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PubMed2001

An animal model of nonconvulsive status epilepticus: a contribution to clinical controversies.

PURPOSE: To characterize electroencephalographic and behavioral effects as well as electrophysiologic and morphologic consequences of a subconvulsive dose of pilocarpine in lithium chloride-pretreated rats. METHODS: Pilocarpine (15 mg/kg) was administered intraperitoneally to adult rats pretreated with lithium chloride (3 mEq/kg, i.p.). Behavior was observed for 2 h and videotaped in three consecutive sessions. At the same time, EEG was recorded from the sensorimotor cortex and the dorsal hippocampus. Threshold intensities of currents necessary to elicit hippocampal afterdischarges were determined 24 h and 1 week after the pilocarpine administration. The brains were histologically examined 1 week after pilocarpine administration using Nissl stain. RESULTS: Pilocarpine induced time-limited nonconvulsive status epilepticus (NCSE). Epileptic EEG activity concurrent with prominent behavioral features was observed both in the neocortex and, predominantly, in the hippocampus. No changes in afterdischarge thresholds were observed in the dorsal hippocampus 24 h and 1 week after NCSE. One week after NCSE, seizure-related brain damage was found mainly in the motor neocortical fields. CONCLUSIONS: Pilocarpine-induced NCSE in rats strongly resembles a short-term human complex partial status epilepticus. Our animal model is suitable for studying the possible adverse effects of prolonged nonconvulsive seizures.

Animals↗
PubMed2002

Behavioral tests after intracerebral hemorrhage in the rat.

BACKGROUND AND PURPOSE: In humans, intracerebral hemorrhage (ICH) causes marked perihematomal edema formation and neurological deficits. A rat ICH model, involving infusion of autologous blood into the caudate, has been used extensively to study mechanisms of edema formation, but an examination of behavioral outcome would improve its preclinical utility and provide a more rigorous assessment of the pathological cascade of events over time. The purpose of this study was to use a battery of sensorimotor function tests to examine the neurological effects of ICH in the rat and to examine which components of the hematoma are involved in generating those effects. METHODS: The behavioral tests used were forelimb placing, preference for forelimb use for weight shifts during vertical exploration of a cylindrical enclosure, and a corner turn test. Rats were tested from day 1 to day 28 after injection of autologous whole blood; injection of blood plus hirudin (thrombin inhibitor), packed red blood cells, thrombin, or saline; or needle placement only. RESULTS: The battery of tests indicated that there were marked neurological deficits by day 1 after ICH, with progressive recovery of function over 4 weeks. The forelimb placing score paralleled changes in edema. Injection of thrombin caused and injection of hirudin reduced the ICH-induced neurological deficits. Injection of packed red blood cells, which causes delayed edema formation, induced delayed neurological deficits CONCLUSIONS: These tests allow continuous monitoring of neurological deficits after rat ICH and assessment of therapeutic interventions. The time course of the neurological deficit closely matched the time course of cerebral edema for both ICH and injection of blood components. There was marked recovery of function after ICH, which may be amenable to therapeutic manipulation.

Animals↗
PubMed1990

GABAergic projection from nucleus accumbens to ventral pallidum mediates dopamine-induced sensorimotor gating deficits of acoustic startle in rats.

Previous studies have demonstrated that increased mesolimbic dopamine (DA) activity disrupts sensorimotor gating as measured by prepulse inhibition (PPI) of the acoustic startle response (ASR) in rats. Other behavioral changes following mesolimbic DA activation are mediated through GABAergic efferent projections from the nucleus accumbens (NAC) to the ventral pallidum (VP). In this experiment, we examined whether PPI deficits in rats following mesolimbic DA activation are mediated through these same GABAergic substrates. PPI was significantly disrupted in rats following infusion of DA (40 micrograms) into the NAC, and this effect was reversed by infusion of a low dose (10 ng) of the GABA agonist muscimol into the VP. In a second experiment, we tested the hypothesis and the loss of PPI following intra-NAC DA infusion results from a disruption of GABAergic activity within the VP. Consistent with this hypothesis, infusion of the GABA antagonist picrotoxin (0-0.2 micrograms) into the VP caused a significant loss of PPI. These findings strongly suggest that the accumbens-ventral pallidal GABAergic circuitry is a substrate for the decrease in sensorimotor gating induced by mesolimbic DA overactivity.

Acoustic Stimulation↗
PubMed2000

New media technology and youth: trends in the evolution of new media.

An information environment is emerging from the simultaneous, rapid, and interconnected evolution of transmission systems, interfaces, and content quantity, quality, and structure. It will be easy to underestimate the collective impact of the sum of these changes on how young people communicate and absorb information. Ultimately, it will be more important to understand how these technologies will facilitate, amplify, or alter the cognitive processes and/or social behavior of the Internet generation. The article analyzes the impact of the following trends on media use and cognition among youthful users: * Information expansion and overload: Accessible networked information will continue to grow at a rapid pace for at least the next 10-20 years. * Rapid increase in interface diffusion: The number of access points into the Internet is expanding in number, variety, and mobility. * Evolution toward more embodied computing: Interfaces are evolving to use more of the sensorimotor system to transfer information to and from the user. * The evolution of more intelligent sensors to interpret use behavior and intentions. * Evolution toward anthropomorphic agent techniques: Computers are evolving to use more social and interpersonal communication techniques to interact with the user.

Adolescent↗
PubMedDate not supplied

[The role of neuromediators and proteins in genetic and functional organization of animal brain].

It was shown that animals that differ in behavioral characteristics (August and Wistar rats) also differ in neurotransmitter and protein metabolism, which can be considered as tests that adequately reflect the functional condition of the central nervous system. These differences are expressed at the level of both subcortical structures (hippocampus and caudate nucleus) and various morphofunctional types of the sensorimotor cortex neurons (layers III and V). Studies on genetically different animals strains have revealed metabolic features that allow determination of individual behavioral features and estimation of individual brain structures in these processes.

Acetylcholinesterase↗
PubMed1994

Synaptic augmentation by 5-HT at rested Aplysia sensorimotor synapses: independence of action potential prolongation.

Short-term augmentation of synaptic transmission at sensory neuron synapses of Aplysia contributes to behavioral sensitization and is one of the current models for a cellular mechanism of learning. This neuromodulatory process, mediated at least in part by the facilitatory neurotransmitter serotonin (5-HT) acting through cAMP, has been thought to result largely from prolongation of the sensory neuron action potential (AP). The quantitative contribution of AP prolongation to synaptic augmentation was examined using a new culture preparation that is favorable for controlling the voltage at the presynaptic terminals. Preventing AP prolongation by using unvarying voltage-clamp commands in place of triggered APs did not reduce augmentation significantly, and pharmacological prolongation of APs caused by a high concentration of 5-HT led to a negligible increase in the synaptic response. Together with earlier evidence against the involvement of changes in Ca2+ current, these results suggest that synaptic augmentation may result from modulation of steps in the secretory process that lie distal to the flow of ion currents across the nerve terminal membrane.

Action Potentials↗
PubMed2001

Behavioral abnormalities of Zic1 and Zic2 mutant mice: implications as models for human neurological disorders.

Zic1 and Zic2 encode closely related zinc finger proteins expressed in dorsal neural tube and its derivatives. In previous studies, we showed that the homozygous Zic1 null mutation (Zic1-/-) results in cerebellar malformation with severe ataxia and that holoprosencephaly and spina bifida occur in homozygotes for Zic2 knockdown mutation (Zic2kd/kd). Since human ZIC2 haploinsufficiency is a cause of holoprosencephaly, the Zic2kd/kd mice are regarded as an animal model for holoprosencephaly in humans. In this study, the behavioral characteristics of the Zic1 and Zic2 mutant mice were investigated in heterozygotes (Zic1-/+ or Zic2kd/+), and significant abnormalities were found in the hanging, spontaneous locomotor activity, stationary rod (Zic1-/+), acoustic startle response, and prepulse inhibition tests (Zic2kd/+). The abnormalities in the Zic1-/+ mice may be explained in part by the hypotonia caused by hypoplasia of the cerebellar anterior vermis, and these mice are regarded as a model of Joubert syndrome. In contrast, the sensorimotor gating abnormality in the Zic2kd/+ mice may be attributable to the presumed abnormality in the dorsomedial forebrain, which was strongly affected in the Zic2kd/kd mice. Zic2kd/+ mice can serve as a model for diseases involving sensorimotor gating abnormalities, such as schizophrenia.

Animals↗
PubMed1998

Connecting cortical and behavioral dynamics: bimanual coordination.

For the paradigmatic case of bimanual coordination, we review levels of organization of behavioral dynamics and present a description in terms of modes of behavior. We briefly review a recently developed model of spatiotemporal brain activity that is based on short- and long-range connectivity of neural ensembles. This model is specified for the case of motor and sensorimotor units embedded in the neural sheet. Focusing on the cortical left-right symmetry, we derive a bimodal description of the brain activity that is connected to behavioral dynamics. We make predictions of global features of brain dynamics during coordination tasks and test these against experimental magnetoencephalogram (MEG) results. A key feature of our approach is that phenomenological laws at the behavioral level can be connected to a field-theoretical description of cortical dynamics.

Brain↗
PubMed2004

To act or not to act. Neural correlates of executive control of learned motor behavior.

Successful behavior requires contextual modulation of learned "programs", that is, the retrieval or nonretrieval (inhibition) of behavioral elements depending on situative context. Here we report neural correlates of these elementary aspects of behavior as identified with functional magnetic resonance imaging (fMRI). Inhibition of a "ready-to-go" behavioral program was represented in the brain by reduction of net synaptic activity in the cerebro-cerebellar pathway. The metabolic correlate of inhibition was a multifocal (premotor, primary sensorimotor, superior parietal, cingulate cortex, and cerebellum) decrease of the blood oxygenation level-dependent (BOLD) signal to below the resting state (negative BOLD) with a concomitant decrease of motor cortical excitability. The reverse was true for retrieval. We propose that contextual modulation of learned behavioral programs depends on an interplay of focal increases and decreases of neural activity and that the inhibitory changes are reflected by negative BOLD responses in an extended cerebro-cerebellar network of sensorimotor structures.

Adult↗
PubMed1998

Lack of sensitization to the effects of d-amphetamine and apomorphine on sensorimotor gating in rats.

This study assessed whether repeated injections of d-amphetamine or apomorphine could induce sensitization to the disruptive effects of these psychomotor stimulants on sensorimotor gating in rats. In the first experiment, rats were given six pre-exposures to either 2.0 mg/kg d-amphetamine or saline before being tested for the effects of d-amphetamine (0.0, 0.5, 1.0, 2.0 or 4.0 mg/kg, i.p.) on prepulse inhibition of acoustic startle (PPI) and locomotor activity. The tests for PPI confirmed that sensorimotor gating could be disrupted by a high dose of d-amphetamine (4.0 mg/kg). However, comparison of the dose-response curves for the drug and saline pre-exposed groups did not reveal evidence for sensitization to this d-amphetamine effect in drug-pre-exposed rats, despite indications that sensitization had developed to the locomotor stimulant effects of d-amphetamine. A similar pattern of results was obtained in a second experiment that examined the effects of apomorphine (0.0, 0.1, 0.2, 0.4 and 0.8 mg/kg, s.c.) on PPI and locomotion in rats pre-exposed to 2.0 mg/kg of this drug or its vehicle. These findings demonstrate that treatments which induce sensitization to the behavioral activating effects of psychomotor stimulants do not necessarily produce sensitization to the disruptive effects of stimulants on sensorimotor gating. The implications of these results for hypotheses linking sensitization-like processes to the etiology of schizophrenia are discussed.

Animals↗
PubMed2006

Neurobehavioral and immunological consequences of prenatal immune activation in rats. Influence of antipsychotics.

Increasing evidence suggests that pre- or perinatal events that influence the immune system contribute to the development of behavioral or neuropsychiatric disorders. For instance, exposure of pregnant rats to the bacterial endotoxin lipopolysaccharide (LPS) disrupts sensorimotor information processing, as assessed by the prepulse inhibition test (PPI), and also the immune function in adult offspring, which might be of particular relevance as regards schizophrenia. However, the consequences of maternal LPS exposure during pregnancy on synaptic functioning in adult offspring and, more importantly, the therapeutic opportunity to re-establish PPI and immune function have still to be demonstrated. In this work, we analyzed the consequences of prenatal LPS exposure on dopaminergic neurotransmission and presynaptic markers in adult brain areas related to PPI circuitry. In addition, we tested whether oral treatment with the typical antipsychotic drug haloperidol (HAL) could reinstate PPI performances and cytokine serum levels in six-month-old male rats with prenatal LPS exposure. Both sensory information processing deficits and immune anomalies induced by prenatal exposure to LPS were accompanied by changes in dopaminergic neurotransmission and synaptophysin expression. It is important to note that PPI disruption and serum increases in cytokines induced by prenatal LPS exposure were both reversed by HAL. Taken together, these results demonstrate the critical influence of prenatal immune events on the functioning of adult nervous and immune systems, in association with the putative role of the immune system in the development of behavior relevant to schizophrenia.

Analysis of Variance↗
PubMed1994

Neonatal infraorbital nerve damage and the development of eating behavior in the rat.

It has been previously shown that bilateral infraorbital nerve (ION) transection in adult rats has little effect upon body weight regulation or eating behavior. However, in neonatal mouse, unilateral ION cut produces a profound decrease in body weight, beginning around the time of weaning. To help clarify the role of the ION in the development and sensorimotor control of eating solid food in rodents, the present experiment examined the effects of unilateral, neonatal ION transection in rats, upon body weight regulation and post-weaning eating behaviors. Comparison of normal and lesioned groups of rats, up to postnatal day (PND) 61, revealed no significant difference in mean adjusted (for sex) body weight. In addition, no significant differences were detected between the groups on post-weaning (PND 26 to PND 61) measures of mean adjusted (for weight) food intake, responsiveness to food, biting ability or inefficiency of mandibulation. At the end of the experiment, the effectiveness of the lesion was histologically evaluated. A significant 48.5% mean reduction in the cross-sectional area of the ophthalmic-maxillary portion of the trigeminal ganglion was observed on the lesioned side, relative to the intact side. There appears to be a differential influence of unilateral, neonatal ION cut upon eating in rat and mouse.

Afferent Pathways↗
PubMed1983

Recovery of function and basal ganglia [14C]2-deoxyglucose uptake after nigrostriatal injury.

Rats with unilateral 6-hydroxydopamine injections along the mesotelencephalic dopaminergic projection showed a profound impairment in localizing somatosensory stimuli on the contralateral body surface at 3 days postoperatively. Approximately one-half of the affected animals recovered the ability to localize tactile stimuli during 6 weeks postoperatively, whereas the remainder did not. When it occurred, the recovery of sensorimotor function began between the third and fifth day postoperatively and plateaued between days 14 and 21. Unilateral damage to these dopaminergic neurons resulted in hemispheric asymmetries of [14C]2-deoxyglucose incorporation at 3 days postoperatively. For structures that normally receive a dopaminergic innervation (e.g., neostriatum, nucleus accumbens septi, olfactory tubercle) the autoradiographic density of the injured side was decreased relative to the intact hemisphere. For structures that receive striatal inputs (globus pallidus, entopeduncular nucleus, substantia nigra pars reticulata), the autoradiographic density was increased on the side of the injury. This pattern of altered [14C]2-deoxyglucose incorporation was still present at 6 weeks postoperatively in animals that showed no recovery of somatosensory localization during that time. In contrast, rats that did recover showed no hemispheric asymmetries within the anterior neostriatum, globus pallidus, or substantia nigra pars reticulata at 6 weeks postoperatively, and the time course of normalization of metabolic activity in these structures was similar to that for behavioral restoration. These results directly demonstrate the importance of the neostriatum and particular structures efferent to it in the recovery of sensorimotor functions after striatal dopamine depletion. The types of neuronal plasticity within this basal ganglia circuitry responsible for the normalization of [14C]2-deoxyglucose incorporation and behavior are discussed.

Afferent Pathways↗
PubMed2003

The behavioral effects of magnesium therapy on recovery of function following bilateral anterior medial cortex lesions in the rat.

Magnesium (Mg(++)) therapy has been shown to be neuroprotective and to facilitate recovery of motor and sensorimotor function in a variety of animal models of traumatic brain injury. However, few studies have investigated the efficacy of Mg(++) therapy on cognitive impairments following injury. The present study evaluated the ability of magnesium chloride (MgCl(2)) to facilitate recovery of function following bilateral anterior medial cortex lesions (bAMC). Rats received electrolytic bAMC lesions or sham surgery and were then treated with 1 mmol/kg, i.p. MgCl(2), 2 mmol/kg, i.p. MgCl(2), or 1.0 ml/kg, i.p. 0.9% saline. Drug treatment was administered 15 min following injury with subsequent injections administered at 24 and 72 h. Rats were tested on a battery of behavioral tests that measured both cognitive (reference and working memory in the Morris Water Maze (MWM) and spatial delayed matching-to-sample (DMTS)) and sensorimotor performance (bilateral tactile adhesive removal). The results indicated that bAMC lesions produced significant cognitive impairments in reference memory and working memory in the MWM, DMTS and sensorimotor impairments compared to shams. Mg(++) therapy exhibited a dose-dependent effect in facilitating recovery of function. Administration of 2mmol of MgCl(2) significantly improved performance on the bilateral adhesive tactile removal test, DMTS and working memory tests. The 1 mmol dose of MgCl(2) reduced the initial deficit on the tactile adhesive removal test and reduced the working memory impairment on the second day of testing. These results suggest Mg(++) therapy improves cognitive performance following injury in a dose-dependent manner.

Analysis of Variance↗
PubMed2004

Abilities in tactile discrimination of textures in adult rats exposed to enriched or impoverished environments.

In previous studies, we have shown that housing in enriched environment for about 3 months after weaning improved the topographic organization and decreased the size of the receptive fields (RFs) located on the glabrous skin surfaces in the forepaw maps of the primary somatosensory cortex (SI) in rats [Exp. Brain Res. 121 (1998) 191]. In contrast, housing in impoverished environment induced a degradation of the SI forepaw representation, characterized by topographic disruptions, a reduction of the cutaneous forepaw area and an enlargement of the glabrous RFs [Exp. Brain Res. 129 (1999) 518]. Based on these two studies, we postulated that these representational alterations could underlie changes in haptic perception. Therefore, the present study was aimed at determining the influence of housing conditions on the rat's abilities in tactile texture discrimination. After a 2-month exposure to enriched or impoverished environments, rats were trained to perform a discrimination task during locomotion on floorboards of different roughness. At the end of every daily behavioral session, rats were replaced in their respective housing environment. Rats had to discriminate homogeneous (low roughness) from heterogeneous floorboards (combination of two different roughness levels). To determine the maximum performance in texture discrimination, the roughness contrast of the heterogeneous texture was gradually reduced, so that homogeneous and heterogeneous floorboards became harder to differentiate. We found that the enriched rats learned the first steps of the behavioral task faster than the impoverished rats, whereas both groups exhibited similar performances in texture discrimination. An individual "predilection" for either homogeneous or heterogeneous floorboards, presumably reflecting a behavioral strategy, seemed to account for the absence of differences in haptic discrimination between groups. The sensory experience depending on the rewarded texture discrimination task seems to have a greater influence on individual texture discrimination abilities than the sensorimotor experience related to housing conditions.

Analysis of Variance↗
PubMedDate not supplied

On the nature and consequences of early loss.

OBJECTIVE: To describe how an animal model system can be used to explore basic questions about the nature of loss and the effects of early loss on later vulnerability to disease. METHOD: The physiological and behavioral responses of infant rats to separation from their mothers are first described and then analyzed experimentally into component mechanisms. RESULTS: These studies have revealed an extensive layer of processes underlying the psychological constructs generally used to understand the response to loss. Hidden within the observable interactions of parent and offspring, we found a number of discrete sensorimotor, thermal, and nutrient-based events that have unexpected long-term regulatory effects on specific components of infant physiology and behavior. Release from all of these inhibitory and excitatory regulators together during maternal separation constitutes a novel mechanism by which the experience of loss can be translated into a complex patterned response. Evidence for early regulatory processes has also been found in monkey and human mother-infant interactions. Here they may well constitute the building blocks from which attachment and object representations develop. We and others have found long-term effects of loss, and of selective replacement of regulators, on behavioral development and on later vulnerability to disease. CONCLUSIONS: The results give us a new understanding of early attachment as a developmental force and of human grief as a risk to health.

Age Factors↗
PubMedDate not supplied

Prenatal heroin exposure. Effects on development, acoustic startle response, and locomotion in weanling rats.

The purpose of this study was to investigate the effects of prenatal heroin exposure on the offspring in postnatal behavioral development. Pregnant Sprague-Dawley rats were injected daily (s.c.) with 10mg/kg of heroin from gestational day 8 to 20. The control dam received saline injections and the pair-fed dam received saline and was yoked to a weight-matched heroin-treated dam. Litters were culled to eight to ten pups and weighed at postnatal day (PND) 1, 8, 15, and 22. Acoustic prepulse inhibition and habituation were parameters used for evaluating the sensorimotor gating and simple form of learning respectively. Locomotor activity and rearing were assessed using the photobeam activity system. All behavioral tests were performed on the offspring at PND 21 to 23. Results showed that heroin treatment significantly reduced maternal food intake, water consumption, and weight gain. Both heroin-exposed and pair-fed groups showed a marked reduction in birth weight in both male and female pups when compared with controls; however the postnatal weight gain in heroin-exposed pups was significantly lower than the pair-fed group by 3 weeks postnatally, particularly in the female pups. These female pups also showed a significant increase in ambulation and rearing when compared to the pair-fed pups. The habituation rate in both types of behavioral tests was also decreased in these female pups as compared to control and pair-fed groups. The present study indicated that prenatal heroin exposure could result in a marked retardation of postnatal development and learning. These effects are sex related.

Acoustic Stimulation↗
PubMed1989

Dissociation between biochemical and behavioral recovery in MPTP-treated mice.

Injection of a low dose of haloperidol, that has no obvious behavioral effects in normal mice, produces akinesia, catalepsy, and somatosensory neglect in MPTP-treated mice. These neuroleptic-induced sensorimotor impairments are exhibited soon after MPTP treatments and coincide with a decrease in both striatal DA and DOPAC levels. DA and DOPAC content gradually return to near-control levels over a 3-5 month period. Interestingly, while the haloperidol-induced somatosensory deficits declined in parallel with the rise in DA and DOPAC levels, the motor deficits persisted for up to 5 months after MPTP administration. These data suggest subtle differences in the neurochemical mediation of these behaviors and that the persistence of neuronal impairments may not necessarily be revealed by near-normal transmitter levels.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗