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Biomedical subjects

M F Hawkins

Publications and source records attributed to M F Hawkins.

28 records · Page 2Linked to original sources

Aphagia in the rat following microinjection of neurotensin into the ventral tegmental area.

Neurotensin was microinjected into the lateral cerebral ventricle and the ventral tegmental area of rats which had been deprived of food for 18 hours. Both routes of administration resulted in a significant reduction of food intake compared to vehicle control injections. Additionally, the dose of neurotensin required to produce aphagia following ventral tegmental injection was substantially less than the dose required by the ventricular route. The results are discussed in relation to a possible site and mode of action for this neuropeptide.

Animals↗

Central nervous system neurotensin and feeding.

A variety of evidence indicates that neurotensin may be involved in the regulation of ingestive behavior. Cerebral ventricular injections of this peptide produced a dose-dependent decrease in the food intake of food-deprived rats. The duration of the aphagia was found to be approximately 90 minutes for the highest dose employed (100 micrograms). The possibility that tolerance might develop to the aphagic effect of neurotensin was investigated. No evidence of tolerance was found after 6 consecutive days of ventricular injection. In addition to ventricular injections, 2 possible central sites of action were examined: the ventromedial nucleus of the hypothalamus and the nucleus accumbens. While microinjections of neurotensin into the nucleus accumbens did not alter food intake, ventromedial hypothalamic administration resulted in a dose-related reduction in food intake. The results are discussed in relation to the possible role of central nervous system neurotensin in the control of feeding.

Animals↗

Synergistic effects of dopamine agonists and centrally administered neurotensin on feeding.

Several lines of evidence indicate that neurotensin may modulate the activity of dopamine systems in the central nervous system. The present study investigated the possibility that intraperitoneal injections of the dopamine agonists l-dopa and bromocriptine would alter the aphagia produced by central administration of neurotensin. It was found that neurotensin suppressed feeding in food-deprived rats when injected into the lateral ventricle or the ventromedial hypothalamus. Food intake was not affected, however, when the peptide was placed in the lateral hypothalamus. A dose-dependent aphagia was also observed following peripheral injections of l-dopa and bromocriptine. Additionally, the anorectic effect of centrally administered neurotensin was potentiated by concurrent administration of doses of l-dopa or bromocriptine which, when given alone, had no effect on food intake. The data suggest that neurotensin aphagia may be mediated by the peptide's ability to increase the activity of dopamine systems in the central nervous system.

Animals↗

Effects of centrally-administered bombesin and adrenalectomy on behavioral thermoregulation and locomotor activity.

Bombesin is an oligopeptide which has been implicated as a possible neurotransmitter or neuromodulator in the central nervous system. Central administration of the peptide produces physiological and behavioral responses which suggest a downward shift in the set point of body temperature. These include hypothermia, decreased metabolic rate and increased behavioral responding to escape from radiant heat. Contradictory data also exist. Therefore, a series of experiments was conducted to evaluate further the effects of the central administration of bombesin on behavioral thermoregulation and general locomotor activity. It was found that microinjections of bombesin into the preoptic area of the anterior hypothalamus increased the number of behavioral responses to radiant heat. The increased responding for heat-reinforcement and heat-escape suggested an activation of general locomotor activity. This was confirmed by the finding that centrally-administered bombesin increased the number of responses to escape from radiant heat without altering the duration of exposure to heat. Additionally, bombesin had no effect on the number of heat-escape responses following adrenalectomy. It was concluded that bombesin acts within the hypothalamus to increase general locomotor activity via the sympathetic outflow to the adrenals. This behavioral excitation is apparently expressed as an increase in responding to heat, or escape from heat, independent of thermoregulatory mechanisms. Therefore, the behavioral data do not indicate that bombesin decreases the set point of body temperature.

Adrenalectomy↗

The role of hyperdipsia in aggression following septal lesions in rats.

Lesions of the septum in animal subjects are known to produce an increase in aggressiveness and an increase in water intake. A series of experiments was carried out to examine the possibility that aggression was secondary to hyperdipsia. When rats with septal lesions were restricted to preoperative levels of water intake, aggression scores declined significantly. When animals without lesions were preloaded, with either water or saline, aggression increased. Neither decreased shock threshold nor increased cell hydration provided a full explanation for the results. It is suggested that the aversive nature of the stomach turgescence caused by increased water intake may be an additional mediating factor in septal aggression.

Aggression↗

Incoherence of neuroimaging studies of attention deficit/hyperactivity disorder.

Neuroimaging studies have been conducted with increasing frequency in recent years in attempts to identify structural and functional abnormalities in the brains of persons with attention deficit/hyperactivity disorder. Although the results of these studies are frequently cited in support of a biologic etiology for this disorder, inconsistencies among studies raise questions about the reliability of the findings. The present review shows that no specific abnormality in brain structure or function has been convincingly demonstrated by neuroimaging studies. Implications regarding stimulant treatment for attention deficit/hyperactivity disorder are discussed.

Animals↗