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Behavioral responses to osmotic upshift were characterized by temporal assays of free-swimming cells of Escherichia coli. Small osmotic upshifts (200 to 300 mosM) elicited tumble responses which were chemotaxis dependent, while large osmotic upshifts (400 to 500 mosM) elicited stopping followed by pseudotumbling which was chemotaxis independent.
Cardiovascular and behavioral responses induced by intravenous administration of the serotonin (5-HT)1A receptor agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), were studied in conscious normotensive rats either after a single administration, after repeated subcutaneous treatments (1 mg/kg daily for 3 days), or after chronic intravenous infusion (200 micrograms/kg per h for 72 h). In naive rats, a single intravenous treatment with 10, 30 or 100 micrograms/kg 8-OH-DPAT produced a blood pressure reduction of approximately 10% and a heart rate reduction of 15-20%. The duration of blood pressure and heart rate reduction was dose-dependent. Behavioral responses were observed (i.e. reciprocal forepaw treading, flat body posture, hind limb abduction and headweaving), the severity and duration of which were also dose-dependent. Subcutaneous pretreatment with 8-OH-DPAT greatly reduced the behavior responses but did not alter the hypotensive or the heart rate response to a single intravenous administration of 8-OH-DPAT. Blood pressure and behavior were not monitored during the subcutaneous pretreatment period. Intravenous infusion of 8-OH-DPAT attenuated both the cardiovascular and behavioral effects to post-infusion intravenous treatment. The differential tolerance development to these responses suggests that 8-OH-DPAT may exert its blood pressure response and its behavior response through two distinct mechanisms.
A method for measuring behavioral responses of rats to both anxiolytic and anxiogenic manipulations, the open field drink test (OFDT), is described. This method utilizes the concept that in the open field, appetitive behavior is reduced because of the ambient level of fear experienced in such an environment. For the OFDT, rats were given restricted access to water for 1 h per day for 3 days, and then their behavior was assessed in an open field that contained a water spout at its center. Use of the open field permitted a number of measures to be taken; of these, "time spent drinking" was most sensitive in detecting differences. Three experiments showed that the OFDT: a) permitted dissociation between behavioral responses to an anxiolytic (diazepam) and an anxiogenic (FG7142) drug, b) detected a dose-response relationship for an anxiolytic drug (diazepam), and c) detected behavioral responses to environmental manipulations designed to increase fear (presence of an olfactory cue from rats that had received foot shock). Advantages of this test over previously described methods are outlined, and several guidelines are provided to aid investigators in using this behavioral test.
Sex differences in responsiveness to infants were investigated by comparing physiological responses to infants with overt behavioral reactions. The former were assumed to be more biologically determined than the latter whereas overt behavioral responsiveness was presumed to be more affected by societal norms than were psychophysiological indices. The subjects were boys and girls in middle childhood and early adolescence. Psychophysiological indices showed that children, like parents, responded differentially to infant smiles and cries. As predicted, there were no sex differences on psychophysiological measures of responsiveness to babies. When permitted to interact with a baby, however, girls interacted more and ignored less than boys did. The results suggest that sex differences in overt responsiveness to babies are attributable to societal pressures rather than innate factors. Sex differences appear to wax and wane depending on the salience of sex stereotypy in differing developmental phases.
CRF in the central nervous system appears to have activating properties on behavior and to coordinate behavioral responses to stress. These behavioral effects of CRF appear to be independent of the pituitary-adrenal axis and can be reversed by a CRF antagonist, alpha-helical CRF9-41. The CRF antagonist reverses not only decreases in behavior associated with stress, but also increases in behavior associated with stress, thus suggesting that the role of CRF is stress dependent and not intrinsic to a given behavioral response. Further, microinjection of alpha-helical CRF9-41 and immunotargeting of CRF neurons in separate brain compartments reveal a link between the anatomical sites that contain CRF and the nature of the behavioral response to stress that can be modified by suppression of endogenous CRF activity therein. Hence, consistent with the dual role of other hypothalamic-releasing factors in integrating hormonal and neural mechanisms by acting both as secretagogues for anterior pituitary hormones and as extrapituitary peptide neurotransmitters, CRF may coordinate coping responses to stress at several bodily levels (Fig. 6). Moreover, dysfunction in such a fundamental homeostatic system may be the key to a variety of pathophysiological conditions including mental disorders.
A comparison was made in the behavioral responses of spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) normotensive rats to d-amphetamine. Animals were tested at a young age (6 weeks) to minimize the effects of elevated blood pressure on drug responsiveness. SHR rats were more active than WKY rats after injections of 1.0, 2.0, and 4.0 mg/kg d-amphetamine. A significant strain difference in stereotypy was also noted; rearing occurred in SHR rats while lateral or vertical head movements (head waving) occurred in WKY rats. The lack of significant strain differences in the behavioral responses of rats to apomorphine, a direct acting dopamine agonist, suggested that the differential behavioral responses to d-amphetamine were not a result of differences between strains in receptor sensitivity. Pretreatment of rats with reserpine eliminated the strain differences in behavioral responses to d-amphetamine. Pretreatment of rats with alpha-methyl-p-tyrosine prior to administration of d-amphetamine elminated the strain differences in stereotyped behavior; however, WKY rats remained less active than SHR rats. Pretreatment of SHR rats with parachlorophenylalanine had no effect on the behavioral responses to d-amphetamine. In contrast, pretreatment of WKY rats with parachlorophenylalanine resulted in an increase in rearing and a decrease in head waving following an injection of d-amphetamine. These findings suggest that the differences in responses to d-amphetamine of SHR and WKY rats are due in part to variations in the activities of central catecholaminergic and serotonergic neurons.
The effects of intracerebroventricular (i.c.v.) injections of mu- and delta-selective opioid agonists on the methamphetamine-induced behavioral alterations in the mouse were determined by using multi-dimensional behavioral analyses. Methamphetamine (1.0 mg/kg) produced a marked increase in linear locomotion, circling, rearing and grooming behavior. Although the mu-selective opioid agonist [D-Ala2,NMePhe4,Gly-ol]enkephalin (DAMGO) (0.003 and 0.01 microgram) itself did not significantly affect different behavioral responses, DAMGO (0.003 and/or 0.01 microgram) antagonized the methamphetamine (1.0 mg/kg)-induced increase in behavioral responses such as linear locomotion, circling, rearing and grooming. Additionally, the effects of DAMGO (0.01 microgram) on the methamphetamine (1.0 mg/kg)-induced behavioral responses were fully reversed by pretreatment with the mu-selective alkylating agent beta-funaltrexamine (beta-FNA) (5.0 micrograms). In contrast, the delta-selective opioid agonist [D-Pen2,L-Pen5]enkephalin (DPLPE) (0.3 or 1.0 microgram) had no marked effects on the methamphetamine (1.0 mg/kg)-induced behavioral responses. These results suggest that the stimulation of mu but not delta opioid receptors plays an inhibitory role in the methamphetamine-induced behavioral responses.
OBJECTIVE: To investigate at the individual practice level physician behavioral responses to the Medicare fee reductions mandated in the Omnibus Budget Reconciliation Act of 1989. Symmetric and nonsymmetric behavioral responses are modeled and investigated. DATA SOURCES: Volume index calculated from data in the Part B Medicare Annual Data (BMAD) Provider Files for 1989 and 1990. The pricing data are from the Procedure Files. STUDY DESIGN: A fixed-effects model in carrier and in specialty is employed. DATA COLLECTION: No direct data collection is required as BMAD files are used in the study. Price and volume variables are expressed as Fisher indexes of change. PRINCIPAL FINDINGS: The results show nonsymmetrical behavioral response because practices that did not face significant fee reductions do not exhibit behavioral change. By contrast, losers partially compensate for the fee reductions. For every dollar cut in their fees, physicians recoup approximately 40 cents by increasing volume. Loser behavioral responses vary by specialty. CONCLUSIONS: The presence of a volume response suggests that price control alone is not sufficient to cap rising healthcare costs. This indicates that additional or other tools must be considered if cost containment is to be attained.
We investigated behavioral responses to noxious cold and heat stimuli in mice. Similar to the hot-plate test, mice showed licking or jumping responses on a cold-plate (0 degrees C). The sensitivity to noxious heat (55 degrees C) was not correlated to the sensitivity to noxious cold, indicating that nociceptive processing of cold and heat are different. Behavioral responses to noxious cold are inhibited by systemic morphine or intrathecal administration of morphine. Lesion of the medial frontal cortex, including the anterior cingulate cortex, or selective activation of two types of opioid receptors in the anterior cingulate cortex produces dose-dependent antinociceptive effects on behavioral responses to noxious cold stimuli. These results suggest that activation of opioid receptors in the anterior cingulate cortex can produce powerful antinociception.
The functional significance of alterations in brain serotonin (5HT) associated with normal aging in both animals and humans is largely unknown. Using the effects of the 5HT agonist, m-chlorophenylpiperazine (m-CPP), as a measure of central serotonergic responsivity, we compared the behavioral and neuroendocrine responses of older normal volunteers (mean age +/- SD = 62.4 +/- 4.12) to those of younger normal volunteers (mean age +/- SD = 31.6 +/- 5.52). When m-CPP was administered intravenously, older subjects showed decreased behavioral responses but similar neuroendocrine responses, compared to younger subjects. The decreased behavioral responsivity was unrelated to pharmaco-kinetic differences between the groups, since m-CPP plasma levels were similar in both groups. This report is the first in vivo study in humans to demonstrate decreased behavioral responsivity with age following serotonergic stimulation, and may indicate a functionally less responsive 5HT subsystem in older subjects.
This study investigated the influence of age on the behavioral responses elicited by psychostimulants in male CD-1 mice. Behavioral activity including locomotion and stereotypy was measured following acute or repeated administration of cocaine, methylphenidate, amphetamine or saline to postweanling (24 days old), periadolescent (33 days old) and adult (60 days old) mice. Postweanling mice exhibited less total and ambulatory activity than periadolescent mice following a single acute injection of cocaine (20 or 30 and 30 mg/kg, respectively). Further, postweanling mice showed less total activity than both periadolescent and adult mice at a dose of 10 mg/kg methylphenidate. Less stereotypy was also seen in postweanling mice when compared to adolescent mice after 30 mg/kg amphetamine. Seven daily injections of cocaine resulted in a heightened behavioral response on day 7 as compared to day 1, indicative of behavioral sensitization in adult and periadolescent, but not postweanling mice. Repeated methylphenidate resulted in increased total activity in adult, but not periadolescent or postweanling mice. None of the animals were sensitized to the behavioral activating effects of amphetamine. The magnitude of behavioral response and the development of sensitization were dependent upon the age of the animal and the agent tested.
Toluene is a major component of numerous commercial organic solvent formulations. It is often listed among the chemicals capable of producing the organic solvent syndrome and a neurobehavioral hypersensitivity condition. The hypersensitivity condition (continued long-term intensification of some behavioral reactions in response to pharmacological or environmental stressors) is usually associated with the increased tonus of the functional dopaminergic system. The aim of our current research was to determine whether, under conditions of inhalation exposure, toluene can produce long-term behavioral changes or modify the intensity of the behavioral response to apomorphine, a dopaminergic receptor agonist. In our experiment, male rats were exposed to 25, 100 and 250 ppm toluene for 4 weeks (5 days/week, 6h/day). The following behaviors were tested: finding water in a radial maze; open field motor activity, acquiring the conditional response of passive avoidance; sensitivity to a thermal pain stimulus (hot plate test) and changes in this sensitivity caused by stress; and acquiring the conditional response of two-directional active avoidance. The behavioral response to apomorphine, i.e. the increased spontaneous locomotor activity, was assessed on day 10 after the termination of the exposure in the rotary drum test. In the behavioral experiment, significant differences between groups were recorded only for the hot plate test; in the 100 and 250 ppm rats, electric-shock-related anxiety response was stronger than in the control group. In the experiment using pharmacological provocation, the behavioral response to apomorphine in the rats exposed to 100 ppm or 250 ppm toluene was significantly lower. Our results indicate that low concentrations of toluene may produce long-term behavioral changes in rats. However, these changes seem to be linked with reduced rather than increased functional tonus of the dopaminergic system.
OBJECTIVES: Perceptions and associated behavioral responses to H5N1 avian influenza were investigated. METHODS: A random telephone survey interviewed 805 Hong Kong adults in November 2005. RESULTS: Of respondents, 37.9% believed that bird-to-human transmission had occurred somewhere in the last year (Hong Kong: 17.3%). Similar figures for human-to-human transmission were 16.8% (some locale) and 6.8% (Hong Kong). Many perceived bird-to-human H5N1 are transmittable via long-distance airborne transmission (35.8%), contaminated water sources (44%) and insect bites (48%). Corresponding figures for human-to-human H5N1 transmission were 47.9%, 47.3% and 48.9% respectively. In the last 3 months, 49.4% of the respondents exhibited one of the 4 studied behavioral responses; the variable was associated with unconfirmed beliefs that past-year human-to-human H5N1 transmission had occurred in Hong Kong (adjusted OR=2.08). Beliefs that human-to-human transmission had occurred somewhere were associated with the 4 individual behaviors studied (adjusted OR=1.58-4.24). Perceptions that human-to-human H5N1 should be transmittable via contaminated water sources was associated with avoidance of visiting hospitals and eating less poultry (adjusted OR=1.69 and 1.64). Belief about airborne transmission of human-to-human H5N1 was associated with perceived stress (adjusted OR=2.32). CONCLUSIONS: Widespread unconfirmed beliefs about status of HN51 epidemic are associated with the general public's behavioral responses. Timely dissemination of up-to-date information is greatly warranted.
Responsiveness (yes/no decisions) to sound has been found to be similar for normal infants and profoundly multihandicapped children of comparable developmental ages (Flexer & Gans, 1985). The purpose of this investigation is to extend the comparison of these two groups by examining the distribution of their response behaviors to sound. Ten normal and 10 multihandicapped children were videotaped while various auditory signals were presented. Without knowledge of stimulus type, five judges listed the behaviors that occurred during 24 sound and 24 catch trials for each child. The behaviors were then evaluated as a function of the stimulus parameters of meaningfulness, bandwidth, and intensity. Results revealed that the profoundly multihandicapped children displayed relatively more reflexive than attentive type behaviors and exhibited fewer behaviors per response. The effects of stimulus-type on the numbers and distribution of responses are discussed.
To define the molecular pathways modulating adrenal and behavioral responses to stress, we have generated mice with inactivation of hypothalamic neuropeptides and signaling pathways. Studies in mice deficient in corticotropin-releasing hormone (CRH) have revealed the essential role for CRH in adrenal glucocorticoid production in response to many physiological and psychological stressors. Immune system activation in CRH-deficient mice provides a unique exception to the necessity for CRH in stimulating adrenal glucocorticoid production. By analyzing mice deficient in interleukin-6 (IL-6) and CRH, we find that restoration of glucocorticoid output with inflammation is largely mediated by dysregulated IL-6 production. Current studies focus on identifying cellular and gene targets by which glucocorticoids regulate immune system function. In contrast to impaired adrenocortical responses to stress, CRH-deficient mice exhibit normal behavioral responses to stress. To determine signaling pathways that may contribute to the behavioral responses to stress, we have generated and analyzed mice deficient in adenylyl cyclase type 8 (AC8). AC8 deficient mice have intact adrenocortical responses to stress, but an inability to undergo stress-induced alterations in behavior.
BACKGROUND: A recent study showed that inhaled furosemide greatly improves experimentally induced dyspnea in humans. The objective of the current study is to test the hypothesis that inhaled furosemide suppresses the behavioral response to airway occlusion without changing the behavioral response to a somatic noxious stimulus in anesthetized animals. METHODS: In 10 spontaneously breathing cats anesthetized with isoflurane, anesthetic ED(50) was determined by measuring an end-tidal anesthetic concentration while observing escape behavior. The monitored behavior consisted of purposeful movement of the head and forearm after endotracheal tube occlusion. The duration from the start of airway occlusion to the onset of the positive response (DOCCL) was measured at the highest concentration of isoflurane permitting the positive motor response to airway occlusion before pretreatment. ED(50) values (minimum alveolar concentration) for the suppression of a somatic motor response to a noxious stimulus induced by toe pinch (toe-pinch ED(50)) were also determined. Then, the effects of inhaled furosemide or vehicle on the ED(50) for the suppression of the behavioral response to airway occlusion, DOCCL, and toe-pinch ED(50) were evaluated in a randomized, cross-over design. RESULTS: The ED(50) for the suppression of the behavioral response to airway occlusion significantly decreased (P < 0.01) and DOCCL was significantly prolonged (P < 0.01) after furosemide inhalation, whereas vehicle inhalation did not change these measurements. The decrease in ED(50) for the suppression of the behavioral response to airway occlusion after furosemide inhalation lasted 3 h. Furosemide inhalation did not affect the toe-pinch ED(50). CONCLUSION: Inhaled furosemide suppressed the behavioral response to airway occlusion in anesthetized animals without affecting the response to somatic noxious stimulus. The authors' animal model of respiratory distress may be applicable to the study of dyspnea in regard to its mechanism and treatment.
Long-term treatment of Parkinson's disease with dopamine-replacing agents such as L-3,4-dihydroxyphenylalanine (L-DOPA) is compromised by many side-effects, most notably involuntary movements, L-DOPA-induced dyskinesia. Acute challenge with dopamine-replacing drugs elicits a rotational response in the 6-hydroxydopamine (6-OHDA)-lesioned rat model of Parkinson's disease. This rotation is contraversive to the lesion and is considered to represent an antiparkinsonian effect. More recently, it has become clear that the rotational response shows plasticity and that repeated L-DOPA or apomorphine therapy is accompanied by a marked enhancement in this response. In this study, we demonstrate that the enhanced behavioral response to repeated dopamine-replacement therapy seen in the 6-OHDA-lesioned rat has pharmacological characteristics similar to L-DOPA-induced dyskinesia seen in MPTP-lesioned primates and man. Thus, the magnitude and rate of development of the enhanced response to L-DOPA treatment is related to both the number of doses and the size of the dose of L-DOPA administered. In contrast, de novo administration of dopaminergic drugs that are associated with a lower incidence of dyskinesia, e.g., bromocriptine or lisuride, does not lead to an enhanced behavioral response following repeated treatment. However, following a single "priming" administration of apomorphine, the rotational response elicited by subsequent bromocriptine administrations is enhanced with repeated treatment. Once established, the enhanced behavioral response to repeated L-DOPA-administration (6.5 mg/kg, twice daily) can, like L-DOPA-induced dyskinesia in man and MPTP-treated monkeys, be selectively reduced by coadministration of L-DOPA with the alpha2-adrenergic receptor antagonist yohimbine (10 mg/kg, -95%), the 5-HT uptake inhibitor 5-MDOT (2 mg/kg, -90%), or the beta-adrenergic receptor antagonist propranalol (10 mg/kg, -35%). While these rats do not exhibit symptoms of dyskinesia per se, this rodent model does exhibit behaviors, the underlying mechanism of which is likely to be similar to that underlying L-DOPA-induced dyskinesia and may prove useful in studying the molecular and cellular mechanisms of L-DOPA-induced dyskinesia in Parkinson's disease.
RATIONALE: Most lifelong drug addiction in humans originates during adolescence. Important structural and functional changes in the brain occur during adolescence, but there has been little direct study of how this impacts on drug abuse vulnerability. An emerging literature suggests that adolescents exhibit different behavioral responses to single doses of several addictive drugs, including ethanol, amphetamine, and cocaine. However, few studies have explored behavioral responses to the repeated dosing that is characteristic of human abuse of these substances. OBJECTIVES: We have investigated age-related behavioral responses to acute "binge" cocaine treatment between adults and adolescents. RESULTS: Adolescent rats displayed an exaggerated behavioral response to cocaine administered in two different binge patterns. Total locomotion after cocaine administration was the same in adolescents and adults. However, adolescent rats engaged in more intense stereotypic behaviors, including paw treading, head weaving, and focused sniffing than adult rats. These differences were observable following a modest dose of cocaine and became more robust following subsequent doses within a binge. Cocaine [corrected] brain levels were not significantly different between age groups during any of the exposure sessions. CONCLUSIONS: These findings suggest that equivalent tissue concentrations of cocaine produce a greater behavioral response in young rats, and that adolescent animals display an apparent form of intrabinge sensitization.