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PubMed1994

Alterations in central monoamine systems after postnatal lead acetate treatment in rats.

The present study was undertaken to investigate the effects of postnatal lead exposure on central monoamine systems. Newborn male Sprague-Dawley rats were given 1 or 8 mg/kg lead acetate intraperitoneally for 20 days postnatally. Two groups of control rats received sodium acetate, or sodium acetate in oversized litters to compensate for lead-induced malnutrition in the high lead dose group, while nontreated animals also served as controls. At Day 21 or 51 regional tissue levels of monoamines were determined using HPLC techniques. No major changes were seen after the lead exposures in the levels of dopamine, noradrenaline, and serotonin, or metabolites of dopamine and serotonin, when compared to respective control groups. On the other hand, in the control group given sodium acetate in over-sized litters some alterations of the monoamine levels were observed in frontal cortex and striatum at Day 21 compared to controls. At Day 51, the striatal homovanillic acid and 5-hydroxyindoleacetic acid levels were higher in the low lead dose group compared to those in the controls. No other changes in the monoamine levels were seen at Day 51. At 50-70 days postnatally, potassium-stimulated dopamine overflow was studied in striatum with in vivo chronoamperometry. In the high lead dose group the amplitudes of signals were lower in both the dorsal and ventral striatum compared to the controls, while no difference was seen in the clearance time of dopamine. The capacity of the dopamine terminals to respond to repeated stimulation was not affected by the lead exposure. Thus, the steady-state levels of monoamines were essentially unaltered after postnatal lead exposure in rats, while functional aspects of striatal dopamine transmission were affected after exposure to the higher dose of lead. These findings support the hypothesis that lead-induced changes in motor skills and exploratory behavior may be related to altered dopamine neurotransmission.

Adolescent↗
PubMed1997

Calcium-binding protein phenotype defines metabolically distinct groups of neurons in barrel cortex of behaving hamsters.

Physiological/anatomical studies of rat frontal cortex in vitro have distinguished subpopulations of gamma-aminobutyric acid (GABA)-expressing inhibitory interneurons defined by expression of the calcium-binding proteins, parvalbumin (PV) and calbindin (CA). Using a novel 2DG/immunostaining technique to double-label hamster barrel cortex for metabolism and phenotype, we have recently shown that while many GABAergic neurons are heavily 2DG labeled during normal exploratory behavior, a subset of GABAergic cells shows relatively sparse 2DG labeling. For this study we used the 2DG/immunostaining technique to test whether, in awake behaving animals, calcium-binding protein expression in a given cell in barrel cortex (as indicated by immunohistochemistry for PV or CA) was related to the degree of 2DG labeling. We found that most PV+ cells were moderately to heavily 2DG labeled, while most CA+ cells were lightly 2DG labeled. Our data indicate that the PV+ and CA+ cells represent metabolically distinct subpopulations of GABAergic neurons in barrel cortex. This distinction corresponds well with the in vitro physiological and anatomical data from frontal cortex and suggests functional implications for the expression of PV and CA, or other colocalized factors, in normally functioning cortical circuitry.

Animals↗
PubMed1996

Spatial and nonspatial learning in mice: effects of S100 beta overexpression and age.

S100 beta, a Ca2+ binding astrocytic brain protein implicated in brain development and neurophysiology, has elevated levels in progressive neurodegenerative diseases, Down's Syndrome, and Alzheimer Disease. Transgenic mice carrying multiple S100 beta gene copies exhibited abnormal exploratory behaviors and synaptic processes suggesting hippocampal dysfunction. Here we analyze learning in a hippocampal-dependent (spatial) as well as a non-hippocampal-dependent (nonspatial) version of the Morris water maze and compare CD1 control and CD1-derived S100 beta transgenic mice. We also investigate possible progressive age-dependent effects of S100 beta overexpression by comparing two age groups of the above mice: 3- and 16-month-old. We show that 3-month-old S100 beta transgenic mice have a spatial task-specific impairment confirming a hippocampal dysfunction. However, we found the 16-month-old transgenic mice statistically indistinguishable from their normal counterparts, a result that does not confirm progressive S100 beta transgene effects. We also show that age, independently of the transgene, impairs spatial learning, spares nonspatial learning and reference memory, but leads to behavioral rigidity.

Age Factors↗
PubMed2000

Genetic differences in response to novelty and spatial memory using a two-trial recognition task in mice.

A two-trial memory task, based on a free-choice exploration paradigm in a Y-maze, was previously developed to study recognition processes in Sprague-Dawley rats. Because this paradigm avoids the use of electric shock or deprivation that may have nonspecific effects and does not require learning of a rule, it may be particularly useful for studying memory in mice. Four inbred strains (Balb/cByJ, DBA/2J, C57BL/6J, and SJL/J), an F1 hybrid (C57BL/6 x SJL/J), and one outbred strain (CD1) were used to validate this task in mice and to characterize a strain distribution in response to novelty and working memory. Exploration was measured with a short (2 min) intertrial interval (ITI) between acquisition and retrieval, while memory was examined with longer intervals (30 min, 1 h, and 2 h). A study of the time course of the response to novelty revealed varying degrees of preference and/or habituation to novelty among the different strains, with CD1 exhibiting a very high response to novelty and others showing lower (C57 x SJL hybrids) to complete absence (SJL) of exploration of novelty. Memory span, assessed with increasing ITIs, varied widely among strains from 30 min (C57 x SJL hybrids) to at least 2 h (C57 and BALB). Such demonstrated sensitivity to a wide range of behavioral phenotypes supports the use of this spatial memory task as an effective tool for the study of genetic influences on the response to novelty and recognition processes in mice.

Animals↗
PubMed1975

Induction of physical dependence on alcohol in rodents.

An ethanol withdrawal syndrome consisting of tremors and seizures can be induced in rats and mice. This syndrome closely resembles the physical signs observed in human patients during alcohol withdrawal. The criteria for an animal model of a human disease appear to be fulfilled regarding the etiological agent, course of illness, the similarity of physical and electrophysiological manifestations and response to therapeutic agents. Therefore these models should lend themselves for the elucidation of the pathogenesis at the molecular level of biological organization and for the development of new therapeutic approaches. Criteria for an optimal animal model of ethanol dependence are outlined. Withdrawal signs are classified into minor (startle threshold and exploratory behavior) and major types (tremors and seizures). Methods for quantification of tremors and seizures are described. The procedures for induction of the major withdrawal signs are classified according to the mode of ethanol administration designed to circumvent the animal's inherent aversion to the taste of ethanol: Oral (free feeding, behavioral modifications of free feeding and force feeding), parenteral and inhalation. Auxiliary procedures consist of pyrazole administration and weight reduction resulting in a decreased rate of ethanol metabolism. Exposure to low environmental temperatures increases consumption of ethanol containing diets without proportionately increasing the rate of ethanol metabolism. Auxiliary procedures for the induction of seizures during withdrawal consist of handling the animals and audiogenic stimuli. Advantages and limitations of various rodent models are evaluated in terms of the procedures (practicability, compounding variables) and their results (reproducibility, severity and yield of major withdrawal signs, objective quantification). It is concluded that none of the current methods fulfill all requisites for all types of experiments. The selection of methods best suited for a particular experiment depend upon its objectives.

Acoustic Stimulation↗
PubMed1984

Naloxone administration following brief exposure to novelty reduces activity and rearing in mice upon 24-h retest: a conditioned aversion?

It has recently been reported that naloxone treatment, prior to initial exposure to a novel arena, results in significant behavioural change when animals are retested 24 h later. In an attempt to clarify the nature of this delayed action of the opiate antagonist, three further studies have been performed. In the first experiment, male mice were injected with naloxone hydrochloride (0-10 mg/kg, IP) immediately after their initial experience of the test arena. When retested 24 h later, all groups that had previously received naloxone exhibited greatly reduced activity and rearing, with no evidence of a dose-response relationship. In the second experiment, naloxone (0-10 mg/kg) failed to induce a conditioned place aversion when administered according to the above regimen. In the final experiment, no evidence for a naloxone-induced taste aversion to saccharin was observed. It is concluded that the behavioural changes observed in the open-field study may reflect either (a) subtle aversive properties of naloxone which are insensitive to traditional one-trial paradigms or (b) opioid modulation of memory for non-painful experiences.

Animals↗
PubMed1985

The effects of compounds related to gamma-aminobutyrate and benzodiazepine receptors on behavioural responses to anxiogenic stimuli in the rat: choice behaviour in the T-maze.

Two methods were used to test rats' responses to novelty in the T-maze: (1) a test of spontaneous alternation allowing separate measurement of place and body turn alternation; and (2) a test of entry into an arm of changed brightness ("response to stimulus change"). Chlordiazepoxide reduced spontaneous alternation by specifically weakening body turn alternation and eliminated the response to stimulus change. These findings are similar to those previously reported for the barbiturate sodium amylobarbitone. The same pattern of change in the two tests was seen after a low dose of the GABAA agonist muscimol (0.00125 mg/kg); when the dose of muscimol was raised (0.01 and 0.25 mg/kg), place alternation was also reduced. Picrotoxin but not bicuculline (both GABAA blockers) reversed the effects of muscimol and partially those of chlordiazepoxide on the response to stimulus change; in the spontaneous alternation test picrotoxin only marginally affected the response to 0.25 mg/kg muscimol and actually enhanced the effect of 0.000125 mg/kg. The GABAB agonist baclofen (1 mg/kg) acted in the test of response to stimulus change like chlordiazepoxide and muscimol; however, when baclofen was combined with muscimol, the two drugs tended to show mutual blocking. These results are generally consistent with the hypothesis that GABAergic mechanisms play a role in anxiolytic behavioural activity, but many details are difficult to explain.

Animals↗
PubMed1993

A comparison of behaviour following stimulation of the anterior substantia nigra by direct cholinergic agonists and anticholinesterases.

Microinjections of carbachol, a muscarinic cholinergic receptor agonist, into the anterior substantia nigra increase feeding, drinking and sexual behaviour if there is a pre-existing tendency to respond and a low baseline rate of behaviour. The present experiment was undertaken to compare the effects of carbachol with other cholinergic stimulants. Groups of 6-12 satiated rats received 0.5 microliter microinjections into the anterior substantia nigra of 0.1-5.0 micrograms carbachol, 0.1-5.0 micrograms nicotine, 2.5-10.0 micrograms eserine, and 1.25-5.0 micrograms or 0.1-1.0 microgram neostigmine (each dissolved in sterile saline) and the effects on feeding, drinking, locomotion, grooming, rearing and sniffing were examined. Carbachol, nicotine and low doses of neostigmine stimulated eating in a dose-dependent manner. The increased feeding following neostigmine was over a shorter time-period than following carbachol or nicotine. Neither carbachol nor nicotine had any significant effect on behaviour other than eating. The higher doses of neostigmine increased the frequency of sniffing and rearing, but not eating, and no dose of eserine had a clear effect on behaviour. These data are discussed in terms of their relationship to the cholinergic input to substantia nigra which excites pars compacta dopamine-containing neurones.

Animals↗
PubMed1995

The pharmacology of VA21B7: an atypical 5-HT3 receptor antagonist with anxiolytic-like properties in animal models.

VA21B7 (3-[2-(4'-piperonylpiperazinyl) indolyl] carboxaldehyde) was synthesized as a potential 5-HT3 receptor antagonist. Even though VA21B7 showed a higher affinity towards 5-HT3 receptors as compared to other receptors studied, it was not a potent 5-HT3 receptor antagonist either in the periphery or in the brain. In a simple animal model of anxiety such as the two-compartment box in mice, a remarkable anxiolytic-like effect was found at doses of 2-500 micrograms/kg IP and also at low oral doses, in the microgram range. These drug doses did not produce any significant effect on spontaneous motor activity of mice. The anxiolytic profile of VA21B7 was further explored using other models of anxiety in rats such as the elevated plus-maze and punished-drinking. VA21B7 was compared with standard 5-HT3 receptor antagonists such as ondansetron, tropisetron and granisetron, with the 5-HT1A agent buspirone and with diazepam. In the plus-maze, VA21B7 showed an anxiolytic-like profile after doses of 0.25-0.5 mg/kg IP or 2-4 mg/kg PO which did not modify the number of total entries into the open and closed arms of the maze. Diazepam, granisetron and tropisetron were also effective in this test but not ondansetron and buspirone. VA21B7 was also able to release suppressed behaviour in the punished-drinking test. The dose-response curve was bell-shaped with a peak at 2-4 mg/kg. At variance with other studies, 5-HT3 receptor antagonists also increased the number of shocks taken in this test and the dose-response curve was also bell-shaped. VA21B7 was not anticonvulsant like diazepam, its anxiolytic action in the light/dark test was not flumazenil-sensitive and there was no rebound anxiogenic effect on withdrawal from chronic VA21B7 treatment for 15 consecutive days. Moreover, VA21B7 was not amnesic like the benzodiazepines but low doses of 2-4 mg/kg reduced the memory deficits induced in rats by scopolamine. Much higher doses were necessary to decrease spontaneous motor activity in rats. Since VA21B7 appears to be well tolerated in rodents at high doses, we think that it is of potential interest as an anxiolytic in humans.

Analgesics↗
PubMed1995

Aggression, anxiety and vocalizations in animals: GABAA and 5-HT anxiolytics.

A continuing challenge for preclinical research on anxiolytic drugs is to capture the affective dimension that characterizes anxiety and aggression, either in their adaptive forms or when they become of clinical concern. Experimental protocols for the preclinical study of anxiolytic drugs typically involve the suppression of conditioned or unconditioned social and exploratory behavior (e.g., punished drinking or social interactions) and demonstrate the reversal of this behavioral suppression by drugs acting on the benzodiazepine-GABAA complex. Less frequently, aversive events engender increases in conditioned or unconditioned behavior that are reversed by anxiolytic drugs (e.g., fear-potentiated startle). More recently, putative anxiolytics which target 5-HT receptor subtypes produced effects in these traditional protocols that often are not systematic and robust. We propose ethological studies of vocal expressions in rodents and primates during social confrontations, separation from social companions, or exposure to aversive environmental events as promising sources of information on the affective features of behavior. This approach focuses on vocal and other display behavior with clear functional validity and homology. Drugs with anxiolytic effects that act on the benzodiazepine-GABAA receptor complex and on 5-HT1A receptors systematically and potently alter specific vocalizations in rodents and primates in a pharmacologically reversible manner; the specificity of these effects on vocalizations is evident due to the effectiveness of low doses that do not compromise other physiological and behavioral processes. Antagonists at the benzodiazepine receptor reverse the effects of full agonists on vocalizations, particularly when these occur in threatening, startling and distressing contexts. With the development of antagonists at 5-HT receptor subtypes, it can be anticipated that similar receptor-specificity can be established for the effects of 5-HT anxiolytics.

Aggression↗
PubMed1993

Neuropharmacology of a new potential anxiolytic compound, F 2692, 1-(3'-trifluoromethyl phenyl) 1,4-dihydro 3-amino 4-oxo 6-methyl pyridazine. 1. Acute and in vitro effects.

F 2692 [1-(3'-trifluoromethyl phenyl) 1,4-dihydro 3-amino 4-oxo 6-methyl pyridazine] exhibited dose-dependent "anxiolytic" properties in the elevated plus-maze and the punished drinking tests in rats. It was also active in the two-compartment test in mice. The "anxiolytic" effects were antagonised by the benzodiazepine antagonists, flumazenil and ZK 93426. The compound exhibited anticonvulsant, sedative, myorelaxant and amnesic effects at doses 3-30 times higher than those required for "anxiolytic" activity. F 2692 has a very low affinity for benzodiazepine binding sites in vitro and in vivo (about 1000 and 160 fold lower than diazepam respectively). In addition it displayed no affinity for GABAA, alpha 2-adrenergic, 5-HT1A or 5-HT2 receptors. These data suggest that F 2692 may be a potential anxiolytic compound with an unusual mechanism of action.

Animals↗
PubMed1989

Effects of repeated administration of low doses of apomorphine in three behavioural models in the rat.

A low dose of the dopamine (DA) receptor agonist apomorphine (APO 0.05 mg/kg) was given repetitively and the effects were tested in three different behavioural models: reduction of spontaneous locomotion, induction of yawning and decrease in water intake in water-deprived animals. The APO-induced suppression of exploration and decrease in water intake were not affected by a previous injection of APO given 1 or 3 hours before the test dose of APO. There was a small, but significant, decrease in the induction of yawning by a previous dose of APO given 1 hour or 30 min before the test dose. However, pretreatment with APO 3 hours before the test dose did not diminish the yawning response. It is suggested that the dopaminergic mechanisms mediating APO induced yawning are different from those mediating decrease in water intake and suppression of exploration. The results are also discussed in relation to the proposed efficiency of low doses of DA agonists in the treatment of various neurological and psychiatric disorders.

Animals↗
PubMed2002

Acamprosate reduces context-dependent ethanol effects.

RATIONALE: Previous studies have indicated that the conditioned effects of environmental stimuli contribute to ethanol tolerance and abuse. Acamprosate was recently suggested to reduce the effects of environmental stimuli previously associated with ethanol administrations. This action is believed to contribute to the clinical benefits of acamprosate treatment in alcoholics. OBJECTIVES: In the present experiment, a classical drug-conditioning paradigm was used to test whether acamprosate modulates the effects of ethanol-paired environmental stimuli on spontaneous motor activity. METHODS: Wistar rats were divided into three groups: cued, uncued and control. The cued group daily received ethanol injections (2.0 g/kg, IP) in a specific testing environment. The uncued group daily received ethanol injections (2.0 g/kg, IP) in their home cage but never experienced ethanol in the testing environment. The control group was injected with saline and never experienced ethanol. After 8 conditioning days, the rats were IP injected with various ethanol doses (saline, 1.0, 1.5 or 2.0 g/kg) and their spontaneous motor activity in the testing environment was recorded to investigate their respective tolerance to ethanol inhibitory effects. In the second part of the study, the same procedure was repeated with chronically acamprosate-treated rats. The chronic acamprosate treatment (400 mg/kg per day) started 2 weeks before the conditioning procedure by diluting acamprosate in the drinking bottles and was maintained throughout the whole experiment. RESULTS: The cued rats showed a significant environment-dependent tolerance to ethanol inhibitory effects relative to the uncued and control rats. This higher ethanol tolerance of the cued rats was mainly due to a faster recovery from ethanol's inhibitory effects on spontaneous activity. Furthermore, the cued rats showed a higher level of activity in the testing environment after the saline injection. However, it is not clear whether this hyperactivity is a conditioned compensatory response or an increased exploratory behavior. Acamprosate totally abolished the environment-dependent tolerance to ethanol, whereas it did not alter the hyperactivity of the cued rats in the testing environment. CONCLUSIONS: The results of the present study suggest that acamprosate reduces ethanol-conditioned effects. Such an action may be of importance to explain the anti-relapse effects of acamprosate.

Acamprosate↗
PubMed2004

Angiotensin II blocks memory consolidation through an AT2 receptor-dependent mechanism.

RATIONALE AND OBJECTIVES: Several studies suggest that the brain renin-angiotensin system is involved in memory consolidation. However, the participation of angiotensin II (AII) in this process is controversial. This is probably due to the fact that many of the studies carried out to elucidate this matter employed multitrial learning paradigms together with pretraining intracerebroventricular infusions, and therefore were unable to distinguish between consolidation and retrieval related events and lacked anatomical specificity. To circumvent this problem, we analyzed the role played in memory consolidation by AII using the hippocampal-dependent, one-trial, step-down inhibitory avoidance task (IA) in combination with stereotaxically localized intrahippocampal infusion of drugs. METHODS AND RESULTS: Rats bilaterally implanted with infusion cannulae into the CA1 region of the dorsal hippocampus (CA1) were trained in IA and tested for memory retention 24 h later. We found that when infused into CA1 immediately or 30 min after training but not later, AII produced a dose-dependent amnesic effect without altering locomotor activity, exploratory behavior or anxiety state. The amnesic effect of AII was not mimicked by angiotensin IV (AIV) and was totally blocked by the AII-type 2 receptor (AT2) antagonist, PD123319, but not by the AII-type 1 receptor (AT1) antagonist, losartan. Importantly, when infused alone, neither PD123319 nor losartan produced any effect on memory retention. CONCLUSIONS: Our data indicate that, when given into CA1, AII blocks memory formation through a mechanism involving activation of AT2 receptors; however, endogenous AII does not seem to participate in the consolidation of IA long-term memory.

Amnesia↗
PubMed2005

Combined treatment of ascorbic acid or alpha-tocopherol with dopamine receptor antagonist or nitric oxide synthase inhibitor potentiates cataleptic effect in mice.

RATIONALE: Drugs like haloperidol (Hal) that decrease dopamine (DA) neurotransmission in the striatum induce catalepsy in rodents and Parkinson disease-like symptoms in humans. Nitric oxide synthase (NOS) inhibitors interfere with motor activity, disrupting rodent exploratory behavior and inducing catalepsy. Catalepsy induced by NOS inhibitors probably involves striatal DA-mediated neurotransmission. Antioxidants such as ascorbic acid (vitamin C) and alpha-tocopherol (vitamin E) have also been shown to interfere with movement modulation and the DA system. OBJECTIVE: The objective of the study is to investigate if the antioxidants vitamins C and E would influence the catalepsy produced by Hal and NOS inhibitors. METHODS: The effects of the following treatments on catalepsy were examined using the hanging-bar test on male Swiss mice (25-30 g): (1) vitamin C (30-1,000 mg/kg)xHal (1 mg/kg); (2) vitamin C (90-1,000 mg/kg)xN (G)-nitro-L: -arginine (LNOARG, 10 and 40 mg/kg); (3) vitamin C (300 mg/kg)xN (G)-nitro-L: -arginine methylester (LNAME, 20-80 mg/kg); (4) vitamin C (300 mg/kg) x 7-nitroindazole (7NI, 3-50 mg/kg); (5) vitamin C (90 mg/kg i.p.) x LNOARG [40 mg/kg twice a day during 4 days (subchronic treatment)]; (7) vitamin E (3-100 mg/kg) x Hal (1 mg/kg); and (6) vitamin E (3-100 mg/kg) x LNOARG (40 mg/kg). RESULTS: Vitamin C enhanced the catalepsy produced by NOS inhibitors and Hal. Treatment with vitamin C did not affect tolerance to LNOARG cataleptic effect induced by subchronic treatment. Vitamin E potentiated the catalepsy induced by LNOARG at all doses tested; in contrast, catalepsy induced by Hal was enhanced only by the dose of 100 mg/kg. CONCLUSIONS: Results support an involvement of dopaminergic and nitrergic systems in motor behavior control and provide compelling evidence that combined administration of the antioxidants vitamins C and E with either Hal or NOS inhibitors exacerbates extrapyramidal effects. Further studies are needed to assess possible clinical implications of these findings.

Animals↗
PubMed2006

Acculturation and aggression in Latino adolescents: a structural model focusing on cultural risk factors and assets.

The specific aim of this investigation was to map cultural factors associated with aggressive behavior in Latino adolescents. Interviews were conducted with a sample of 481 foreign- and U.S.-born Latino adolescents living in North Carolina and Arizona. Structural Equation Modeling was used to validate a conceptual model linking adolescent and parent culture-of-origin and U.S. cultural involvement, acculturation conflicts, and perceived discrimination to family processes (familism and parent-adolescent conflict) and adolescent aggression. Parent-adolescent conflict was the strongest cultural risk factor followed by perceived discrimination. Familism and adolescent culture-of-origin involvement were key cultural assets associated with less aggressive behavior. Exploratory mediation analyses suggested that familism and parent-adolescent conflict mediated the effects of acculturation conflicts, parent and adolescent culture-of-origin involvement, and parent U.S. cultural involvement on adolescent aggression. Implications for prevention programming were discussed.

Acculturation↗
PubMed1981

Increase in spontaneous motor activity following infusion of neurotensin into the ventral tegmental area.

Microinjection of neurotensin (NT) into the ventral tegmental area (VTA) of the rat produced a dose-dependent increase in spontaneous motor activity. The NT-induced hyperactivity consisted of an increase in exploratory behaviors, such as locomotion, rearing and sniffing, and a decrease in sleep or resting. The structural specificity of this response was demonstrated by microinjecting NT analogues endogeneous neuropeptides into the VTA. The fact that high levels of immunoreactive NT have been demonstrated in the VTA indicates that the observed behavioral effects may reflect an underlying physiological action by endogenous NT.

Animals↗