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Biomedical subjects

K Johannessen

Publications and source records attributed to K Johannessen.

At least 19 recordsLinked to original sources
PubMed2001

Preventing alcohol-related problems at the University of Arizona's homecoming: an environmental management case study.

In 1995, the University of Arizona installed and publicized new policies to provide better alcohol control during its annual homecoming event. Systematic observation at pregame tents revealed that, compared to 1994, these policies led to a lower percentage of tents selling alcohol, elimination of beer kegs, greater availability of food and nonalcoholic beverages, the presence of hired bartenders to serve alcohol, and systems for identification checks. These changes were still in evidence through 1998. In 1995, campus police also saw a downward shift in the number of neighborhood calls for complaints related to homecoming activities, which was maintained through 1998. Statistics on law enforcement actions were inconsistent. There was a sharp drop in 1995, but 1996 and 1998 saw enforcement levels similar to what was seen prior to the new policies. This case study underscores the importance of environmental management strategies for campus-based alcohol and other drug prevention.

Alcoholic Intoxication↗
PubMed2001

Challenging the collegiate rite of passage: a campus-wide social marketing media campaign to reduce binge drinking.

A social marketing media campaign, based on a normative social influence model and focused on normative messages regarding binge drinking, on a large, southwestern university campus has yielded positive preliminary results of an overall 29.2 percent decrease in binge drinking rates over a three-year period. The Core Alcohol and Drug Survey and the Health Enhancement Survey provided information on student knowledge, perceptions, and behaviors regarding alcohol and binge drinking. This study represents the first in-depth research on the impact of a media approach, based on a normative social influence model, to reduce binge drinking on a large university campus and has yielded promising initial results.

Adolescent↗
PubMed1994

Effect of local infusion of glutamate analogues into the nucleus accumbens of rats: an electrochemical and behavioural study.

In vivo voltammetry at electrochemically pretreated carbon fibre electrodes was used to investigate the effect of local infusion of glutamate analogues on dopamine (DA) release in rat nucleus accumbens. Infusion of a low dose of NMDA or AMPA (1 mM/0.2 microliter), but not L-glutamate or kainate, was followed a few minutes later by a large but short-lived increase in the extracellular concentration of DA. The involvement of spreading depression was indicated since this response could be repeated only after a short refractory period, and the response magnitude did not seem to be dependent on the dose infused. Furthermore, the increase in DA release was accompanied by a marked negative shift in brain field potential and a similar increase in release could be induced by local infusion of K+. The infusion of NMDA, AMPA or kainate was followed by behavioural activation of the animals but not convulsions. The behavioural response induced by NMDA was dose-dependently reduced by haloperidol, which suggests the involvement of a DA-dependent mechanism in this effect. Co-infusion of the DA transport inhibitors, nomifensine or GBR 12909, failed to alter the DA response to NMDA, while this response was completely blocked by co-infusion of tetrodotoxin or pretreatment with reserpine. It is evident from this study that local infusion of NMDA or AMPA may induce spreading depression in rat nucleus accumbens and that this condition is associated with a vast release of DA and behavioural activation.

Animals↗
PubMed1993

Effect of ageing on extracellular ascorbate concentration in rat brain.

In vivo voltammetry at electrochemically pretreated carbon fibre electrodes was used to investigate the effect of ageing on extracellular ascorbate (AA) concentration in the rat brain. Recordings from the nucleus accumbens in 3-, 6- and 18-month-old Sprague-Dawley rats revealed an age-related decrease in basal extracellular AA concentration. The mean AA current measured in 18-month-old rats was less than 10% of the current measured in 3-month-old rats. Systemic administration of ethanol (1.0 g/kg, i.p.) caused an increase in the AA signal measured in this area in all 3 age groups tested. However, the effect on AA was significantly less pronounced in 18-month-old rats. Further analysis of the AA signal revealed a gradual increase in AA release during terminal anoxia. Also in this case the effect on AA was significantly less pronounced in 18-month-old rats. This difference was also observed in the caudate putamen, another dopamine (DA) rich area in the brain. No significant difference in AA release was observed in the frontal cortex where the DA concentration is low. The increase in AA was followed by a pronounced increase in extracellular DA in the nucleus accumbens and caudate putamen. This release of DA was accompanied by a prompt reversal of the AA signal possibly explained by a DA-dependent autoxidation of AA. These results suggest a role for brain AA in the process of ageing.

Aging↗
PubMed1992

Rapid changes in ascorbate and dopamine release in rat nucleus accumbens after intracerebroventricular administration of NMDA.

In vivo voltammetry at electrochemically pretreated carbon fibre electrodes was used to investigate the effect of intracerebroventricular (i.c.v.) administration of N-methyl-D-aspartic acid (NMDA) on neuronal activity in rat nucleus accumbens. Infusion of a low dose of NMDA (1 nmol) was followed a few minutes later by rapid changes in both Peak 1 and Peak 2 heights indicating large but short-lived increases in the extracellular concentrations of ascorbate and catecholamines, respectively. These responses did not seem to be dependent on the dose infused since infusion of NMDA for a longer time period neither changed the amplitude nor the time-course of these effects. The increase in Peak 2 height was resistant to pargyline pretreatment indicating that this response mainly reflected the release of dopamine. The administration of NMDA was followed by behavioural activation in the animals but not convulsions. Co-administration of the competitive NMDA receptor antagonist, CPP (1 nmol), completely blocked these effects while the acetylcholine receptor antagonist, atropine (1.5 nmol), and the GABA receptor antagonist, picrotoxin (1 nmol), failed in this respect. The phenomenon spreading depression is discussed as a possible explanation of these results.

Animals↗
PubMed1992

Intracerebroventricular 5,7-DHT alters the in vitro function of rat cortical GABAA/benzodiazepine chloride ionophore receptor complexes.

We have earlier presented data indicating that the anxiolytic-like effect obtained in rats after depletion of brain 5-HT by means of PCPA or 5,7-DHT treatment is indirect and appears to involve the GABAA/benzodiazepine chloride ionophore receptor complex (GABAA/BDZ-RC), and that it is abolished by adrenalectomy. In the present series of experiments we have therefore investigated the 36Cl(-)-uptake in rat synaptoneurosomal preparations of central cortices from 5,7-DHT- and SHAM-lesioned animals. The GABA as well as the 3 alpha,5 alpha-tetrahydrodeoxycorticosterone (THDOC) induced picrotoxin-sensitive increase in 36Cl(-)-uptake was significantly lower than that observed in the SHAM-lesioned animals, indicating that the 5,7-DHT lesion has rendered the GABAA/BDZ-RC subsensitive to two of its tentative endogenous ligands. This effect of the 5,7-DHT lesion on the function on the GABAA/BDZ-RC was reversed by adrenalectomy, indicating that an intact adrenocortical function is required for the development of GABAA/BDZ-RC subsensitivity in 5,7-DHT-lesioned rats. A tentative conclusion of these findings is that the 5,7-DHT lesion induces an increase in release of GABA and/or barbiturate-like steroids and that this increase is reversed by adrenalectomy. The findings from these in vitro studies parallel those from our previous behavioral experiments and provide further support for the notion that a decreased serotonergic influence in the central nervous system may, possibly via the adrenocortical system, enhance the function of the GABAA/BDZ-RC.

5,7-Dihydroxytryptamine↗
PubMed1992

Surveying University of Arizona students' health.

The authors sampled more than 600 University of Arizona students to determine how student attitudes, beliefs, and practices should be considered by healthcare personnel in planning campus health education programs. The survey found that students worried more about diet, exercise, and weight than they did about more serious health problems and that, although generally positive and optimistic, the students frequently felt anxious and overwhelmed. Two thirds of the students were sexually active, 74% of those who were active used various contraceptive methods. More than three quarters of those surveyed indicated they currently drank alcoholic beverages; one quarter of the drinkers said they frequently downed three or more drinks on one occasion, and 44% of the drinkers reported driving while under the influence of alcohol.

Arizona↗
PubMed1991

Evidence for a role for dopamine in the diazepam locomotor stimulating effect.

It is well known that benzodiazepines produce dependence in humans and locomotor stimulation in experimental animals. In this study the possible involvement of catecholamines in the diazepam-induced locomotor stimulation in mice were investigated. Diazepam was found to have a biphasic effect; increasing locomotor activity at a low dose (0.25 mg/kg), while decreasing it at higher doses (greater than 0.5 mg/kg). The locomotor stimulating effect of diazepam was effectively blocked by pretreatment with the benzodiazepine receptor antagonist flumazenil, as well as with the catecholamine synthesis inhibitor alpha-methyltryrosine and the dopamine receptor antagonists haloperidol, spiperone and SCH 23390. Taken together, these data indicate that the locomotor stimulating effect observed after low doses of diazepam is due to activation of brain dopaminergic systems involved in locomotor activity. The observations are discussed in relation to the hypothesis that dependence-producing drugs activate specific brain reward systems.

Animals↗
PubMed1990

Effect of amperozide on the synthesis and turnover of monoamines in rat brain.

The effects of amperozide on the synthesis and the turnover of monoamines in different brain regions of the rat were determined using both ex vivo and in vivo biochemical techniques (i.e. post-mortem measurements of the tissue levels by HPLC-EC, and direct measurements with the in vivo voltammetry technique). It was found that amperozide slightly increased the DOPA accumulation and the DOPAC content in limbic brain areas but not in the striatum. The DOPA accumulation was also slightly increased in the noradrenaline rich cortical region indicating increased synthesis of noradrenaline. Furthermore, amperozide increased the utilization of noradrenaline after tyrosine hydroxylase inhibition by alpha-methyl-p-tyrosine. The synthesis of 5-HT was not significantly altered by amperozide. In conclusion, the biochemical data obtained in this study suggest that amperozide produces preferential effects on the mesolimbic dopaminergic system. In addition, amperozide also interacts with the noradrenergic system.

3,4-Dihydroxyphenylacetic Acid↗