Cadmium exposure results in decreased responsiveness to ethanol

Nation, Jack R.; Wellman, Paul J.; Stultz, Jeannine Von; Taylor, Betty; Clark, Donald R.; Bratton, Gerald R.

doi:10.1016/0741-8329(88)90003-1

Cited by 12 publications

(5 citation statements)

References 18 publications

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“…Lower dopamine levels may translate into a functionally lower dose of a set ethanol delivery (drug attenuation), yet stimulate voluntary consumption, in a manner similar to that observed with the genetic and lesion models (see above). Prima facie, this rationale is consistent with previous cadmium–ethanol findings from the laboratory (Grover et al, 1991; Nation et al, 1987, 1988), but more direct challenges to the mesolimbic dopamine system of cadmium-treated animals are needed before confident assertions are possible.…”

Section: Discussionsupporting

confidence: 78%

“…Evidence of cadmium-based disturbances in transmitter processes has stimulated interest in other areas in which such chemical events play a regulatory role. In the laboratory, issues relating to the interaction of cadmium and psychoactive drugs such as ethanol (e.g., Nation et al, 1987Nation et al, , 1988Nation, Frye, Von Stultz, & Bratton, 1989;Nation, Horger, Pugh, Bratton, & Rowe, 1990) and cocaine (Nation et al, 1991) have been a central concern. With regard to the effects of cotreatment with cadmium and ethanol, chronic exposure to inorganic cadmium stimulates increased volitional intake of a nonpreferred ethanol solution (Nation et al, 1987;Nation, Pugh, Von Stultz, Bratton, & Clark, 1989) but attenuates responsiveness to acute applications of the drug.…”

mentioning

confidence: 99%

“…With regard to the effects of cotreatment with cadmium and ethanol, chronic exposure to inorganic cadmium stimulates increased volitional intake of a nonpreferred ethanol solution (Nation et al, 1987; Nation, Pugh, Von Stultz, Bratton, & Clark, 1989) but attenuates responsiveness to acute applications of the drug. For example, cadmium-burdened animals exhibit a hyposensitivity to ethanol in studies in which a hypnotic dose of the drug is administered (Nation et al, 1988), in tests of ethanol's hypoalgesic effects (Burkey, Nation, Grover, & Bratton, 1993), and in ethanol self-administration paradigms in which animals lever press for ethanol reinforcement (Grover et al, 1991). There is current speculation that these effects may derive from toxicant-related antagonism of the pharmacologic action of ethanol (Burkey et al, 1993).…”

mentioning

confidence: 99%

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Effects of cadmium contamination on ethanol-induced changes in locomotor activity and rota-rod performance.

Nation¹,

Burkey²,

Bratton³

1995

Experimental and Clinical Psychopharmacology

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Twelve rats exposed to water containing 100 ppm cadmium and 12 control rats received intraperitoneal injections of 0.5, 1.0, and 1.5 g/kg ethanol prior to activity testing. Eleven rats exposed to cadmium and 11 control rats received comparable injections of saline prior to activity testing. In addition, all rats were tested on a rota-rod task. Activity results showed that parallel behavioral decreases occurred for cadmium-treated and control subjects. However, cadmium attenuated ethanol-induced impairment of rota-rod performance. These data indicate that the external chemical environment may alter drug responsiveness.Editor's Note. Because of unexpected delays with the editor's office, the publication of this article was postponed beyond its originally scheduled issue. The editor apologizes for the delay.-CRS

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Section: Discussionsupporting

confidence: 78%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Effects of cadmium contamination on ethanol-induced changes in locomotor activity and rota-rod performance.

Nation¹,

Burkey²,

Bratton³

1995

Experimental and Clinical Psychopharmacology

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“…Twenty-four hr after the final day of testing, animals were rendered unconscious with 60 mg/kg sodium pentobarbital (IP), and 3-5 ml blood samples were drawn via cardiac puncture. Cadmium tissue residues in blood were then measured via dry ashing and atomic absorption spectrophotometry as described in detail previously (Nation et al, 1988).…”

Section: Cadmium Residues In Bloodmentioning

confidence: 99%

Chronic cadmium exposure alters cocaine self-administration in adult male rats.

Nation¹,

Livermore²,

Bratton³

et al. 1996

Experimental and Clinical Psychopharmacology

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Adult male rats (Rattus norvegicus) were exposed to a water supply in the home cage containing 100 ppm cadmium chloride and sodium saccharin (.65% wt/vol; cadmium group) or water containing only the saccharin amendment (group control). On Day 65 of exposure, animals from each group received jugular catheter implants and were subsequently trained over the course of 15 daily 2-hr sessions to self-administer a .25 mg/kg/infusion of cocaine HC1 under a fixed-ratio 1 schedule. Immediately following acquisition training, the full dose-effect function was determined for all animals by using cocaine doses of .03, .06, .125, .25, .50, and 1.0 mg/kg. Cadmium-exposed animals executed more active (cocaine) lever responses during acquisition training but were not different from controls in depressing a pharmacologically inactive lever. For dose-effect testing, cadmiumexposed animals exhibited greater self-administration than controls at the higher doses of cocaine, and there was evidence that the cocaine dose that produced maximum responding was higher in cadmium-exposed than control animals.The pathologic consequences of recurrent exposure to metallic pollutants have been a research priority in toxicology for many years (see Klaassen, 1990, for a review). Within this investigatory framework, attempts to document human health risks attendant to repeated contact with cadmium have accelerated. The increasing interest in cadmium stems partly from the expanding literature on the links between the toxicant and the use of tobacco. Cadmium selectively accrues in tobacco leaves and is present in all commercial tobacco products (Landsberger & Larson, 1995;Piascik, Champney, Kasarskis, & Forrester, 1985;Yue 1992). Consequently, it is not surprising that cigarette smokers suffer greater body burdens of cadmium than nonsmokers (e.g., Klaassen, 1990;Piascik et al., 1985;Wolfsperger, Hauser, Gossler, & Schlagenhaufen, 1994), to an extent that individuals smoking 10-20 cigarettes or more per day have more than double the levels of blood cadmium as compared with the nonsmoking population (Maranelli, Apostoli, & Ferrari, 1990). Even filtering the tobacco smoke confers no protection, as it has been shown that unlike other heavy metals, cadmium is not prominently retained in the filter (Kalcher, Kern, & Pietsch, 1993).Included in the list of health concerns associated with cadmium toxicity are the effects of the contaminant on drugs that possess abuse liability. Using an animal model, it has been shown that chronic low-level exposure to cadmium results in

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“…Elsewhere, it has been shown that cadmium exposure causes an increase in ethanol intake but does not increase intake of a sucrose–quinine solution equated for caloric value and palatability (Nation, Pugh, Von Stultz, Bratton, & Clark, 1989). Apart from issues relating to drug self-administration, the hypnotic properties of a 3.5 g/kg intraperitoneal administration of ethanol are attenuated by cadmium exposure (Nation et al, 1988).…”

mentioning

confidence: 99%

Effects of cadmium on cocaine-induced changes in activity.

Nation¹,

Grover²,

Salinas³

et al. 1991

Behavioral Neuroscience

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Adult male rats were exposed to a diet that contained 100 parts per million added cadmium or a control diet for 72 days before being tested in a Digiscan activity monitor. During the 1-hr test period, each animal's baseline activity levels were recorded for 20 min. Animals then received intraperitoneal injections of 0, 10, 20, or 40 mg/kg cocaine HCl, and their activity levels were recorded for the remaining 40 min of the test session. The results showed that the 10, 20, and 40 mg/kg doses of cocaine produced behavioral activation in the control-diet animals. For cadmium-treated animals, cocaine-induced behavioral changes at the 10 mg/kg dose were not observed, but increased activity was evident at the two higher doses.

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Cadmium exposure results in decreased responsiveness to ethanol

Cited by 12 publications

References 18 publications

Effects of cadmium contamination on ethanol-induced changes in locomotor activity and rota-rod performance.

Effects of cadmium contamination on ethanol-induced changes in locomotor activity and rota-rod performance.

Chronic cadmium exposure alters cocaine self-administration in adult male rats.

Effects of cadmium on cocaine-induced changes in activity.

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