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   <subfield code="a">Dextrorphan effects on cocaine and brainstem perturbation</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[M. Lundien, O. Andy, R. Rockhold, M. Andrews, C. Dearman]</subfield>
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   <subfield code="a">Dextrorphan is a noncompetitive blocker of N-methyl-D-aspartate (NMDA) receptors. Since NMDA blockers are known to reduce the locomotor stimulatory and toxic effects of cocaine, it was speculated that dextrorphan would attenuate cocaine-induced behavioral excitatory motor activity associated with and without mechanical perturbation of the brainstem. Technique: Motor activity was recorded following dextrorphan and/or cocaine challenge in 25 SHR rats. Ten were naive subjects. Mini-osmotic pumps delivering cocaine (2.5 mg/0.49 ul/hr) were placed in 15 subjects, and infusion was halted after the third infusion day. On the fifth day either a dextrorphan (25 mg/kg, subcutaneous) or a dextrorphan and cocaine (40 mg/kg, intraperitoneal) challenge was done. Ten rats had bipolar electrode implants in the bilateral brainstem. Five were treated with DC current lesions in each of 12 days over a 3-week period. The effects of brainstem lesions on escape behavior were also evaluated in those five subjects. Results: In the naive subjects, dextrorphan reduced motor activity (P=.0001), whereas combined cocaine and dextrorphan increased motor activity (P=0.04). In lesioned subjects, dextrorphan decreased motor activity (P=0.0001). In electrode implant subjects, combined dextrorphan and cocaine challenge decreased the motor activity (P=0.04). Hyperactivity in the electrode implant group was greater than in the lesioned subjects. Midbrain electrolytic lesions attenuated escape behavior. A variety of behaviors were produced by brainstem lesions. Conclusions: Dextrorphan and brainstem lesions reduced motor hyperactivity and escape behavior. In electrode implant subjects dextrorphan counteracted the expected cocaine excitatory motor effects. Dextrorphan did not activate nor facilitate seizures.</subfield>
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   <subfield code="a">Transaction Publishers, 1996</subfield>
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   <subfield code="a">dextrorphan</subfield>
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   <subfield code="a">Lundien</subfield>
   <subfield code="D">M.</subfield>
   <subfield code="u">Depts. of Neurosurgery, Pharmacology and Toxicology and Preventive Med., U. of Mississippi Med. Center, Jackson, MS</subfield>
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   <subfield code="a">Andy</subfield>
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   <subfield code="u">Depts. of Neurosurgery, Pharmacology and Toxicology and Preventive Med., U. of Mississippi Med. Center, Jackson, MS</subfield>
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   <subfield code="t">Integrative Physiological and Behavioral Science</subfield>
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