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PubMed1997

Orphanin FQ acts as an anxiolytic to attenuate behavioral responses to stress.

Orphanin FQ (OFQ, Nociceptin) is a recently discovered 17-amino acid neuropeptide that is structurally related to the opioid peptides but does not bind opioid receptors. OFQ has been proposed to act as an anti-opioid peptide, but its widespread sites of action in the brain suggest that it may have more general functions. Here we show that OFQ plays an important role in higher brain functions because it can act as an anxiolytic to attenuate the behavioral inhibition of animals acutely exposed to stressful/anxiogenic environmental conditions. OFQ anxiolytic-like effects were consistent across several behavioral paradigms generating different types of anxiety states in animals (light-dark preference, elevated plus-maze, exploratory behavior of an unfamiliar environment, pharmacological anxiogenesis, operant conflict) and were observed at low nonsedating doses (0.1-3 nmol, intracerebroventricular). Like conventional anxiolytics, OFQ interfered with regular sensorimotor function at high doses (>3 nmol). Our results show that an important role of OFQ is to act as an endogenous regulator of acute anxiety responses. OFQ, probably in concert with other major neuropeptides, exerts a modulatory role on the central integration of stressful stimuli and, thereby, may modulate anxiety states generated by acute stress.

Animals↗

PubMedDate not supplied

[The correction of the manifestations of a neurosis-like state in white rats by using the vitamin complex Aekol].

Behavior of neurotized white rats was studied in two experimental situations: during training for passive and active avoidance of electroshock applied to the limbs and during testing the acquisition of the conditioned avoidance. It was shown that in behavior of rats in the neurosis-like state the signs of anxiety and fear dominated, the orienting-exploratory behavior was suppressed. The state correction was performed by per os introduction of the natural vitamin complex Aekol during the neurotization of animals.

Animals↗

PubMed1997

Loss of perikaryal parvalbumin immunoreactivity from surviving GABAergic neurons in the CA1 field of epileptic gerbils.

The Mongolian gerbil (Meriones unguiculatus) is known as a genetic model of epilepsy. Seizure behavior ranges from subtle events like arrest of motor activity and facial spasms to grand mal seizures followed by automatisms. Exploratory behavior in a stressful situation represents the most effective environment for provoking seizures in gerbils. Modifications of the inhibitory hippocampal circuits have been suggested as a cause of seizure susceptibility in the gerbil. This study presents a quantitative analysis of the hippocampal parvalbumin (PV)-immunoreactive and gamma-aminobutyric acid (GABA)-immunoreactive neurons in gerbils whose seizure sensitivity had been scored. PV is a cytosolic calcium-binding protein synthesized by a subpopulation of GABAergic neurons and thought to be responsible for the fast spiking capability of this subset of neurons. We show that the number of PV-immunoreactive neurons in the CA1 field of the gerbil hippocampus decreases in repeatedly seizing animals as compared to non-seizing controls. The lowest density of PV-immunoreactive neurons was observed 1 hour after the last generalized seizure. No changes in the density of GABA-immunoreactive neurons in field CA1 paralleled the obvious loss of perikaryal PV-immunoreactivity. The CA1 field represents the final output region to extrahippocampal brain areas, and its recruitment or not into seizure activity is crucial for the spreading of hippocampal discharges to the adjacent neocortex. A reduction of such a calcium-buffering system in the soma and dendrites may affect the spike characteristics of PV-containing GABAergic neurons and may alter their response to glutamatergic transmission. A reduced inhibitory control of pyramidal cells may ensue, facilitating neuronal excitability as a result.

Animals↗

PubMed1986

Anticonvulsant properties of spirohydantoins derived from optical isomers of camphor.

Natural camphor exists as the d (+) form but the l (-) form has been synthesized. Replacement of the keto group on carbon 2 of each form with a hydantoin moiety led to only one spirohydantoin derivative. Both d and l derivatives were synthesized. Both forms and their racemic mixture were tested in vivo for toxicity and behavioral effects in mice. A dose of 100 mg/kg of the d form was not toxic: mice showed normal grooming and exploratory behavior; the l form induced hunched posture, body jerks and myoclonic manifestations followed by quiescence. The dl form showed intermediate effects. Challenge with the convulsant pentylenetetrazol (Metrazol) 2 hr after treatment with placebo or the camphor spirohydantoins produced seizure manifestations in all controls, in half of the subjects pretreated with the d-camphor derivative, in none of those pretreated with the l derivative and an intermediate response in those pretreated with racemic mixture. Thus, a spirohydantoin moiety added to camphor conferred strong anticonvulsive properties on the l form and modest ones on the d form; the d form did not seem to antagonize the l form.

Animals↗

PubMed2004

Bupropion effects on aggressiveness and anxiety in OF1 male mice.

RATIONALE: Bupropion is an antidepressant drug that is being used to help in giving up smoking. Its behavioral effects have been evaluated in different animal models, although limited information is available regarding its effects on aggressiveness, anxiety and exploratory behavior. OBJECTIVES: Evaluate acute effects of bupropion on locomotor activity, isolation-induced aggression, hole-board and elevated plus-maze tests in OF1 male mice. METHODS: In the first experiment, effects of bupropion (2.5, 5, 10, 20 and 40 mg/kg) on locomotion were evaluated. In the second experiment, isolation-induced aggression was assessed in isolated male mice previously classified as short attack latency (SL) and long attack latency (LL). Mice were treated with bupropion or vehicle and confronted with standard opponents for 10 min. In experiments 3 and 4, mice were treated with bupropion or vehicle and 30 min later examined in the plus-maze or in the hole-board apparatus. RESULTS: In the actimeter, bupropion induced a dose-dependent increase in locomotion. During agonistic encounters, bupropion (10 mg/kg and 40 mg/kg) increased time devoted to attack in LL mice. In the plus-maze, no significant differences were found between bupropion-treated and vehicle-treated mice in the percentage of entries or time spent in open arms. In the hole-board, the highest dose of bupropion (40 mg/kg) significantly decreased number of head-dips and increased latency to the first head-dip. CONCLUSIONS: During agonistic encounters the two sub-groups of mice (SL and LL) may display differential sensitivity in drug-induced changes on aggressiveness, since bupropion increased attack only in mice with "long attack latency" in the pre-screening test. In the plus-maze, this drug does not seem to have specific actions on anxiety and in the hole-board a high dose had similar effects to those induced by anxiogenic drugs.

Aggression↗

PubMedDate not supplied

Regulatory role of brain angiotensins in the control of physiological and behavioral responses.

Considerable evidence now indicates that a separate and distinct renin-angiotensin system (RAS) is present within the brain. The necessary precursors and enzymes required for the formation and degradation of the biologically active forms of angiotensins have been identified in brain tissues as have angiotensin binding sites. Although this brain RAS appears to be regulated independently from the peripheral RAS, circulating angiotensins do exert a portion of their actions via stimulation of brain angiotensin receptors located in circumventricular organs. These circumventricular organs are located in the proximity of brain ventricles, are richly vascularized and possess a reduced blood-brain barrier thus permitting accessibility by peptides. In this way the brain RAS interacts with other neurotransmitter and neuromodulator systems and contributes to the regulation of blood pressure, body fluid homeostasis, cyclicity of reproductive hormones and sexual behavior, and perhaps plays a role in other functions such as memory acquisition and recall, sensory acuity including pain perception and exploratory behavior. An overactive brain RAS has been identified as one of the factors contributing to the pathogenesis and maintenance of hypertension in the spontaneously hypertensive rat (SHR) model of human essential hypertension. Oral treatment with angiotensin-converting enzyme inhibitors, which interfere with the formation of angiotensin II, prevents the development of hypertension in young SHR by acting, at least in part, upon the brain RAS. Delivery of converting enzyme inhibitors or specific angiotensin receptor antagonists into the brain significantly reduces blood pressure in adult SHR. Thus, if the SHR is an appropriate model of human essential hypertension (there is controversy concerning its usefulness), the potential contribution of the brain RAS to this dysfunction must be considered during the development of future antihypertensive compounds.

Amino Acid Sequence↗

PubMed2006

Effects of glucose-dependent insulinotropic peptide on behavior.

Glucose-dependent insulinotropic peptide (GIP) is an incretin hormone that rises rapidly in response to nutrient ingestion. The GIP receptor is widely expressed in the brain including the brain stem, telencephalon, diencephalon, olfactory bulb, pituitary, and cerebellum. Until recently it was not clear what the endogenous ligand for this receptor was because no GIP expression had been demonstrated in the brain. GIP synthesis has now been documented in the dentate gyrus of the hippocampus. To define GIP effects on behavior we utilized a mouse model a GIP-overexpressing transgenic mouse (GIP Tg). Specifically, anxiety-related behavior, exploration, memory, and nociception were examined. Compared to age-matched adult male C57BI/6 controls GIP Tg mice displayed enhanced exploratory behavior in the open-field locomotor activity test. GIP Tg mice also demonstrated increased performance in some of the motor function tests. These data suggest that the GIP receptor plays a role in the regulation of locomotor activity and exploration. To our knowledge, this is the first report of effects of GIP on behavior.

Animals↗

PubMed2006

Receptor crosstalk: characterization of mice deficient in dopamine D1 and adenosine A2A receptors.

Here we report the development of D1A2A receptor knockout mice to investigate whether interactions between dopamine D1 and adenosine A2A receptors participate in reward-related behavior. The combined deletion of D1 and A2A receptors resulted in mice with decreased weight and appetitive processes, reduced rearing and exploratory behaviors, increased anxiety, and a significantly poorer performance on the rotarod, compared to wild-type littermates. D1A2A receptor knockout mice shared phenotypic similarities with mice deficient in D1 receptors, while also paralleling behavioral deficits seen in A2A receptor knockout mice, indicating individual components of the behavioral phenotype of the D1A2A receptor knockout attributable to the loss of both receptors. In contrast, ethanol and saccharin preference in D1A2A receptor knockout mice were distinctly different from that observed in derivative D1 or A2A receptor-deficient mice. Compared to wild types, preference and consumption of ethanol were decreased in D1A2A receptor knockout mice, the reduction in ethanol consumption greater even than that seen in D1 receptor-deficient mice. Preference and consumption of saccharin were also reduced in D1A2A receptor knockout mice, whereas saccharin preference was similar in wild-type, D1, and A2A receptor knockout mice. These data suggest an interaction of D1 and A2A receptors in the reinforcement processes underlying the intake of rewarding substances, whereby the A2A receptor seems involved in goal-directed behavior and the motor functions underlying the expression of such behaviors, and the D1 receptor is confirmed as essential in mediating motivational processes related to the repeated intake of novel substances and drugs.

Alcohol Drinking↗

PubMed1982

Behavioral toxicity of trihalomethane contaminants of drinking water in mice.

The behavioral toxicity of trichloromethane (TCM), dichlorobromomethane (DCBM), dibromochloromethane (DBCM) and tribromomethane (TBM) was evaluated following oral administration in mice. A variety of dosage regimens and behavioral measures were used. Studies included acute dose effect, 14-and 90-day treatments at 300 and 3000 times the estimated average human daily intake of contaminated drinking water, 30 days of 100 mg/kg/day, and 60 days of 100 and 400 mg/kg/day. In addition, TCM was tested for the production of taste aversions with 10-day administration and for behavioral teratology in offspring following extensive perinatal exposure. The ED50 for acute effects on a screen test of motor performance was about 500 mg/kg for all four trihalomethanes. The 14-day treatments had no effect on swimming behavior and the 90-day treatments had no effect on bar clinging, a test of motor coordination, and a measure of exploratory behavior. None of the compounds produced effects on passive-avoidance learning following 100 mg/kg/day for 30 days. TCM, DBCM and TBM elicited clear effects at both 100 and 400 mg/kg/day on operant behavior when administered for 60 days. DBCM elicited clear effects at 400 mg/kg/day. These effects on operant behavior were seen following the first dose and tolerance tended to develop. Thus, there was no evidence from these studies for a progressive neurotoxicity from trihalomethanes in adult mice. A behavioral teratology study was also conducted with TCM. Both parents were treated with 31.1 mg/kg/day TCM, and treatment of the dam continued throughout gestation and lactation. No clear evidence for behavioral effects in the offspring were observed. The most sensitive measure for the effects of TCM was the taste aversion paradigm in which saccharin aversions were produced after a single treatment of 30 mg/kg.

Administration, Oral↗

PubMed1977

[Social effects of the behavior of male and female mice in open field].

Canonical discriminant analysis is used to differentiate behaviors, in male and female mice, either isolated, either grouped by two, or grouped by five, and placed into two different open-fields, one of 1 m X 1 m and one of 2.5 m X 2.5 m. Social effects are experimentally demonstrated. In addition the evidenced complexity of the behavior of mice in an openfield cannot be merely reduced to a decrease or increase of an emotional or of an exploratory behavior, as it has been previously stated.

Animals↗

PubMed1983

Behavioral outcome after prenatal exposure to phenytoin in rats.

The long-term behavioral outcome subsequent to prenatal exposure to phenytoin was examined in an animal model for the Fetal Hydantoin Syndrome. Behavioral outcome was determined by two different techniques--the residential maze, which provided a 24-hour measure of horizontal movement frequency in a group of animals, and time-lapse photography, which allowed quantification of frequency, duration, distribution, and sequencing of 15 motor acts performed by individual rats. Phenytoin induced significant, sex-related changes in motor behavior. Ten-week-old females exposed in utero to phenytoin displayed hypoactivity comprised of a longer duration, greater frequency, and more random distribution of grooming behaviors. Prenatally exposed males at that age displayed an opposite effect of hyperactivity consisting of a longer duration and greater frequency of exploratory behaviors. It appears that prenatal exposure to phenytoin may affect normal maturational changes in motor behavior so that immature activity levels are maintained in the adult animal.

Aging↗

PubMed2002

The mGluR5 antagonist MPEP, but not the mGluR2/3 agonist LY314582, augments PCP effects on prepulse inhibition and locomotor activity.

Phencyclidine (PCP), a non-competitive antagonist of ionotropic N-methyl-D-aspartate (NMDA) receptors, produces psychotomimetic effects, such as a disruption in prepulse inhibition (PPI) of the startle response. NMDA antagonists also induce locomotor hyperactivity in rodents. We hypothesized that, like NMDA receptors, metabotropic glutamate receptors (mGluRs) modulate PPI and locomotor activity either alone or, in the case of mGluR5, via interaction with NMDA receptors. Rats treated with the mGluR5 antagonist MPEP (2-methyl-6-phenylethynylpyridine) or the mGluR2/3 agonist LY314582, either alone or in combination with PCP, were tested in PPI and locomotor activity paradigms. Neither MPEP nor LY314582 altered PPI. MPEP, but not LY314582, potentiated the PPI-disruptive effects of PCP. MPEP alone did not alter locomotor or exploratory behavior, but augmented the complex, time-dependent locomotor-stimulating effects of PCP. LY314582 dose-dependently decreased locomotor activity and exploratory holepokes. LY314582 did not alter the PCP-induced increases in locomotor activity, but further decreased the number of holepokes. The effects of MPEP on the response to PCP may reflect the cooperation and co-localization of NMDA and mGlu5 receptors.

Animals↗

PubMed2000

Female presence during postejaculatory interval facilitates penile erection and 22-kHz vocalization in male rats.

During the postejaculatory interval (PEI), male rats exhibit prolonged immobility, 22-kHz vocalization, and penile erections. To test whether females modulate these behaviors, females were removed after the first or second ejaculation or left in the test chamber. Female presence during the PEI delayed exploratory behavior and facilitated vocalization and erection. Female stimulation of vocalization is consistent with the hypothesis that vocalization has a communicative function, not just a thermoregulatory one. The timing of the effect of females on erection suggests that males are sexually arousable well before they resume copulation. Therefore, erection may be better than vocalization as an indicator of the male's sexual refractoriness. The findings also challenge the conventional view that the PEI comprises absolute and relative sexual refractory periods marked, respectively, by the presence and absence of 22-kHz vocalization.

Animals↗

PubMed2002

Thalamocortical [correction of Thalamcortical] optimization of tactile processing according to behavioral state.

We propose a conceptual model that describes the operation of the main thalamocortical loop of the rat somatosensory system. According to this model, the asynchronous convergence of ascending and descending projections dynamically alters the physiological properties of thalamic neurons in the ventral posterior medial (VPM) nucleus as rats shift between three behavioral states. Two of these states are characterized by distinct modes of rhythmic whisker movements. We posit that these simultaneous shifts in exploratory behavioral strategy and in the physiological properties of VPM neurons allow rats to either (i) optimize the detection of stimuli that are novel or difficult to sense or (ii) process complex patterns of multi-whisker stimulation.

Afferent Pathways↗

PubMed2000

(Over)correction of FMR1 deficiency with YAC transgenics: behavioral and physical features.

Fragile X syndrome is a common cause of mental retardation involving loss of expression of the FMR1 gene. The role of FMR1 remains undetermined but the protein appears to be involved in RNA metabolism. Fmr1 knockout mice exhibit a phenotype with some similarities to humans, such as macroorchidism and behavioral abnormalities. As a step toward understanding the function of FMR1 and the determination of the potential for therapeutic approaches to fragile X syndrome, yeast artificial chromosome (YAC) transgenic mice were generated in order to determine whether the Fmr1 knockout mouse phenotype could be rescued. Several transgenic lines were generated that carried the entire FMR1 locus with extensive amounts of flanking sequence. We observed that the YAC transgene supported production of the human protein (FMRP) which was present at levels 10 to 15 times that of endogenous protein and was expressed in a cell- and tissue-specific manner. Macro-orchidism was absent in knockout mice carrying the YAC transgene indicating functional rescue by the human protein. Given the complex behavioral phenotype in fragile X patients and the mild phenotype previously reported for the Fmr1 knockout mouse, we performed a more thorough evaluation of the Fmr1 knockout phenotype using additional behavioral assays that had not previously been reported for this animal model. The mouse displayed reduced anxiety-related responses with increased exploratory behavior. FMR1 YAC transgenic mice overexpressing the human protein did produce opposing behavioral responses and additional abnormal behaviors were also observed. These findings have significant implications for gene therapy for fragile X syndrome since overexpression of the gene may harbor its own phenotype.

Animals↗

PubMed1988

RO 15-4513 and its interaction with ethanol.

It has recently been claimed that RO 15-4513 selectively opposes some of the behavioral actions of ethanol. Our studies on the intrinsic effects of this compound have shown it to be proconvulsant and to reduce exploratory behavior in mice. In these respects RO 15-4513 resembles a benzodiazepine receptor partial inverse agonist. Such intrinsic actions may well explain its alcohol-antagonizing properties, and argue against its potential in humans. In addition to partially reversing the effects of ethanol, RO 15-4513 also partially reverses the behavioral effect of a barbiturate and completely reverses the effects of a benzodiazepine.

Animals↗

PubMed1997

Effects of intracerebroventricular injection of histamine on memory deficits induced by hippocampal lesions in rats.

The influence of bilateral hippocampal lesions on active avoidance response was studied in rats, as well as the effect of intracerebroventricular (i.c.v.) injection of histamine on memory deficits caused by hippocampectomy. Retardation of learning acquisition was produced by lesioning of the bilateral dorsal hippocampus in active avoidance response. Memory retention was also impaired by hippocampectomy. Although locomotor activity and rearing behavior measured by open-field test increased after hippocampal lesions, there was no relation between impairment of learning and increase in exploratory behavior. I.c.v. injection of histamine and i.p. injection of histidine resulted in an improvement of memory deficits (not only learning acquisition but also memory retrieval) induced by hippocampal lesions in rats. Histamine contents of the hippocampus and hypothalamus decreased after hippocampectomy, and a decrease in histamine contents of both areas was restored by histamine (i.c.v.) and histidine (i.p.) injection. In addition, a close relationship was found between decrease in response latency of avoidance response and an increase in histamine content of the hippocampus and hypothalamus after histamine injection.

Animals↗

PubMed1997

Purkinje cell expression of a mutant allele of SCA1 in transgenic mice leads to disparate effects on motor behaviors, followed by a progressive cerebellar dysfunction and histological alterations.

Spinocerebellar ataxia type 1 (SCA1) is an autosomal dominant neurological disorder caused by the expansion of a CAG repeat encoding a polyglutamine tract. Work presented here describes the behavioral and neuropathological course seen in mutant SCA1 transgenic mice. Behavioral tests indicate that at 5 weeks of age mutant mice have an impaired performance on the rotating rod in the absence of deficits in balance and coordination. In contrast, these mutant SCA1 mice have an increased initial exploratory behavior. Thus, expression of the mutant SCA1 allele within cerebellar Purkinje cells has divergent effects on the motor behavior of juvenile animals: a compromise of rotating rod performance and a simultaneous enhancement of initial exploratory activity. With age, these animals develop incoordination with concomitant progressive Purkinje neuron dendritic and somatic atrophy but relatively little cell loss. Therefore, the eventual development of ataxia caused by the expression of a mutant SCA1 allele is not the result of cell death per se, but the result of cellular dysfunction and morphological alterations that occur before neuronal demise.

Alleles↗