Cadmium exposure attenuates the initiation of behavioral sensitization to cocaine

Nation, Jack R.; Livermore, Christina L.; Bratton, Gerald R.

doi:10.1016/0006-8993(95)01060-2

Cited by 19 publications

(11 citation statements)

References 32 publications

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“…This pattern of antagonism parallels that observed with ethanol (e.g., Burkey et al 1994), as well as cocaine (e.g., Nation et al 1991Nation et al , 1995. The significance of the present findings derives jointly from the high probability of cadmium burdens stemming from the use of commercially available tobacco products (Piascik et al 1985;Yue 1992;Landsberger and Larson 1995;Wu et al 1995), and the realization that the behav-…”

Section: Referencessupporting

confidence: 73%

“…Employing an animal model, it has been shown that chronic low-level cadmium exposure diminishes the sensitivity to acute ethanol effects (Burkey et al 1994), thus stimulating an increase in the volitional intake of higher concentrations of ethanol (Nation et al 1987(Nation et al , 1989. Parallel antagonistic effects have been demonstrated in studies of intravascular cocaine self-administration (Nation et al 1996), in the effects of acute (Nation et al 1991) and repeated cocaine challenges on locomotor activity (Nation et al 1995), and on the rate-enhancing impact of cocaine on schedule-controlled responding (Burkey et al 1997).…”

Section: Introductionmentioning

confidence: 93%

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Chronic exposure to cadmium attenuates behavioral sensitization to morphine

1997

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The purpose of this investigation was to assess the impact of dietary cadmium on morphine-induced changes in locomotor activity. Adult male rats were exposed ad libitum to an adulterated food supply containing 100 ppm added cadmium chloride, or an identical diet containing no added cadmium, for 45 days prior to testing for the locomotor activating effects of successive daily morphine administration (0, 5, 10, or 20 mg/kg per session) on locomotor activity. On day 1 of testing, increasing doses of morphine produced a dose-related suppression of activity, and this sedative effect was greater in control than in cadmium-exposed animals. Repeated morphine administration resulted in tolerance to the sedative effects of the drug, and a systematic elevation of locomotor activity over the 14-day testing period was observed, with the augmentation (sensitization) effect more pronounced in control than cadmium-exposed animals. There was no indication that conditioning (context) events played a role in the effects observed here.

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Section: Referencessupporting

confidence: 73%

Section: Introductionmentioning

confidence: 93%

Chronic exposure to cadmium attenuates behavioral sensitization to morphine

1997

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“…injections of 0, 10, 20, and 40 mg/kg cocaine. This range of cocaine doses has been shown to be sufficient to characterize the complete dose-effect function produced by increasing doses of the drug (Nation et al 1995). Finally, as described in detail elsewhere , atomic absorption spectrophotometry procedures were used to determine blood lead concentrations in samples drawn from littermates as well as subjects sacrificed 24 hr after the final day of testing, Separate groups of animals that begin testing on PND 90 for sensitivity to the stimulatory effects of cocaine were tested precisely according to the procedures outlined for PND 30 testing.…”

Section: Methodsmentioning

confidence: 99%

Developmental Lead Exposure Alters the Stimulatory Properties of Cocaine at PND 30 and PND 90 in the Rat

Nation

Miller

Bratton

2000

Neuropsychopharmacology

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The aim of this study was to examine the effects of perinatal lead exposure on locomotor responding following acute and repeated cocaine challenges (sensitization).Lead poisoning continues to present major health concerns nationwide, and this situation is especially problematic among children. Recent sociodemographic data indicate the threat of lead toxicity is especially great among economically disadvantaged, nonwhite, and inner-city children (Goldman and Carra 1994;Pirkle et al. 1994). Along these lines, a 1999 report alarmingly places the "at risk" figure for children suffering from excessive lead exposure at around 70% in major metropolitan areas of the United States (cf., Mielke 1999).The sizable literature on developmental lead poisoning understandably has focused on global disturbances produced by early contaminant exposure that may have an enduring impact on the quality of life. In this sense, the data are compelling with respect to showing that even low-level lead exposure during development can occasion long-lasting neurobehavioral disturbances that compromise adult adaptive abilities and threaten stability. In this regard, functional deficits in cognitive and intellectual processing have been shown to persist well into the adult cycle of humans, rodents, and nonhuman primates (e.g., Bellinger et al. 1987). In addition, it seems that even emotional expression and attendant psychosocial phenomena may be influenced by lead ex- N EUROPSYCHOPHARMACOLOGY 2000 -VOL . 23 , NO . 4 Developmental Lead Exposure and Cocaine 445 posure during early development (Needleman et al. 1996).In the present report, our objective was to investigate interactive relations between developmental lead exposure and drug sensitivity later in the life cycle. This is an especially pertinent issue given that lead uniquely threatens sub-populations where drug abuse is more common, i.e., urban minorities . Clearly, experiential elements, availability, drug history, poverty, etc., must be considered in the list of dispositional factors that determine drug habits in humans. But it also must be considered that other types of environmental events may contribute to the abuse potential of selective drugs. That is, to the extent that lead or any other xenobiotic chemical alters the impact of a set delivery of a drug, motivational features related to drug seeking and taking may be redefined and therein influence maintenance responding and/or the effectiveness of certain pharmacotherapies for drug abuse (Mello et al. 1995).The development of behavioral sensitization during repeated administration of psychomotor stimulants is a well-characterized phenomenon which has received considerable attention because of its proposed relevance to drug addiction (Robinson and Berridge 1993;Wise and Bozarth 1987;Wolf et al. 1995) and psychosis (Post et al. 1992;Segal and Schuckit 1983). Therefore, the procedure was employed here in an effort to determine the effects of lead exposure during lactation and gestation on cocaine-induced changes in locomotor re...

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“…Furthermore, it must be emphasized that sensitization to cocaine and amphetamines is prevented not only by non-competitive antagonists such as MK-801 but also by other classes of NMDA receptor antagonists. These include competitive antagonists (Karler et al 1991(Karler et al , 1994Kalivas and Alesdatter 1993;Ohmori et al 1994;Haracz et al 1995;Wolf et al 1995), the glycine site partial agonist (+)-HA966 (Morrow et al 1995;Shoaib et al 1995;Khan and Shoaib 1996), and toxic metals such as cadmium and lead that interfere with NMDA transmission (Nation et al 1995(Nation et al , 1996. These agents have markedly different pharmacological and behavioral profiles.…”

Section: Repeated Coadministration Of Mk-801 With Amph: Emergence Of mentioning

confidence: 97%

Can the ”state-dependency" hypothesis explain prevention of amphetamine sensitization in rats by NMDA receptor antagonists?

Wolf

1999

Psychopharmacology

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Many laboratories have reported that coadministration of N-methyl-D-aspartate (NMDA) receptor antagonists with psychomotor stimulants prevents the development of behavioral sensitization and therefore concluded that NMDA receptor transmission is necessary for sensitization. According to an alternative "state-dependency" interpretation, NMDA receptor antagonists do not prevent sensitization. Rather, they become a conditioned stimulus for the sensitized response, i.e., it is only elicited in response to combined administration of the NMDA receptor antagonist and the stimulant. This hypothesis is supported by progressive augmentation of the locomotor response to the drug combination during the induction phase, and expression of sensitization when challenged with the combination but not the stimulant alone. To test this hypothesis, rats were treated during a 6-day induction phase with amphetamine (Amph) alone or in combination with the competitive NMDA receptor antagonist CGS 19755 (10 mg/kg) or the non-competitive NMDA receptor antagonist MK-801 (0.05, 0.1 and 0.25 mg/kg). When CGS 19755 was coadministered with Amph, there was no progressive augmentation of response to the drug combination. When challenged with Amph alone, rats did not exhibit the biphasic pattern of locomotor activity characteristic of Amph sensitization. No sensitization of stereotyped behaviors was evident, although the ambulatory response was greater than that exhibited by naive rats. Results with MK-801 were complex, but progressive augmentation of response to the drug combination appeared to in part reflect sensitization to MK-801 and could be dissociated from the ability of MK-801 to prevent the development of sensitization as assessed by response to challenge with Amph alone. Many of these findings are inconsistent with predictions of the "state-dependency" hypothesis. Moreover, the ability of NMDA receptor antagonists to prevent biochemical and electrophysiological correlates of sensitization is difficult to reconcile with the idea that sensitization develops in the presence of NMDA receptor blockade but cannot be expressed. Together, these findings suggest that the ability of NMDA receptor antagonists to prevent Amph sensitization reflects a requirement for NMDA receptor transmission during its induction.

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Cadmium exposure attenuates the initiation of behavioral sensitization to cocaine

Cited by 19 publications

References 32 publications

Chronic exposure to cadmium attenuates behavioral sensitization to morphine

Chronic exposure to cadmium attenuates behavioral sensitization to morphine

Developmental Lead Exposure Alters the Stimulatory Properties of Cocaine at PND 30 and PND 90 in the Rat

Can the ”state-dependency" hypothesis explain prevention of amphetamine sensitization in rats by NMDA receptor antagonists?

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