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J.E. Rose

Publications and source records attributed to J.E. Rose.

3 recordsLinked to original sources

Chronic nicotinic stimulation and blockade effects on working memory.

Acute and chronic nicotine treatment has been found to improve learning and memory function in a variety of tasks. In several studies we have found that chronic nicotine infusion improves working memory performance. Replicating these results, the current study showed that chronic nicotine treatment (12mg/kg/day) significantly improved working memory performance in the radial-arm maze. The nicotine effect did not diminish during the 2 weeks following withdrawal. The nicotine-induced improvement was eliminated when the nicotinic antagonist mecamylamine (3mg/kg/day) was given concurrently, suggesting that the nicotine effect was mediated via actions on the nicotinic receptor. Surprisingly, when this chronic dose of mecamylamine was given alone, it caused a transient improvement in choice accuracy during the first week of administration. This improvement subsequently became attenuated and was not evident at all by the third and fourth weeks of administration.

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Effects of spirometric administration of tobacco smoke containing varying amounts of nicotine on physiological measures and subject ratings.

A previously developed spirometric methodology of tobacco smoke administration was evaluated by determining the effects of varying nicotine delivery on various physiological and subjective measures. Eight male tobacco smoking subjects were administered 60cc volumes of tobacco smoke drawn from University of Kentucky research cigarettes, or air. Subjects were exposed to four bouts of smoke administration conducted over an 8h day. Each smoking bout was separated by 2h and involved 20 smoke administrations at the rate of one every 30sec. Each smoke administration consisted of 60cc of air or 60cc drawn from 0.3, 1.2 or 2.7mg nicotine yield cigarettes, followed by 1 liter of air which forced the smoke or air deep into the lungs. Carbon monoxide (CO), blood pressure, and heart rate were measured before and after each smoking bout, and subject ratings of smoke effects were completed after each smoking bout. In a separate study, blood samples were collected on two occasions before and after administration of the two highest nicotine yield cigarettes to determine changes in nicotine plasma levels. Data indicated that the spirometric method produced: (1) similar CO boosts across nicotine yields, and (2) changes in heart rate, blood pressure, subject ratings and plasma nicotine levels which were directly related to the nicotine yield of cigarettes.

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Anticholinergic sensitivity following chronic nicotine administration as measured by radial-arm maze performance in rats.

Chronic nicotine administration in rats has been previously found to improve choice accuracy performance of rats in the radial-arm maze. A nicotine-induced choice accuracy improvement was also seen in the current study. Rats were trained to asymptotic levels of choice accuracy performance on a working memory paradigm in an 8-arm radial maze. During and after 3 weeks of chronic nicotine treatment, rats were tested for sensitivity to acute doses of the nicotinic and muscarinic receptor antagonists, mecamylamine and scopolamine. During the first week of administration, nicotine-treated rats were supersensitive to the sedation caused by mecamylamine. This suggests that nicotine may not have been acting as a simple nicotinic agonist, since in this case, the opposite effect, an attenuated effect of mecamylamine in the nicotine-treated group, would have been expected. Three to 4 weeks after withdrawal from chronic nicotine administration, the treated rats were more sensitive to the choice accuracy deficits caused by the muscarinic blocker scopolamine (0.16 mg/kg) and the nicotinic blocker mecamylamine (10 mg/kg). This supersensitivity may have been due to a lasting change caused by chronic nicotine in the cholinergic bases of memory function.

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