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Featured researches published by David C. Jewett.


Journal of American College Health | 2005

Illicit Use of Prescribed Stimulant Medication Among College Students

Kristina M. Hall; Melissa M. Irwin; Krista A. Bowman; William Frankenberger; David C. Jewett

The authors investigated illicit use of stimulant medications at a midwestern university. They used a questionnaire to (a) examine the extent to which university students illicitly used stimulant medications prescribed for attention-deficit hyperactivity disorder; (b) determine why college students abused such drugs; and (c) identify the factors that predicted illicit use of prescribed stimulant medication. Findings revealed that 17% of 179 surveyed men and 11% of 202 women reported illicit use of prescribed stimulant medication. Forty-four percent of surveyed students stated that they knew students who used stimulant medication illicitly for both academic and recreational reasons. Students reported they experienced time pressures associated with college life and that stimulants were said to increase alertness and energy. Regression analysis revealed that the factor that predicted mens use was knowing where to get easily acquired stimulant medication, whereas the main predictor for women was whether another student had offered the prescribed stimulants.


Psychopharmacology | 1995

Effects of neuropeptide Y, insulin, 2-deoxyglucose, and food deprivation on food-motivated behavior

David C. Jewett; J. Cleary; Allen S. Levine; David W. Schaal; Travis Thompson

The current study demonstrates the ability of neuropeptide Y (NPY) to increase break points under a progressive ratio 1 (PR1) reinforcement schedule. An initial response resulted in delivery of a food reinforcer (45 mg pellet) under the PR1, and an additional response was required foreach successive reinforcer. The break point, the number of responses emitted to obtain the last reinforcer, is considered a measure of reinforcing efficacy or motivational strength of the food reinforcer. NPY (0.3–10 µg) significantly increased break point to levels comparable to those produced by 36–48 h of food deprivation. Although insulin (3–8 U/kg) and 2-deoxyglucose (150–250 mg/kg) also increased food intake, neither increased break points to levels produced by NPY or food deprivation. These data suggest that NPY may change the value of food in ways that cannot be accounted for by changes in insulin, glucose levels or intracellular glucoprivation. These results emphasize that simply measuring the amount of freely available food eaten is not a fully adequate measure of the strength of the feeding behavior.


Brain Research | 1991

The discriminative stimulus effects of neuropeptide Y

David C. Jewett; David W. Schaal; J. Cleary; Travis Thompson; Allen S. Levine

Neuropeptide Y (NPY), an endogenous peptide which strongly induces food intake, is demonstrated to have discriminative stimulus properties when administered intracerebroventricularly. Rats rapidly learned to press the appropriate lever during training. NPY discrimination was dose-dependent. NPYs discriminative stimulus properties were compared to those of two doses of Peptide YY (PYY) and 24 and 48 h of food deprivation, conditions which also increase feeding. Both doses of PYY generalized to NPY, supporting previous findings that PYY has effects similar to NPY. Although food deprivation increases feeding in a manner similar to NPY, food deprivation did not result in NPY-appropriate responding.


Peptides | 2004

Our journey with neuropeptide Y: effects on ingestive behaviors and energy expenditure.

Allen S. Levine; David C. Jewett; J. Cleary; Catherine M. Kotz; Charles J. Billington

Clark and colleagues first described the robust orexigenic effects of neuropeptide Y (NPY) in 1984. Our group as well as Stanley et al. confirmed these effects in the same year. During the next 20 years, we investigated the effects of NPY on diet preferences, opioid-related feeding, distributed neural feeding networks, energy metabolism, motivation and discriminative stimulus effects. These data together with data from other laboratories indicate that NPY increases feeding, even when rats work for food; that NPY decreases energy expenditure, particularly by altering thermogenesis; and that NPYs effects on energy metabolism are mediated by a widely distributed neural network involving other neuroregulators known to be involved in energy regulation.


Brain Research | 2001

The kappa-opioid antagonist GNTI reduces U50,488-, DAMGO-, and deprivation-induced feeding, but not butorphanol- and neuropeptide Y-induced feeding in rats

David C. Jewett; Martha K. Grace; Robert M. Jones; Charles J. Billington; Phillip S. Portoghese; Allen S. Levine

Antagonists selective for either kappa- [e.g. nor-binaltorphimine (nor-BNI)] and mu- (e.g. beta-funaltrexamine) opioid receptors have previously been shown to reduce both kappa- and mu-opioid-induced feeding. In the present studies, the anorectic effects of GNTI, a newly synthesized antagonist selective for kappa-opioid receptors, were studied in rats. GNTI (0.032-0.32 nmol; i.c.v.), administered 15 min prior to food access, reduced feeding induced by the kappa-opioid agonist U50,488 (producing a 70% maximal decrease), the mu-opioid agonist DAMGO (90% maximal decrease), and 24 h acute food deprivation (60% maximal decrease). GNTI did not reduce the orexigenic effects of butorphanol, an agonist that binds to both kappa- and mu-opioid receptors, and neuropeptide Y (NPY). Taken together, these results suggest that GNTI is a potent anorectic agent and opioid antagonist in rats. Like nor-BNI, GNTI reduced feeding induced by both kappa- and mu-opioid agonists. However, unlike nor-BNI, GNTI did not alter the orexigenic effects of butorphanol or NPY. Given the selectivity of GNTI and its effectiveness in several of the present experiments, its potency, and its short duration of action compared to nor-BNI, GNTI may serve to be a useful tool to study behavioral effects mediated by kappa-opioid receptors.


Brain Research | 2005

Chronic sucrose ingestion enhances mu-opioid discriminative stimulus effects

David C. Jewett; Martha K. Grace; Allen S. Levine

Sucrose affects a variety of opioid-related behaviors. We hypothesized that, if sucrose ingestion alters opioidergic circuitry, opioid-induced discriminative stimulus effects would be enhanced following sucrose intake. In the present study, rats were trained to discriminate nalbuphine (3.2 mg/kg, s.c.) from saline in an operant choice procedure. After acquiring the discrimination, subjects were injected with a single nalbuphine dose (0.1-3.2 mg/kg) and given 30-min access to 30% sucrose or water. Sucrose consumption did not alter nalbuphines discriminative stimulus effects under these conditions. During subsequent tests, training was suspended, and rats received continuous access to sucrose (9 days) or water (8 days). Chronic sucrose consumption increased the potency of nalbuphine to produce its discriminative stimulus effects by 3-fold. These findings suggest chronic sucrose consumption results in changes in opioid-system function that modulates the effects of exogenously administered opioids.


Brain Research | 1993

[Leu31,Pro34]neuropeptide Y (NPY), but not NPY 20-36, produces discriminative stimulus effects similar to NPY and induces food intake.

David C. Jewett; J. Cleary; David W. Schaal; Travis Thompson; Allen S. Levine

Rats were trained to discriminate between an intracerebroventricular injection of 1.15 nmol of Neuropeptide Y (NPY) and a sham injection. Rats rapidly learned to press the appropriate lever during training. NPYs discriminative stimulus effects were compared to those of saline, and 1.15-3.45 nmol [Leu31,Pro34]NPY, a Y1 receptor agonist and NPY 20-36, Y2 receptor agonist. [Leu31,Pro34]NPY resulted in NPY-appropriate responding, whereas saline and NPY 20-36 did not. [Leu31,Pro34]NPY also increased food intake, but NPY 20-36 did not. This suggests that NPYs discriminative stimulus and orexigenic effects involve the Y1, but not the Y2, receptor.


Behavior Analyst | 2004

A forgotten resource critical to the future of behavior analysis: Undergraduate psychology majors

Gregory J. Madden; Kevin P. Klatt; David C. Jewett; Larry A. Morse

The demand for board-certified applied behavior analysts is not being met, and there is a perception that fewer students are exposed to systematic courses in basic and applied behavior analysis than was true a generation ago. This article outlines how we have successfully implemented an undergraduate curriculum in behavior analysis within a traditional department of psychology. Certification credentials offered by the Behavior Analysis Certification Board facilitated the approval of this curriculum, and the cultural practice selection contingencies that supported the creation of our curriculum in behavior analysis may be similar at other comprehensive universities. Advice for developing an undergraduate program in behavior analysis within a psychology department is outlined. We also summarize strategies we have used to attract talented students to the courses and the significant impact these strategies have had on the number of our graduates who pursue graduate training in basic and applied behavior analysis. Attracting the best and brightest students to behavior analysis is critical to the future of the field.


Pharmacology, Biochemistry and Behavior | 1992

Effects of neuropeptide Y on food-reinforced behavior in satiated rats

David C. Jewett; J. Cleary; Allen S. Levine; David W. Schaal; Travis Thompson


Psychopharmacology | 2009

Effects of sibutramine and rimonabant in rats trained to discriminate between 22- and 2-h food deprivation

David C. Jewett; Thomas W. Hahn; Travis R. Smith; Britta L. Fiksdal; Jason M. Wiebelhaus; Andrew R. Dunbar; Catherine R. Filtz; Noah Novinska; Allen S. Levine

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J. Cleary

University of Minnesota

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Andrew R. Dunbar

University of Wisconsin–Eau Claire

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Breanna Pagel

University of Wisconsin–Eau Claire

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Britta L. Fiksdal

University of Wisconsin–Eau Claire

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