Effects of a cold environment or age on methamphetamine-induced dopamine release in the caudate putamen of female rats

Bowyer, John F.; Gough, B.; Slikker, William; Lipe, George W.; Newport, Glenn D.; Holson, R.Robert

doi:10.1016/0091-3057(93)90284-z

Cited by 100 publications

(67 citation statements)

References 25 publications

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“…A progressive decline in caudate DA response has also been reported after successive injections of lower doses of both AMPH (Segal and Kuczenski, 1997b) and METH (Nash and Yamamoto, 1992;Bowyer et al, 1993;Segal and Kuczenski, 1997b; but see Weihmuller et al, 1992), and it seems likely that the prolonged AMPH-induced release of DA could result in a decrease in the availability of relevant transmitter pools. In fact, we showed previously that CP tissue levels of DA were decreased by ϳ20% at the fourth injection of an 8.0 mg /kg run.…”

Section: Discussionmentioning

confidence: 98%

An Escalating Dose/Multiple High-Dose Binge Pattern of Amphetamine Administration Results in Differential Changes in the Extracellular Dopamine Response Profiles in Caudate-Putamen and Nucleus Accumbens

Kuczenski

Segal

1997

J. Neurosci.

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Amphetamine (AMPH)-induced psychosis is most frequently associated with a chronic high-dose "binge" or "run" pattern of stimulant abuse, generally preceded by a period of gradually escalating doses of the drug. We showed previously that animals subjected to such a regimen of AMPH administration developed, over multiple daily binges, a unique pattern of behavioral response that included a decrease in stereotypy and a pronounced increase in locomotion. Because of the involvement of mesolimbic and mesostriatal dopamine (DA) pathways in locomotion and stereotypy, respectively, we hypothesized that a persistent shift in the relative magnitude of caudateputamen (CP) and nucleus accumbens (NAC) DA transmission may contribute to this altered behavioral profile. To test this hypothesis, we examined CP and NAC extracellular DA in response to multiple high-dose AMPH binges. Our results revealed that with multiple binges the CP DA response but not the NAC response developed a profound tolerance/tachyphylaxis to the drug-induced increase in extracellular transmitter. These differential regional response alterations seem to correspond to the shift in the relative expression of stereotypy and locomotion. We hypothesize that changes in DA synthesis, perhaps mediated by regionally specific adaptations in DA autoreceptor function, contribute to the differential extracellular transmitter response profiles, and suggest that these neurochemical changes may have important implications for the mechanisms underlying the addictive and psychotogenic properties of AMPH.

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Section: Discussionmentioning

confidence: 98%

An Escalating Dose/Multiple High-Dose Binge Pattern of Amphetamine Administration Results in Differential Changes in the Extracellular Dopamine Response Profiles in Caudate-Putamen and Nucleus Accumbens

Kuczenski

Segal

1997

J. Neurosci.

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“…Interestingly, both of these manipulations have been demonstrated previously to prevent the persistent DA deficits caused by METH treatment (Wagner et al, 1983;Schmidt et al, 1985;Axt et al, 1990;Bowyer et al, 1992;Bowyer et al, 1993;Albers and Sonsalla, 1995;Giovanni et al, 1995), presumably because both contribute to ROS or reactive nitrogen species formation (Cubells et al, 1994;Giovanni et al, 1995;Fleckenstein et al, 1997b;Yamamoto and Zhu, 1998; Figure 7. ␣MT pretreatment prevented the METH-induced higher molecular weight DAT complex formation ( A) although hyperthermia was maintained ( B).…”

Section: Discussionmentioning

confidence: 99%

Methamphetamine Increases Dopamine Transporter Higher Molecular Weight Complex Formation via a Dopamine- and Hyperthermia-Associated Mechanism

Baucum¹,

Rau²,

Riddle³

et al. 2004

J. Neurosci.

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Multiple high-dose administrations of methamphetamine (METH) both rapidly (within hours) decrease plasmalemmal dopamine (DA) uptake and cause long-term deficits in DA transporter (DAT) levels and other dopaminergic parameters persisting weeks to months in rat striatum. In contrast, either a single administration of METH or multiple administrations of methylenedioxymethamphetamine (MDMA) cause less of an acute reduction in DA uptake and little or no persistent dopaminergic deficits. The long-term dopaminergic deficits caused by METH have been suggested, in part, to involve the DAT. Hence, this study assessed the impact of METH and MDMA administration on the DAT protein per se. Results revealed that multiple administrations of METH promoted formation of higher molecular weight (Ͼ170 kDa) DAT-associated protein complexes 24 -48 hr after treatment. This increase was attenuated by either preventing hyperthermia or pretreatment with the tyrosine hydroxylase inhibitor ␣-methyl-p-tyrosine; notably, each of these manipulations has also been demonstrated previously to prevent the persistent deficits in dopaminergic function caused by METH treatment. In contrast, either a single injection of METH or multiple injections of MDMA caused little or no formation of these DAT complexes. The addition of the reducing agent ␤-mercaptoethanol to samples prepared from METH-treated rats diminished the intensity of these complexes. Taken together, these data are the first to demonstrate higher molecular weight DAT complex formation in vivo and that such formation can be altered by both pharmacological and physiological manipulations. The implications of this phenomenon with regard to the neurotoxic potential of these stimulants are discussed.

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“…This is particularly important with respect to the toxic effects of stimulant drugs such as METH. These effects are temperature dependent (Bowyer et al, 1993(Bowyer et al, , 1994Miller and O'Callaghan, 1994;Alberts and Sonsalla, 1995;Farfel and Seiden, 1995;Ali et al, 1996;Davidson et al, 2001), and a wide range of conditions can influence brain as well as core temperature. In the present case, administration of the drug at 9 mg/kg during a social interaction was often sufficient to bring brain temperature close to its biological limit, resulting in the death of one of our animals.…”

Section: High-activity State Exacerbates Meth-induced Hyperthermiamentioning

confidence: 99%

“…The format is the same as described for Figure 1. ANOVA values for temperature elevation are as follows: for Saline-1, F (25,155) ϭ 18.47, 17.04, 20.11, respectively, for the NAcc, muscle, and hippocampus (Hippo); for 1 mg/kg METH, F (32,197) temperature-sensitive toxicity of monoamine terminals (Bowyer et al, 1993(Bowyer et al, , 1994.…”

Section: Meth Induces Pathological Metabolic Neural Activation and Hymentioning

confidence: 99%

“…METH is also known to cause hyperthermia both in humans (Kalant and Kalant, 1975) and rodents (Sandoval et al, 2000), which appears to contribute to METH-induced neurotoxicity and mortality. Hyperthermia potentiates dopamine and tyrosine-hydroxylase depletion and astrocytosis and also exacerbates oxidative stress (Omar et al, 1987;Lin et al, 1991), whereas hypothermia protects against these effects (Bowyer et al, 1993(Bowyer et al, , 1994Miller and O'Callaghan, 1994).…”

Section: Introductionmentioning

confidence: 99%

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Brain Hyperthermia Is Induced by Methamphetamine and Exacerbated by Social Interaction

2003

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Hyperthermia is a symptom of methamphetamine (METH) intoxication and a factor implicated in neurotoxicity during chronic METH use. To characterize the thermic response to METH, it was injected once daily into rats at increasing doses (0, 1, 3, and 9 mg/kg, s.c.) while brain [nucleus accumbens (NAcc), hippocampus] and body (deep temporal muscle) temperatures were continuously monitored. METH produced dose-dependent hyperthermia, with brain structures (especially the NAcc) showing a more rapid and pronounced temperature increase than the muscle. At the highest dose, brain and body temperatures increased 3.5-4.0°C above basal levels and remained elevated for 3-5 hr. Stressful and other high-activity situations such as interaction with a conspecific female are also known to induce a significant hyperthermic response in the rat. A combination of social interaction and METH administration was tested for additive effects. Male rats were exposed daily to a conspecific female for a total of 120 min, and METH was injected at the same doses 30 min after the initial contact with the female. An initial hyperthermic response (ϳ1.5°C) to social interaction was followed by a large and prolonged hyperthermic response (3.5-5.0°C, 5-7 hr at 9 mg/kg) to METH, which was again stronger in brain structures (especially in the NAcc) than in the muscle. Although the combined effect of the hyperthermic events was not additive, METH administration during social interaction produced stronger and longer-lasting increases in brain and body temperature than that induced by drug alone, heating the brain in some animals near its biological limit (Ͼ41°C).

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Effects of a cold environment or age on methamphetamine-induced dopamine release in the caudate putamen of female rats

Cited by 100 publications

References 25 publications

An Escalating Dose/Multiple High-Dose Binge Pattern of Amphetamine Administration Results in Differential Changes in the Extracellular Dopamine Response Profiles in Caudate-Putamen and Nucleus Accumbens

An Escalating Dose/Multiple High-Dose Binge Pattern of Amphetamine Administration Results in Differential Changes in the Extracellular Dopamine Response Profiles in Caudate-Putamen and Nucleus Accumbens

Methamphetamine Increases Dopamine Transporter Higher Molecular Weight Complex Formation via a Dopamine- and Hyperthermia-Associated Mechanism

Brain Hyperthermia Is Induced by Methamphetamine and Exacerbated by Social Interaction

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