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PubMed2003

[Coordination of rhythmic movements: a dynamic approach].

The dynamic theoretic approach regards motor coordination not as a supervised sequential planning but as a spontaneous self-organized process. Owing only to transitory local interactions between sensorimotor areas (without any pre-existing motor program) a coherent collective neural behavior should emerge and underlie voluntary rhythmic synergies (in our example, bimanual on-phase and out-of-phase movements). Therefore this collective behavior should govern and reflect functional constraints slaving independent movement of effectors in a global synergy. In order to understand such a process, it proves necessary to study movement from the effector level to the cerebral level, by experimentally ascertaining: (1) the set of all possible synergies for a given movement, (2) the order parameters and the control parameters, (3) the task-dependent laws for the movement of each effector, and (4) the general and slaving laws responsible for the synergy itself which must be qualitatively similar to those applying to cerebral collective behavior. This paper tries to introduce experimental results for bimanual rhythmic movements as well as the main theoretic tools issued from dynamics of dissipative systems located far from equilibrium (order parameter, multistability, bifurcation, fluctuation...) used to grasp the self-organized nature of motor synergies.

Humans↗
PubMed2004

Effect of intention and visual fixation disengagement on prosaccades in Parkinson's disease patients.

In a previous study, we postulated a divergence in reflexive versus voluntary saccade behavior in Parkinson's disease (PD) patients and hypothesized a fronto-striatal dysfunction. The voluntary saccade tasks included antisaccades (AS) and remembered saccades (RemS). However, multiple cognitive processes are involved in AS and RemS and the procedures lack a visual target. The present study had two main objectives. Firstly, we wanted to extend our previous findings of disturbed AS and RemS to other intentional (endogenous, "voluntary") saccades but now with a visible target. Therefore, an intentional prosaccade (IpS) task was used. Secondly, we investigated whether there is a different saccade behavior in PD patients and controls in conditions where the central fixation stimulus is extinguished shortly before the onset of the peripheral target (the so called gap condition) to assess the role of disengagement of visual fixation. With respect to the first objective, the present study found a clear dissociation between the performances of PD patients on reflexive saccade (RS) versus IpS tasks. Patients did not differ from controls in latency or error rate of RS. However, in the IpS task, latency was longer and error rate was higher in PD patients. Thus, the present study provides evidence that PD patients are deficient in intentional saccade tasks independent from the fact whether a target is visible or not. As to the second objective, saccades of PD patients did show a shorter latency in the gap than in the no gap condition. This suggests that the gap effect is not dominantly dependent on nigro-collicular neuronal circuits that are affected in PD. In the patients, the gap effect was reliable in the RS task, but not in the IpS condition. These discordant gap findings might suggest modulation of selected neuronal circuits involved in early sensorimotor processing. The present findings do not to support the hypothesis that impaired saccade behavior in PD patients is merely dependent on the presence or the absence of visual fixation and suggests a higher order psychomotor dysfunction, presumably of intentional nature. The dorsolateral prefrontal cortex might correspond to the premotor cognitive dysfunction site. However, an additional involvement of the frontal eye field can not be excluded from the present study.

Aged↗
PubMed2000

Ontogeny of phencyclidine and apomorphine-induced startle gating deficits in rats.

NMDA antagonists and dopamine (DA) agonists produce neuropathological and/or behavioral changes in rats that may model specific abnormalities in schizophrenia patients. In adult rats, NMDA antagonists and DA agonists disrupt sensorimotor gating-measured by prepulse inhibition (PPI)-modeling PPI deficits in schizophrenia patients. In addition, high doses of NMDA antagonists produce limbic system pathology that may model neuropathology in schizophrenia patients. We examined these behavioral and neuropathological models across development in rats. Both the NMDA antagonist phencyclidine (PCP) and the DA agonist apomorphine disrupted PPI in 16 day pups, demonstrating early developmental functionality in substrates regulating these drug effects on PPI. In contrast, PCP neurotoxicity was evident only in adult rats. Brain mechanisms responsible for the PCP disruption of PPI, and PCP-induced neurotoxicity, are dissociable across development.

Age Factors↗
PubMed1992

Subcortical deterioration after cortical damage: effects of diazepam and relation to recovery of function.

Agents which enhance the activity of gamma-aminobutyric acid (GABA) can severely disrupt behavioral recovery in rats following damage to the neocortex if delivered during a sensitive postoperative period. The mechanisms of this disruption have not been found. It has been suggested previously that the ipsilateral striatum and related structures may be transiently disabled after cortical lesions and that diazepam may interfere with restoration of function in these areas. In the present experiment, the subcortical anatomical effects of chronic (3 weeks) administration of diazepam, an indirect GABAergic agonist, were assessed following unilateral lesions of the anteromedial cortex (AMC) or the sensorimotor cortex (SMC) in rats. Atrophic and degenerative changes were examined in the striatum, substantia nigra and thalamus. Following either AMC or SMC lesions, there was a reduction in the size of the ipsilateral striatum and thalamus and a loss of neurons in the ipsilateral substantia nigra pars reticulata (SNr). After AMC lesions, striatal atrophy and neuron loss in the SNr were increased by the diazepam regimen relative to vehicle-treated controls. In addition, diazepam interfered with the behavioral recovery from somatic-sensorimotor asymmetries in AMC-lesioned rats. After SMC lesions, the sites of striatal and thalamic atrophy were different from that observed after AMC lesions, and the extent of atrophy and neuron loss was not exaggerated by diazepam treatment. Consistent with these data, diazepam did not significantly affect recovery from SMC lesions. These findings suggest that the long-term disruptive effects of diazepam on recovery of function after AMC lesions may be related to an augmentation of lesion-induced degeneration.

Animals↗
PubMed2005

Kappa opioid receptor activation disrupts prepulse inhibition of the acoustic startle in rats.

BACKGROUND: Compelling evidence indicates that kappa opioid receptor (KOR) agonists produce perceptual distortions in animals and humans, yet the mechanism of action and clinical relevance of such effects remain unclear. Since abnormalities in preattentional functions and informational processing are hypothesized to underlie psychotic disorders, the present study has been designed to assess the role of KOR on sensorimotor gating. METHODS: The effects of the selective KOR agonist U50488 were evaluated on the behavioral paradigm of prepulse inhibition (PPI) of the acoustic startle reflex (ASR). RESULTS: U50488 (1.25, 2.5, and 5 mg/kg, subcutaneous [SC]) induced a dose-dependent reduction of PPI, which was efficiently prevented by the selective KOR antagonist norbinaltorphimine (nor-BNI, 10 mg/kg, SC), as well as by the atypical antipsychotic clozapine (5, 8 mg/kg, intraperitoneal [IP]) but not by the typical antipsychotic haloperidol (.1, .5 mg/kg, IP). Conversely, nor-BNI (10 mg/kg, SC) failed to reverse the PPI disruption mediated by both apomorphine (.25 mg/kg, SC) and dizocilpine (.1 mg/kg, SC). CONCLUSIONS: Our results support a pivotal role of KOR in the regulation of preattentional functions and sensorimotor gating, pointing to these receptors as a possible neurobiological substrate especially relevant to the clusters of psychosis unresponsive to typical antipsychotics.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1998

Using an animal model of deficient sensorimotor gating to study the pathophysiology and new treatments of schizophrenia.

Certain animal models can greatly enhance our understanding of the neurobiology of schizophrenia and can be used to predict the antipsychotic activity of compounds. Prepulse inhibition (PPI), the reduction in startle produced by a prepulse stimulus, is diminished in schizophrenia patients. Theoretically, deficient PPI in schizophrenia patients is a measure of the loss of sensorimotor gating that may lead to sensory flooding and cognitive fragmentation. In rats, PPI is disrupted by systemic administration of dopamine agonists, serotonin agonists, or glutamate antagonists and by a variety of surgical or pharmacological manipulations of neural circuitry linking the limbic cortex, striatum, pallidum, and pontine reticular formation. This article describes several different ways the loss of PPI in rats can be used as a model for studying the pathophysiology and neurobiology of impaired sensorimotor gating in schizophrenia patients and for predicting antipsychotic activity in novel compounds. First, new experimental strategies may be used to distinguish behavioral profiles of "typical" versus "atypical" antipsychotics. Second, this paradigm can be used to study the effects of early developmental insults--including neonatal lesions and isolated rearing--on the adult emergence of deficient sensorimotor gating. Third, using different animal strains and species, as well as gene "knockout" strategies, greatly increases our ability to understand specific genetic or receptor contributions to the regulation of deficient PPI. Each of these uses of the PPI paradigm is enhanced by studies of the basic brain substrates that regulate PPI in rats and by the increasingly sophisticated assessments of PPI and related measures in schizophrenia spectrum patients.

Animals↗
PubMed1982

Study of the neural basis of circling behavior induced by L-dopa in lesioned entopeduncular cats.

Experiments were carried out in cats bearing unilateral electrolytic lesion of the entopeduncular nucleus. The animals were tested for circling 1-2 weeks after surgery. Postoperatively the cats displayed transient spontaneous ipsiversive turning. The administration i.p. of L-DOPA (80 mg/kg) plus CarbiDOPA (30 mg/kg), suspended in 10% Tween 80, induced rotational behavior toward the lesioned side. This effect began about 26 min after drug administration and reached its maximum 40-110 min after the injection. Electrolytic lesions placed in the superior colliculus, strionigral pathway or pedunculopontine nucleus, contralateral to the lesioned entopeduncular nucleus did not modify the circling behavior induced by L-DOPA. Similar results were observed following unilateral lesion of the sensorimotor cortex or the VL thalamic nucleus. These results suggest that the circus movements induced by L-DOPA, in animals with unilateral lesion of the entopeduncular nucleus, is not mediated by the classic outflow of the striopallidal system.

Animals↗
PubMed1985

Comparative electrophysiology of pyramidal and sparsely spiny stellate neurons of the neocortex.

Slices of sensorimotor and anterior cingulate cortex from guinea pigs were maintained in vitro and bathed in a normal physiological medium. Electrophysiological properties of neurons were assessed with intracellular recording techniques. Some neurons were identified morphologically by intracellular injection of the fluorescent dye Lucifer yellow CH. Three distinct neuronal classes of electrophysiological behavior were observed; these were termed regular spiking, bursting, and fast spiking. The physiological properties of neurons from sensorimotor and anterior cingulate areas did not differ significantly. Regular-spiking cells were characterized by action potentials with a mean duration of 0.80 ms at one-half amplitude, a ratio of maximum rate of spike rise to maximum rate of fall of 4.12, and a prominent afterhyperpolarization following a train of spikes. The primary slope of initial spike frequency versus injected current intensity was 241 Hz/nA. During prolonged suprathreshold current pulses the frequency of firing adapted strongly. When local synaptic pathways were activated, all cells were transiently excited and then strongly inhibited. Bursting cells were distinguished by their ability to generate endogenous, all-or-none bursts of three to five action potentials. Their properties were otherwise very similar to regular-spiking cells. The ability to generate a burst was eliminated when the membrane was depolarized to near the firing threshold with tonic current. By contrast, hyperpolarization of regular-spiking (i.e., nonbursting) cells did not uncover latent bursting tendencies. The action potentials of fast-spiking cells were much briefer (mean of 0.32 ms) than those of the other cell types.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1997

Assessment of sensorimotor neglect after occlusion of the middle cerebral artery in the rat.

Evaluating the efficacy of neuroprotective drugs in rat models of focal cerebral ischemia has involved histological and behavioral batteries to examine treatment outcome. However, the behavioral tests used to date provide little insight into the nature of the neurological impairments. To provide an analysis of a possible "neglect" syndrome after occlusion of the middle cerebral artery, M. I. Posner's (1980) visual attentional paradigm was adapted for use in the rat. A paw-reaching task and a test of somatosensory "neglect" also were used to assess forelimb sensorimotor function. The lesion group displayed unilateral deficits; however, there was no evidence of attentional dysfunction. Results are consistent with the conclusion that the behavioral deficits identified arise from a somatosensory deficit rather than hemineglect due to dysfunctional spatial attention.

Animals↗
PubMed1993

Physiological correlates of abnormal behaviors in magnesium-deficient rats.

In order to elucidate the mechanism of behavioral alterations in magnesium-deficient rats, changes in the electroencephalogram (EEG) and electrocardiogram (ECG) were studied during auditory stimulation and correlated with the behavioral alterations. Weanling rats were fed either a Mg-deficient diet or a control synthetic diet for 2-3 weeks before the experiment. EEGs were recorded from the hippocampus and the sensorimotor and auditory cortices, and ECGs with a telemetry system. White noise with an intensity of 100 dB was given continuously to induce behavioral changes. The Mg-deficient rats developed consistent and graded behavioral changes in response to the stimulation, showing running-jumping behavior (stage 1), followed by tonic limb convulsion (stage 2) and finally by falling down on the floor (stage 3). The EEGs also showed consistent changes with spike activity, initiating in the hippocampus (stage 2) and then spreading to the neocortices bilaterally (stage 3). These findings indicate that the behavioral changes induced by auditory stimulation in the Mg-deficient rats are due to seizures arising in deeper brain structures, particularly in the limbic system, and projecting secondarily to the neocortices. The ECG changes, mainly consisting of marked bradyarrhythmia, occurred as early as the appearance of the EEG spikes, indicating that they were also related to the seizure. We conclude therefore that Mg deficiency in rats causes increased excitability of the central nervous system, resulting in seizures possibly originated in the limbic system, later developing secondary generalization, and also causing cardiac dysfunctions.

Acoustic Stimulation↗
PubMedDate not supplied

Life-long diet restriction failed to retard cognitive aging in Fischer-344 rats.

Although the beneficial effects of diet restriction on longevity and the retardation of many somatic age-related processes are well established, the answer to the question of whether anti-aging effects of diet restriction extend to the brain and cognitive function remains unclear. In the present study, the effects of long-term dietary restriction (60% of ad-libitum calories) on an age-related alteration of memory and sensorimotor function have been investigated in Fischer 344 male rats at four different ages: 6 months, 12 months, 18 months, and 24 months. A major drop in reference memory of DR and AL rats occurred at the age of 18 months. The performance deficits in working memory tasks were observed in both diet groups at the age of 24 months. These results indicate that diet restriction failed to provide protection against age-related deficits in memory. Although DR rats outperformed AL rats in sensorimotor tasks throughout the life-span, the slope of the declining function in DR rats paralleled those of AL rats, suggesting that diet restriction failed to alter the rate of aging in sensorimotor performance, as well.

Aging↗
PubMed1997

Prior non-spatial pretraining eliminates sensorimotor disturbances and impairments in water maze learning caused by diazepam.

Diazepam has been reported to impair spatial learning in the water maze. This experiment reexamined this topic using control groups that had first been non-spatially pretrained to familiarize them with the general behavioral strategies required in the water maze task. Naive rats given diazepam (0.5, 3.0, 6.0 mg/kg, IP) displayed dose-related maze acquisition impairments and sensorimotor disturbances (swimming in the periphery of the pool, deflecting off or swimming over the hidden platform, jumping off the platform when placed there after a trial, ataxia on a narrow wooden beam). The sensorimotor disturbances interfered with the acquisition of information about the spatial location of the platform, occurred in the absence of impairments in a subsequent visible platform task or swim speed, and correlated strongly with measures of acquisition. In contrast, the non-spatially pretrained groups did not exhibit sensorimotor disturbances in the water maze and acquired the maze task as rapidly under diazepam as control rats. The non-spatially pretrained groups continued to display diazepam-induced sensorimotor disturbances (ataxia) in a novel beam walking task. CGS8216 (10.0 or 20.0 mg/kg), a benzodiazepine receptor antagonist, attenuated the effect of 3.0 or 6.0 mg/kg diazepam in naive rats, suggesting that the effects of diazepam were mediated by benzodiazepine receptors. Occupancy of benzodiazepine receptors by diazepam does not prevent robust spatial learning in the water maze.

Animals↗
PubMed2002

A transgenic model of comorbid Tourette's syndrome and obsessive-compulsive disorder circuitry.

The tic disorder Tourette's Syndrome (TS) and obsessive-compulsive disorder (OCD) are comorbid behavioral disorders, suggesting a shared but still unknown neuronal basis. To 'circuit-test' such behaviors, we previously engineered transgenic mice expressing a neuropotentiating protein (cholera toxin A1 subunit) within a cortical-limbic subset of dopamine D1-receptor expressing (D1+) neurons known to trigger glutamatergic excitation of orbitofrontal, sensorimotor, limbic and efferent striatal circuits thought to be hyperactive or affected in OCD and TS. These mice exhibited OCD-like behaviors including generalized behavioral perseveration and compulsion-like leaping and grooming-associated pulling and biting of skin and hair. We now report that these OCD-like mice, like humans, also exhibit comorbid TS-like behaviors, including juvenile-onset tics; increased tic number, complexity and flurries; increased tic severity in males; voluntary tic suppression; and tic responsiveness to a non-cataleptic TS+OCD drug therapy (clonidine, 0.01 mg kg(-1)). These data suggest that hormonal gender differences, apart from the influence of genetic or autoimmune etiologic factors, may be sufficient to aggravate tic severity in human TS males compared to TS females. These data also proffer a precise neuronal basis for TS+OCD, wherein tics and primary compulsions or obsessions are evoked by hyperactivity of various cortical-limbic projection neurons' glutamatergic output to efferent targets like the striatum. The 'Cortical-limbic Glutamatergic Neuron' (CGN) neuronal circuit model merges formerly opposed neurotransmitter models of TS and OCD, and is consistent with new clinical reports of increased cortical hyperactivity, striatal glutamate and striatal inhibitory D2 receptors, and reduced striatal responsiveness, in these disorders.

Analgesics↗
PubMed2002

Relationship between the development of autoimmunity and sensorimotor gating in MRL-lpr mice with reduced IL-2 production.

MRL-lpr mice develop systemic lupus-like autoimmune disease associated with changes in emotional reactivity and spatial learning and memory. Although the major immunological deficit in MRL-lpr mice is uncontrolled lymphoproliferation associated with a Fas gene mutation, these mice have a marked deficit in interleukin-2 (IL-2) production which, when treated, can prevent the development of autoimmune disease. Moreover, both MRL-lpr and IL-2 knockout mice manifest alterations in hippocampal cytoarchitecture and cognitive behavior. We found previously that IL-2 knockout mice have alterations in prepulse inhibition (PPI), a measure of sensorimotor gating. Thus, the present study sought to test the hypothesis that that PPI would be altered in MRL-lpr mice. Compared to MRL(+/+) control mice, MRL-lpr mice exhibited different patterns of PPI during development. Whereas 7 and 12-week MRL-lpr mice with evidence of autoimmune disease (the onset and early stages, respectively) showed increased PPI, 5 week predisease MRL-lpr mice did not. MRL-lpr mice also exhibited increased acoustic startle reactivity that was independent of autoimmune disease. These behavioral changes were not associated with increased brain expression of the proinflammatory cytokines genes, IL-1alpha and IL-6, CD3, or c-myc-associated apoptosis.

Acoustic Stimulation↗
PubMed2003

[Compulsive phenomena in children with tic disorder and attention deficit-hyperactive disorder].

Tic disorders (TD), obsessive-compulsive disorders (OCD) and attention-deficit/hyperactivity disorder (ADHD) are often associated with deficits of impulse control and aggressive behavior. Tic disorders and OCD are closely related on epidemiological, psychopathological and neurobiological levels, whereas ADHD and OCD phenomena seem to be at opposite poles. Research evidence on the clinical significance of associated obsessive-compulsive behavior is reviewed and linked to our own new data. Thus the analyses of a worldwide database on Tourette's Syndrome (TS) (N = 4,833) showed that that the associated symptomatology of the OCD spectrum has to emphasized. In further investigations, premonitory sensorimotor phenomena reminiscent of OCD were more frequent in children with tic disorders as they grew older. Obsessive-compulsive behavior concomitant with TS was particularly associated with impulsive and aggressive behavior, as well as with depression and anxiety. The data suggest a reduced serotonergic transmission. Self-reports by children with ADHD, as opposed to those by their parents, mentioned a significantly higher quantitative degree of OC phenomena than those by children with TS. These findings suggest that OC symptoms in children with ADHD have so far been neglected in assessments by others. In summary, a complex psychopathological pattern of tic, OC behavior, impulsivity and internalizing symptomatology emerges that requires discriminating assessment and treatment.

Adolescent↗
PubMed2003

Neural correlates of decision processes: neural and mental chronometry.

Recent studies aim to explain the duration and variability of behavioral reaction time in terms of neural processes. The time taken to make choices is occupied by at least two processes. Neurons in sensorimotor structures accumulate evidence that leads to alternative categorizations, while other neurons within these structures prepare and initiate overt responses. These distinct stages of stimulus encoding and response preparation support variable but flexible behavior.

Animals↗
PubMed2000

Varied duration of congenital hypothyroidism potentiates perseveration in a response alternation discrimination task.

The behavior of five groups of rats (seven rats per group) made hypothyroid for varying lengths of time and one group of seven normal control rats was assessed under forced alternation fixed-ratio (FR1, FR3, FR5 and FR10), alternating lever cyclic-ratio (ALCR) and progressive-ratio (PR3) schedules of reinforcement. Hypothyroidism was produced by adding methimazole (MMI) to the drinking water of pregnant dams from embryonic day E16 to postnatal day P25. Four groups were given replacement thyroxine (T4) injections beginning at specific time points (P1, P7, P13, and P19). There were no differences in behavioral performance between control and experimental groups under the FR schedule, which indicates that the animals' sensorimotor abilities were intact. Under the forced ALCR schedule, all groups reached criteria similarly. However, under the choice lever ALCR schedule, control animals and those which received T4 replacement from early on (P1, P7, P13 groups) performed well and all had reached criteria by 11 sessions. In contrast, animals which did not receive any T4 replacement or received it late (P19 group) took longer to reach criteria and 5/14 animals had not reached criteria at all by 20 sessions. This deterioration in performance was paralleled by an increase in perseverative behavior as evidenced by an increased frequency of pressing the wrong lever when alternation of lever was required. This suggests that congenital hypothyroidism results in increased perseveration leading to a decrease in learning when a discrimination between correct and incorrect operanda is made available.

Animals↗
PubMed1994

The involvement of nucleus accumbens dopamine in appetitive and aversive motivation.

In recent years, considerable emphasis has been placed upon the putative role of nucleus accumbens dopamine systems in appetitive motivation and positive reinforcement. However, considerable evidence indicates that brain dopamine in general, and nucleus accumbens dopamine in particular, is involved in aspects of aversive motivation. Administration of dopamine antagonists or localized interference with nucleus accumbens dopamine systems has been shown to disrupt active avoidance behavior. In addition, accumbens dopamine release and metabolism is activated by a wide variety of stressful conditions. A review of the literature indicates that there are substantial similarities between the characteristics of dopaminergic involvement in appetitive and aversive motivation. There is conflicting evidence about the role of dopamine in emotion, and little evidence to suggest that the profound and consistent changes in instrumental behavior produced by interference with DA systems are due to direct dopaminergic mediation of positive affective responses such as hedonia. It is suggested that nucleus accumbens dopamine is involved in aspects of sensorimotor functions that are involved in both appetitive and aversive motivation.

Animals↗