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At least 739 records · Page 41Linked to original sources
PubMed1992

Behavioral effects of A71623, a highly selective CCK-A agonist tetrapeptide.

We studied the behavioral effects of a novel cholecystokinin tetrapeptide (CCK-4) analogue, A71623, with full agonist activity and high affinity and selectivity for the CCK-A receptor subtype relative to the CCK-B receptor. In tests for anorectic activity, A71623 was found to suppress 60-min intakes of a liquid diet in both deprived and sated rats, and the effects were blocked by a selective CCK-A antagonist, A70104. Compared with CCK-8, A71623 was found to have improved potency and duration of action; the most potent route of administration was intraperitoneal. A71623 also suppressed the intake of a liquid diet and a 0.2 M sucrose solution in lean and obese Zucker rats. In daily injection studies, the anorectic activity of CCK-8 diminished rapidly, whereas the suppressant effects of A71623 on food intakes and body weight gains persisted throughout the 11-day treatment period. Finally, A71623 reduced the spontaneous locomotor activity of rats at doses above those required to suppress intakes. These studies are the first to describe the behavioral effects of a potent and highly selective CCK-A receptor agonist.

Animals↗
PubMed1997

Effects of xanomeline, a selective muscarinic receptor agonist, on cognitive function and behavioral symptoms in Alzheimer disease.

OBJECTIVE: To evaluate the therapeutic effects of selective cholinergic replacement with xanomeline tartrate, an m1 and m4 selective muscarinic receptor (mAChR) agonist in patients with probable Alzheimer disease (AD). DESIGN: A 6-month, randomized, double-blind, placebo-controlled, parallel-group trial followed by a 1-month, single-blind, placebo washout. SETTING: Outpatients at 17 centers in the United States and Canada. PARTICIPANTS: A total of 343 men and women at least 60 years of age with mild to moderate AD. INTERVENTIONS: Patients received 75, 150, or 225 mg (low, medium, and high doses) of xanomeline per day or placebo for 6 months. OUTCOME MEASURES: Scores on the cognitive subscale of the Alzheimer's Disease Assessment Scale (ADAS-Cog), the Clinician's Interview-Based Impression of Change (CIBIC+), the Alzheimer's Disease Symptomatology Scale (ADSS), and the Nurses' Observational Scale for Geriatric Patients (NOSGER). RESULTS: A significant treatment effect existed for ADAS-Cog (high dose vs placebo; P < or = .05), and CIBIC+ (high dose vs placebo; P < or = .02). Treatment Emergent Signs and Symptoms analysis of the ADSS, which assesses behavioral symptoms in patients with AD, disclosed significant (P < or = .002) dose-dependent reductions in vocal outbursts, suspiciousness, delusions, agitation, and hallucinations. On end-point analysis, NOSGER, which assesses memory, instrumental activities of daily living, self-care, mood, social behavior, and disturbing behavior in the elderly, also showed a significant dose-response relationship (P < or = .02). In the high-dose arm, 52% of patients discontinued treatment because of adverse events; dose-dependent adverse events were predominantly gastrointestinal in nature. Syncope, defined as loss of consciousness and muscle tone, occurred in 12.6% of patients in the high-dose group. CONCLUSIONS: The observed improvements in ADAS-Cog and CIBIC+ following treatment with xanomeline provide the first evidence, from a large-scale, placebo-controlled clinical trial, that a direct-acting muscarinic receptor agonist can improve cognitive function in patients with AD. Furthermore, the dramatic and favorable effects on disturbing behaviors in AD suggest a novel approach for treatment of noncognitive symptoms.

Alzheimer Disease↗
PubMed1989

Aggressive behaviors in adult rats deprived of playfighting experience as juveniles.

Matched litter mates were reared in one of three conditions: in pairs or in isolation with or without one hour of daily playfighting experience from 20 to 50 days of age. The rats were then regrouped within condition so that they lived with identically reared cagemates for a month. This regrouping eliminated the transient effects of isolation such as increased fearfulness. When tested as adults, there was no effect of early rearing condition on the probability of intraspecific aggression or muricide, although isolation-reared rats were less likely to retrieve the mice. However, isolation rearing reduced the latency to initiate shock-induced defensive aggression and increased both its frequency and intensity. Isolated animals which had been given daily playfighting during development did not show the effects of early social deprivation. The mechanisms through which playfighting experience shapes later defensive behavior remain to be determined.

Aggression↗
PubMed1993

Sex differences and the role of aromatization in the control of sexually dimorphic behavior and morphology in gray short-tailed opossums (Monodelphis domestica).

Sex differences in the activating effects of an aromatizable (testosterone, T) and a nonaromatizable (dihydrotestosterone, DHT) androgen on sexually dimorphic scent marking and aggressive behavior were examined in gonadectomized gray short-tailed opossums. When compared with males, females showed less chest, head, flank, and hip marking and more fighting behavior in tests with stimulus females and threat behavior in tests with stimulus males following receipt of subcutaneous T, DHT, or blank (B) implants. Testosterone but not DHT activated hip and head marking while both T and DHT activated flank marking. In tests with stimulus females, only males showed clicking vocalizations and T but not DHT or B stimulated clicking. Animals that received T had significantly larger suprasternal scent glands than those that received DHT or B. The significance of these findings is discussed with respect to the development of sex differences in behavior in eutherian mammals.

Aggression↗
PubMed1990

Neuroendocrine effects of benzodiazepines.

Benzodiazepine administration has been associated with alterations in neuroendocrine function both in experimental animals and in humans. Clinical and laboratory data indicate that the beta-carbolines, a class of active benzodiazepine receptor inverse agonists, cause behavioral and neuroendocrine changes characteristic of anxiety and stress. In contrast, the "classic" benzodiazepine receptor agonists such as diazepam can reduce anxiety and inhibit stress-induced increases in anterior pituitary hormone secretion. Although the site of action and mechanisms by which benzodiazepines alter anterior pituitary hormone secretion are still under investigation, evidence suggests that the effects are mediated in the brain, primarily through actions at benzodiazepine receptors in the hypothalamus. The benzodiazepines may act at GABA-coupled benzodiazepine receptors in the hypothalamus or other regions of the brain to potentiate the effects of endogenous GABA. It also is believed that brain monoamines may modulate the effects of endogenous GABA. Brain monoamines have also been reported to modulate the effects of benzodiazepines on stress-induced hypothalamic-pituitary-adrenocortical function. Direct effects of the benzodiazepines on central- and peripheral-type benzodiazepine receptors in the anterior pituitary have also been documented.

Animals↗
PubMed1977

Biochemical correlates in mouse-killing behavior of the rat: prolonged isolation and brain cholinergic function.

After 30 days of isolation, 45% of the rats exhibited mouse-killing behavior. The killing response was suppressed by atropine (5 mg/kg and 8 mg/kg, IP) and scopolamine (8 mg/kg, IP), whereas methylatropine was ineffective. Acetylcholine (ACh) content and acetylcholinesterase (AChE) activity were measured in 5 discrete areas of rat brain. As compared with the aggregated rats only the killer rats exhibited higher ACh levels in the diencephalon. The activity of AChE in all brain areas was unchanged by isolation; no significant difference was found between the killer and nonkiller rats. These results suggest that central cholinergic mechanisms participate in the mediation of mouse-killing behavior in the rat.

Acetylcholine↗
PubMed2002

Comparison of emotional responses in monkeys with rhinal cortex or amygdala lesions.

Four emotionally arousing stimuli were used to probe the behavior of monkeys with bilateral ablations of the entorhinal and perirhinal cortex. The monkeys' behavioral changes were then contrasted with those observed earlier (M. Meunier, J. Bachevalier, E. A. Murray, L. Málková, & M. Mishkin, 1999) in monkeys with either neurotoxic or aspiration lesions of the neighboring amygdala. Rhinal cortex ablations yielded several subtle behavioral changes but none of them resembled any of the disorders typically seen after amygdalectomies. The changes produced by rhinal damage took mainly the form of heightened defensiveness and attenuated submission and approach responses; that is, just the opposite of some of the most distinctive symptoms following amygdala damage. These findings raise the possibility that the rhinal cortex and amygdala have distinct, interactive functions in normal behavioral adaptation to affective stimuli.

Aggression↗
PubMed1990

A truncation mutation in the avian beta-adrenergic receptor causes agonist-induced internalization and GTP-sensitive agonist binding characteristic of mammalian receptors.

Recombinant turkey erythrocyte beta-adrenergic receptors expressed in murine L cells exhibited characteristic avian subtype selectivity for agonists and antagonists. In 10 of the 11 clones studied, no agonist-induced internalization of receptor was observed, although agonist-induced uncoupling of receptor and adenylyl cyclase occurred rapidly. GTP caused little or no decrease in affinity for beta-adrenergic agonists. Such behavior is commonly observed in avian erythrocytes. In contrast, one clone was susceptible to agonist-induced receptor internalization and down-regulation even though it exhibited characteristic avian beta-adrenergic ligand-binding properties. The affinity of this variant receptor for agonists was also notably reduced by GTP. Electrophoresis of affinity-labeled receptor from this clone indicated an apparent size of about 33 kDa, about 12 kDa less than that of the native or recombinant turkey beta-adrenergic receptor. Genomic DNA from this cell line that encodes the receptor was cloned and partially sequenced. The coding region of the original receptor cDNA was interrupted after codon 412 (out of 483) and was followed by 36 base pairs of novel sequence prior to the first in-frame stop codon. These results suggest that the lack of both hormone-induced internalization and GTP-sensitive, high affinity binding of agonists that is characteristic of the beta-adrenergic receptor in avian erythrocytes is due to intrinsic properties of the receptor. The restoration of these phenomena in a C-terminally truncated mutant receptor suggests the importance of the C-terminal domain in determining these processes.

Adenylyl Cyclases↗
PubMed2001

Comparison of the effects of isoproterenol administered into the hippocampus, frontal cortex, or amygdala on behavior of rats maintained by differential reinforcement of low response rate.

RATIONALE: Central administration of isoproterenol, a non-selective beta adrenergic agonist, produces behavioral changes in animal models sensitive to antidepressants. However, it is not clear which brain regions mediate these effects. OBJECTIVES: To investigate the antidepressant-like effects of site-specific administration of isoproterenol and the involvement of beta adrenergic receptor subtypes. METHODS: The effects of isoproterenol, which was administered into the lateral ventricle, hippocampus, frontal cortex, or amygdala, were determined in rats under a differential-reinforcement-of-low-rate (DRL) 72-s schedule. The effects of beta adrenergic antagonists on the actions of isoproterenol also were determined. RESULTS: When injected bilaterally into the hippocampus, isoproterenol (1-30 microg/side) decreased response rate and increased reinforcement rate in a dose-dependent manner. The minimum dose of isoproterenol required for changing DRL behavior was 6 microg (i.e., 3 microg bilaterally), compared to 10 microg for intracerebroventricular and 60 microg (30 microg bilaterally) for administration into the frontal cortex or amygdala. These effects of isoproterenol were blocked by the beta adrenergic antagonist propranolol. In addition, the effects of isoproterenol injected intrahippocampally also were antagonized dose-dependently by the beta-1 selective antagonist betaxolol and the beta-2 selective antagonist ICI 118,551. The relative potency of these antagonists for blocking the effects of isoproterenol suggested predominant mediation by beta-1 adrenergic receptors. CONCLUSIONS: The hippocampus is an important site involved in mediating the antidepressant-like effect of isoproterenol. This suggests a key, although not exclusive, role for this site in the pathophysiology of depression and its pharmacotherapy.

Adrenergic beta-Agonists↗
PubMed2005

Differential behavioral tolerance to the delta-opioid agonist SNC80 ([(+)-4-[(alphaR)-alpha-[(2S,5R)-2,5-dimethyl-4-(2-propenyl)-1-piperazinyl]-(3-methoxyphenyl)methyl]-N,N-diethylbenzamide) in Sprague-Dawley rats.

Nonpeptidic delta-opioid agonists produce a number of behaviors, such as antidepressant-like effects, locomotor stimulation, antinociception, and convulsions. To consider this class of compounds as potential therapeutics for humans, the effects of delta-opioid agonists after repeated administration must be evaluated. Therefore, the present study investigated the effects of repeated delta-opioid agonist, SNC80 ([(+)-4-[(alphaR)-alpha-[(2S,5R)-2,5-dimethyl-4-(2-propenyl)-1-piperazinyl]-(3-methoxyphenyl)-methyl]-N,N-diethylbenzamide), administration on its antidepressant-like effects in the forced swim test, locomotor activity, and convulsions in male Sprague-Dawley rats. Tolerance developed rapidly to the convulsive and locomotor-stimulating effects of SNC80 but not to the antidepressant-like effects. In addition, tolerance was evaluated at the level of the receptor-G protein interaction by measuring 5'-O-(3-[35S]thio)triphosphate binding in brains from rats that were pretreated with SNC80. With various exposure durations to SNC80, some brain regions demonstrated tolerance at different times, suggesting that adaptations in the delta-opioid system may occur during agonist exposure. Overall, the lack of observable tolerance to the antidepressant-like effects of SNC80 indicates that this class of compounds has potential as a novel antidepressant therapy.

Animals↗
PubMed1998

Behavioral responsitivity to dopamine receptor agonists after extensive striatal dopamine lesions during development.

Dopamine (DA) receptor responsitivity was investigated in adult rats that received intrastriatal (i.s.) injections of 6-OHDA (20 micrograms per striatum) on day of birth or postnatal Day 1 (Day 0/Day 1). Neonatally lesioned rats exhibited self-biting behavior and increases in stereotypic gnawing following treatment with the mixed D1/D2 receptor agonist apomorphine (0.32-3.2 mg/kg) or the D1-like receptor agonist SKF38393 (10 mg/kg). Increases in locomotor activity, rearing, and paw treading were also observed in the lesioned rats after SKF38393 (1-10 mg/kg) treatment. The incidences of the prototypical D1 receptor-mediated behaviors, grooming and abnormal perioral movements (i.e., oral dyskinesias) were not increased in the lesioned rats. However, the low dose (0.32 mg/kg) of apomorphien as well as all doses of the D2-like receptor agonist quinpirole (0.32-3.2 mg/kg) induced grooming in the lesioned rats, which was not observed in nonlesioned control rats. Autoradiographs of [3H]mazindol binding to high affinity DA uptake sites revealed an extensive loss of DA terminals in the striata of the neonatally lesioned rats. These data suggest that near-total (> or = 95%) DA depletions on Day 0/Day 1 result in long-term alterations in the functional sensitivity of DA receptors, as well as possible changes in the interactions between D1 and D2 receptors. Comparisons of these results with those seen following lesions of the early-developing DA system ("patch-selective" lesions) and lesions made at other time points will be discussed.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗