greater affinity for the serotonin transporter than methamphetamine.
Comparing dopaminergic dynamics in the dorsolateral striatum between adolescent and adult rats: Effect of an acute dose of WIN55212-2
2019, Brain Research
During adolescence dopaminergic neurotransmission shows transient changes until reaching adulthood. The administration of CB1 agonists such as WIN55212-2 during adulthood increases dopamine extracellular levels. However, the effects of acute administration of cannabinoids on nigrostriatal dopamine neurotransmission during adolescence are not fully elucidated. The aim of this research is to compare dorsolateral striatum (DLS) dopamine (DA) dynamics and to study the effect of WIN55212-2 on DLS DA dynamics during adolescence and adulthood. No-net flux microdialysis experiments were carried out in adolescent (post-natal day 35–40) and young-adult (post-natal day 70–75) urethane-anesthetized rats. Basal DA dialysate, DA extraction fraction (Ed) and extracellular concentration of DA (C_ext) in DLS were assessed after an acute injection of WIN55212-2 (1.2 mg/kg) or vehicle. An increased basal DA dialysate and DA Ed were observed during adolescence compared to adulthood. Moreover, WIN55212-2 increases DLS DA C_ext rising basal DA dialysate in adulthood and decreasing DA Ed in adolescence. Our results suggest that an age-dependent mechanism underlies the effect of WIN 55212-2 on DA balance between release and uptake in DLS.
Early ontogeny of <inf>D</inf>-amphetamine-induced one-trial behavioral sensitization
2013, Pharmacology Biochemistry and Behavior
Citation Excerpt :
Therefore, cocaine increases extracellular neurotransmitter levels by blocking re-uptake of metabolically older DA from vesicular stores, whereas amphetamine-like compounds primarily release newly synthesized DA located in cytostolic pools (Kuczenski, 1983). McNamara et al. (1993) have hypothesized that the size and turnover rate of these DA pools (unbound cytosolic vs. vesicular) are important determinants affecting the induction and ultimate expression of behavioral sensitization (see Castañeda et al., 1988, for a more detailed discussion). On a related issue, DA release capacity increases from adolescence to adulthood, while the ratio of DA uptake to release declines (Walker and Kuhn, 2008).
The early ontogeny of _D-amphetamine-induced one-trial behavioral sensitization was characterized using male and female preweanling and preadolescent rats. In Experiment 1, rats were injected with saline or _D-amphetamine (1, 4, or 8 mg/kg) in activity chambers or the home cage on postnatal day (PD) 12, PD 16, PD 20, or PD 24. One day later, rats were challenged with either 0.5 or 2 mg/kg _D-amphetamine and distance traveled was measured in activity chambers for 120 min. In Experiment 2, saline or _D-amphetamine was administered in activity chambers on PD 24, while a challenge injection of _D-amphetamine (0.25–4 mg/kg) was given on PD 25. At younger ages (PD 13 and PD 17), a strong sensitized response was evident on the test day regardless of whether rats were pretreated with _D-amphetamine (4 or 8 mg/kg) before being placed in the activity chamber or 30 min after being returned to the home cage. Rats did not display _D-amphetamine-induced behavioral sensitization on PD 21, nor was context-dependent sensitization apparent on PD 25 even when a broad dose range of _D-amphetamine was used. When low doses of _D-amphetamine were administered on the pretreatment and test days (1 and 0.5 mg/kg, respectively), sensitized responding was not evident at any age. In summary, _D-amphetamine-induced one-trial behavioral sensitization was only apparent within a narrow developmental window during early ontogeny. This ontogenetic pattern of sensitized responding is similar to the one produced by methamphetamine and distinct from the pattern produced by cocaine. The unique sensitization profiles resulting from repeated _D-amphetamine and cocaine treatment may be a consequence of their different mechanisms of action.
Repeated treatment with the kappa opioid receptor agonist U69593 reverses enhanced K <sup>+</sup> induced dopamine release in the nucleus accumbens, but not the expression of locomotor sensitization in amphetamine-sensitized rats
2012, Neurochemistry International
Citation Excerpt :
Our microdialysis results show that basal dopamine extracellular levels in the NAc are normal after four days of abstinence in rats treated with amphetamine, indicating that amphetamine-induced locomotor sensitization is not associated with modifications in basal dopamine levels in the NAc. Supporting our observations, Castaneda et al., reported that basal levels of dopamine in the NAc are not altered after short or long periods of abstinence to amphetamine (Castaneda et al., 1988; Paulson and Robinson, 1995). More complex observations have been reported during cocaine abstinence.
The effects after the acute activation of the kappa opioid receptor (KOR) can be distinguished from the effect after repeated administration of KOR agonist. Here, we report the effect of repeated administration of U69593 during abstinence after amphetamine-induced locomotor sensitization. Rats were injected once daily with amphetamine for five consecutive days. From day 6 to 9, rats that developed locomotor sensitization, received once daily injection of U69593 or vehicle. On day 10, all rats were injected with a challenging dose of amphetamine and locomotor activity was measured to assess the expression of sensitization. Microdialysis studies were carried out to assess dopamine extracellular levels in NAc. Rats that develop and express horizontal locomotor sensitization to amphetamine show increased dopamine release in the NAc induced by high K⁺. The repeated treatment with U69593 reverses the sensitized depolarization-stimulated dopamine release in the NAc, but not the expression of locomotor sensitization induced by amphetamine. Thus, repeated activation of KORs during early amphetamine withdrawal dissociates the behavioral responses and the neurochemical responses that accompany the expression of sensitization to amphetamine.
Amphetamine-Induced Changes in Dendritic Morphology in Rat Forebrain Correspond to Associative Drug Conditioning Rather than Nonassociative Drug Sensitization
2009, Biological Psychiatry
Citation Excerpt :
The lack of effect in striatum following VTA AMPH exposure is consistent with the fact that this forebrain region is not an A10 DA neuron projection field and supports the integrity and anatomic specificity of the VTA microinjections made. Together with the locomotor sensitization results, these findings confirm and extend earlier reports showing that exposure to AMPH enhances its ability to produce locomotion and to release DA from DA terminals in forebrain (18,25,26). They also show that these effects are produced by either the IP or VTA route of AMPH exposure.
Systemic exposure to amphetamine (AMPH) leads to a number of long-lasting neuroadaptations including changes in dendritic morphology in rat forebrain. It remains unknown whether these changes relate to associative drug conditioning or to nonassociative drug sensitization, two forms of plasticity produced by systemic exposure to AMPH.
We compared the behavioral, neuronal, and morphologic consequences of exposing rats to intraperitoneal (IP) AMPH to those of exposure to AMPH applied to the ventral tegmental area (VTA), infusions that sensitize AMPH-induced locomotion and nucleus accumbens (NAcc) DA overflow but do not produce drug conditioning.
Both IP and VTA AMPH exposure sensitized locomotion and NAcc DA overflow, but only IP AMPH exposure produced conditioned locomotion. Importantly, whereas IP AMPH exposure increased spine density and dendritic length and branching in the NAcc, exposure to VTA AMPH produced the opposite effects. A similar differentiation of effects was observed in cortical areas.
Together these findings suggest that the morphological changes seen following IP AMPH exposure reflect associative drug conditioning rather than nonassociative drug sensitization. The decreases observed in the NAcc of VTA AMPH exposed rats may reflect the inability of these infusions to support conditioning.
The effect of exposure to drugs on the processing of natural rewards
2009, Neuroscience and Biobehavioral Reviews
Why does moderate exposure to a drug reward make natural rewards increasingly attractive to organisms, whereas prolonged exposure to the same drug reward has the opposite effect? The paradox behind that question remains unsatisfactorily captured by current theories of addiction. The incentive-sensitisation theory is viewed as a promising approach to this paradox, although it provides no mechanism to explain the decrease in interest of natural rewards as time exposure to a drug increases. To attempt to remedy this problem, I describe a model called the anticipatory dynamics model (ADM) that suggests a pivotal role of anticipation and attention in motivational interactions. In addition to relying on strong neuropsychopharmacological data, the ADM provides an original conception of motivational specificity. The ADM is an extension of the incentive-sensitisation theory that hypothesizes how drugs interact with natural rewards. It has not been tested empirically, although a possible experiment to test two predictions in the field of addiction is presented.

View all citing articles on Scopus

View full text

The long-term effects of repeated amphetamine treatment in vivo on amphetamine, KCl and electrical stimulation evoked striatal dopamine release in vitro

Abstract

Brain Res. Rev.

Neuropharmacology

Eur. J. Pharmacol.

Brain Res.

Pharmacol. Biochem. Behav.

Pharmacol. Biochem. Behav.

Pharmacol. Biochem. Behav.

J. Neurosci. Meth.

Neuropharmacology

Eur. J. Pharmacol.

Neuroscience

Neuroscience

Pharmacol. Biochem. Behav.

Eur. J. Pharmacol.

Appetite

Eur. J. Pharmacol.

Brain Res.

Life Sci.

Brain Res.

Pharmacol. Biochem. Behav.

Eur. J. Pharmacol.

Pharmacol. Biochem. Behav.

J. Neurosci. Meth.

Biochem. Pharmacol.

Amphetamine Psychosis

Am. J. Psychiatry