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Results for “sensorimotor behavior”

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At least 1,099 records · Page 61Linked to original sources
PubMed2003

Effect of levodopa chronic administration on behavioral changes and fos expression in basal ganglia in rat model of PD.

To study behavioral character and changes of neuronal activity in the basal ganglia of rat model of levodopa-induced dyskinesia, unilateral 6-hydroxydopamine lesioned rat model of Parkinson disease (PD) was treated with levodopa/benserazide twice daily for 4 weeks and the behavior observed on the 1st, 3rd, 4th, 7th, 9th, 10th, 14th, 21st and 28th day. The animals were sacrificed and immunohistochemical technique was used to measure the changes of Fos expression in the caudate putamen (CPU), globus pallidus (GP) and sensorimotor area of cerebral cortex 2 h after the last treatment. The results showed that pulsatile treatment with a subthreshold dose of levodopa gradually induced abnormal involuntary movement (AIM), including stereotypy (limb dyskinesia, axial dystonia and masticatory dyskinesia) towards the side contralateral to the dopamine-denervated striatum and increased contraversive rotation. The motor pattern of each subtype was highly stereotypic across individual rats, and the proportion of each subtype was not consistent among individual rats. Fos positive nuclei in the CPU and GP were increased by levodopa acute administration, and more remarkably in the CPU, but not in the cerebral cortex. After repeated levodopa treatment. Fos positive nuclei were reduced remarkably in the CPU, but were increased in the GP and cerebral cortex. It was concluded that the neural mechanisms underlying levodopa induced AIM in rat model of PD was very similar to those seen in levodopa-induced dyskinesia (LID) in PD patients and MPTP-lesioned monkeys, and increased striatopallidal neuronal activity might be involved in occurrence of LID.

Animals↗
PubMed1993

The distal hindlimb musculature of the cat: interanimal variability of locomotor activity and cutaneous reflexes.

During stereotyped behaviors such as locomotion, patterns of muscle recruitment are usually quite consistent from animal to animal, even in the face of many surgical and pharmacological reductions. However, as studies of musculoskeletal structure, neuromuscular architecture, and sensorimotor circuitry become more detailed, it is important to ask whether there is some level of organization at which individual differences begin to dominate. This study concentrated on the small muscles of the foot and ankle, using standardized methods that consistently record stereotypical electromyographic activity from prime mover muscles and that permit well-calibrated stimulation of cutaneous nerves to elicit reflexes during treadmill locomotion. Some muscles (particularly the main ankle extensors, triceps surae, and plantaris) had stereotyped activity during both unperturbed locomotion and reflex responses. Others had stereotyped activity during locomotion but variable reflex patterns among animals (tibialis anterior, extensor digitorum longus, flexor hallucis longus, and peroneus brevis). Still others had variable locomotor activity but reflexes that were consistent (flexor digitorum longus) or variable for only peroneal nerve stimulation (peroneus longus), only plantar nerve stimulation (peroneus tertius), or the two (flexor digitorum brevis). Among muscles with interanimal variability, there seemed to be no particular correlation between locomotor and reflexive recruitment in a given animal. This functional heterogeneity is discussed in terms of the development of locomotor and reflex programs and in the context of structural heterogeneity of some of these muscles that is described in the companion paper.

Animals↗
PubMed2002

Disruption of prepulse inhibition of startle reflex in a neurodevelopmental model of schizophrenia: reversal by clozapine, olanzapine and risperidone but not by haloperidol.

Neonatal ventral hippocampal (NVH) lesions in rats have been shown to induce behavioral abnormalities at adulthood thought to simulate some aspects of positive, negative and cognitive deficits classically observed in schizophrenic patients. Such lesions induced a post-pubertal emergence of prepulse inhibition deficits reminiscent of the sensorimotor gating deficits observed in a large majority of schizophrenic patients. Here we have investigated the capacity of typical and atypical antipsychotics to reverse PPI deficits seen in NVH-lesioned rats. We show that three atypical antipsychotics (clozapine, olanzapine and risperidone) were able to reverse lesion-induced PPI deficits, in contrast to haloperidol, a classical neuroleptic. These results show that the NVH lesion model seems to be endowed with a fair predictive validity as, like in schizophrenic patients, PPI deficits in lesioned animals were reversed by atypical antipsychotics but not by the typical neuroleptic haloperidol.

Animals↗
PubMed1995

Kindling of the interpeduncular nucleus and its influence on subsequent amygdala kindling in rats.

We examined the effect of interpeduncular nucleus (IPN) kindling on subsequent amygdala (AM) kindling in rats (n = 9). Eleven to 15 daily IPN stimulations at an afterdischarge (AD)-inducing threshold (400-1000 microA, biphasic sine waves, 1-3 s) produced progressive AD growth (9 of 9 rats) and recruitment of behavioral seizures (7 of 9 rats). The final form of the latter was generalized tonic-clonic seizures with or without a limbic seizure component. The latter was associated with ictal involvement of AM and sensorimotor cortex. Subsequent AM kindling resulted not only in more rapid kindling, but also in tonic seizure associated with a protracted loss of postural control (5-20 s) not observed in animals undergoing AM kindling without previous IPN kindling (n = 5). These findings indicate that the IPN can be kindled and that subsequent AM kindling utilizes the proconvulsant neuroplastic changes that have been already established by IPN kindling.

Amygdala↗
PubMed2005

Analysis of 5-HT-induced short-term facilitation at Aplysia sensorimotor synapse during bursts: increased synaptic gain that does not require ERK activation.

The 5-HT-induced synaptic plasticity of Aplysia sensorimotor synapses has typically been probed by firing a single presynaptic spike. In this study, 5-HT-induced synaptic plasticity was probed with brief bursts of spikes (10 Hz, 1 s), which are more behaviorally relevant stimuli. Because such bursts provide a greater challenge to the release machinery than single spikes, their use may reveal additional aspects of synaptic modulation, and, in particular, the role of extracellular signal-regulated protein kinase (ERK), which has recently been implicated in several examples of short- and long-term synaptic plasticity. Excitatory postsynaptic currents (EPSCs) were characterized by their amplitudes. In addition, two kinetic measurements, time to peak and decay time constant, were determined for the initial and last EPSCs of each burst. Application of 5-HT produced a uniform increase in gain by facilitating each EPSC elicited during a burst of spikes without affecting the kinetics of the initial or last EPSC. These data suggest that short-term facilitation during a burst is mediated largely by processes such as those that affect the size of the releasable pool or rate of vesicle mobilization rather than by an increase in the duration of the presynaptic action potential. An ERK cascade inhibitor (U0126) had no effect on the 5-HT-mediated facilitation of either the initial EPSC or EPSCs elicited late in the burst.

Animals↗
PubMed1991

Autistic and dysphasic children. I: Clinical characteristics.

Autism and dysphasia are behaviorally defined disorders of higher cerebral function which in preschool children share the common core symptom of impairment of language. In this study we describe the clinical characteristics of 314 autistic and 237 dysphasic nonautistic children evaluated by one child neurologist. There was no significant difference between autistic and dysphasic children in gestational age, birth weight, or prevalence of associated medical disorders, all of which were infrequent, although a positive history of resuscitation or ventilatory support was more common in dysphasic than autistic children (P = .03). As a group autistic children are more likely than dysphasic children to have language subtypes affecting central processing and formulation, a family history of psychiatric disorders and autism, and a history of regression of language and behavior. After excluding 12 girls with autistic symptoms who met the clinical criteria for Rett syndrome, we found that there was no significant difference in the number of autistic and dysphasic children with an abnormal sensorimotor examination. Girls with autism were more likely than boys to have severe mental deficiency (38% of autistic girls vs 23% of boys) (P = 0.012) and a motor deficit (27% vs 11%) (P = .0009).

Aphasia↗
PubMed1987

An hypothesis about redundancy and reliability in the brains of higher species: analogies with genes, internal organs, and engineering systems.

The phenomena of behavioral resistance to massive brain damage and behavioral recovery from brain damage suggest there is redundancy in neural tissue. This paper uses basic concepts from probability theory and reliability engineering, as a first step toward more rigorously establishing the plausibility of the redundancy hypothesis. Exponential effects in the relevant formulas lead to results that are intuitively surprising. Thus, within a broad range of parametric assumptions related to lifespan and number of neurons or neural subsystems, it appears that the human brain may be at least twice as large as it would have to be for short-term survival. Simple reliability models suggest that redundancies are in parallel connections of smallest subsystems, such as individual neurons. Other implications of the basic formulas concern the relation between backed-up subsystem reliability and lifetime usage frequency for each subsystem, and the evolution of approximately equal allocation of lifetime reliability among components of a system. In addition, the paper briefly reviews more complex reliability engineering approaches. Redundancy as a reason for neural mass action is compared to other theoretical reasons for mass action in sensorimotor function and learning. Relationships of the present hypothesis to other theories of recovery from brain damage and to theories of regressive trophic phenomena in ontogeny are briefly discussed; it is suggested that as stages of ontogeny progress, both redundancy and flexibility in simpler behavioral functions are traded away for a larger, more differentiated repertoire of complex functions and memories.

Animals↗
PubMed2006

Sustained brain-derived neurotrophic factor up-regulation and sensorimotor gating abnormality induced by postnatal exposure to phencyclidine: comparison with adult treatment.

Brain-derived neurotrophic factor (BDNF) is involved in synaptic development and plasticity, and alterations in BDNF expression or signaling are implicated in drug addiction and psychiatric diseases, such as depression and schizophrenia. In this study, we administered phencyclidine to postnatal and adult rats with different time schedules, and determined the correlations between BDNF expression and the behavioral effects. Both single and repeated phencyclidine injections into adult rats induced BDNF up-regulation in the corticolimbic system and a decrease in prepulse inhibition, both of which were transient. In contrast, subchronic postnatal administration increased BDNF protein and mRNA levels in the hippocampus and entorhinal cortex, which were sustained until 8 weeks of age. In parallel, the postnatal rats treated with phencyclidine developed a persistent decrease in prepulse inhibition at the adult stage. The chronic BDNF increase appeared to contribute to the prepulse inhibition abnormality, as subchronic BDNF infusion into the hippocampus of normal rats mimicked the prepulse inhibition deficits. This study suggests that phencyclidine exposure during brain development induces sustained BDNF up-regulation in the limbic system with a biological link to sensorimotor gating deficits.

Aging↗
PubMed2005

Quantitative assessment of forelimb motor function after cervical spinal cord injury in rats: relationship to the corticospinal tract.

Approximately 50% of human spinal cord injuries (SCI) are at the cervical level, resulting in impairments in motor function of the upper extremity. Even modest recovery of upper extremity function could have an enormous impact on quality of life for quadriplegics. Thus, there is a critical need to develop experimental models for cervical SCI and techniques to assess deficits and recovery of forelimb motor function. Here, we analyze forelimb and forepaw motor function in rats after a lateral hemisection at C5 and assessed the relationship between the functional impairments and the extent of damage to one descending motor system, the corticospinal tract (CST). Female Sprague-Dawley rats were trained on various behavioral tasks that require the forelimb, including a task that measures gripping ability by the hand (as measured by a grip strength meter, GSM), a food reaching task, and horizontal rope walking. After 8 weeks of post-injury testing, the distribution of the CST was evaluated by injecting BDA into the sensorimotor cortex either ipsi- or contralateral to the cervical lesion. Complete unilateral hemisection injuries eliminated the ability to grip and caused severe impairments in food retrieval by the forepaw ipsilateral to the lesion. There was no indication of recovery in either task. In cases in which hemisections spared white matter near the midline, there was some recovery of forelimb motor function over time. Assessment of rope climbing ability revealed permanent impairments in forelimb use and deficits in hindlimb use and trunk stability. Sensory testing using a dynamic plantar aesthesiometer revealed that there was no increase in touch sensitivity in the affected forelimb. For the cases in which both histological and behavioral data were available, spared forelimb motor function was greatest in rats in which there was sparing of the dorsal CST.

Animals↗
PubMed1996

Sensorimotor impairments in Wistar Kyoto rats with cerebral infarction, induced by unilateral occlusion of the middle cerebral artery: recovery of function.

Wistar Kyoto (WKY) rats with cerebral infarction induced by permanent unilateral occlusion of the middle cerebral artery (MCA) and sham-operated rats were tested in a series of simple behavioral test 2, 16 and 37 days after surgery. In addition, the motility of the animals was measured over a period of 62 h, after the third test series. A subset of the tests appeared to be suitable to assess the effects of cerebral infarction, namely, grasping reflex of contralateral hindpaw, circling behavior, forelimb flexion, hindlimb flexion, and latency to fall off a square bridge. Except for the impaired grasping reflex of the contralateral hindpaw, there was spontaneous complete recovery of function by the third test session, 37 days after surgery. Some of the other tests might not have been sensitive enough to detect the effects of the unilateral MCA-occlusion (MCA-O) on behavior. Moreover, the WKY rats were very inactive in some of the tests, so that reliable scoring of the effects was not always possible. A rat strain other than the WKY strain might be more suitable to study the behavioral consequences of MCA-O.

Animals↗
PubMed1999

Effects of sustained phencyclidine exposure on sensorimotor gating of startle in rats.

Phencyclidine (PCP), a non-competitive NMDA antagonist with actions at multiple other central nervous system receptors, can cause both acute and lasting psychoses in humans, and has also been used in cross-species models of psychosis. Acute exposure to PCP in rats produces behavioral changes, including a loss of prepulse inhibition (PPI) of the startle reflex, which parallels the loss of PPI observed in schizophrenia patients. Sustained exposure to PCP in rats produces neuropathological changes in several limbic regions and prolonged behavioral abnormalities that may parallel neuropsychological deficits in schizophrenia. It is unclear whether sustained PCP exposure will also produce a loss of prepulse inhibition which parallels the decrease observed in schizophrenia patients. In the present study, we examined changes in PPI during and after sustained PCP administration, using 5-day PCP exposure via subcutaneous osmotic minipumps, or 14-day PCP exposure via repeated intraperitoneal injections. In both forms of drug delivery, PPI was disrupted during, but not after, sustained drug exposure. PPI does not appear to be sensitive to neuropathological effects of sustained PCP exposure.

Animals↗
PubMed1973

Trigeminal deafferentation and feeding in the pigeon: sensorimotor and motivational effects.

The role of oral sensations in the control of hunger and thirst in the pigeon was studied in birds in which the trigeminal sensory nerves had been sectioned bilaterally. Trigeminal deafferentation, although it does not impair drinking, disrupts both the neurosensory and the motivational control of feeding behavior. These two types of deficit may be experimentally dissociated.

Animals↗
PubMed2004

Interactions of the mGluR5 gene with breeding and maternal factors on startle and prepulse inhibition in mice.

Sensorimotor gating, measured by prepulse inhibition (PPI), is a fundamental form of information processing that is deficient in schizophrenia patients and mice lacking the gene for metabotropic glutamate receptor 5 (mGluR5). Both breeding strategies and mothering behaviors are capable of influencing the behavioral phenotype of knockout (KO) mice. Previous studies found a PPI deficit and increased startle magnitudes in mGluR5 KO mice derived from homozygous matings. Here we compared the PPI of mGluR5 wildtype (WT) and KO mice derived from heterozygous matings to that seen in mice derived from homozygous matings. Possible influences of postnatal mothering behaviors were examined using two different methods of cross-fostering. The potential developmental nature of the PPI deficit of the mGluR5 KO mice was also addressed via acute administration of the mGluR5 antagonist 2-methyl-6-(phenylethynyl)-pyridine (MPEP) to C57BL/6J mice. The mGluR5 KO mice exhibited reduced PPI independently of breeding strategy or postnatal mothering behavior. Startle magnitude, however, varied with breeding strategy. The PPI deficit seen in the mGluR5 KO mice is not mimicked by acute administration of an mGluR5 antagonist, and is therefore most likely due to compensatory alterations in neuronal circuitry occurring during development independent of maternal behaviors in the postnatal environment.

Animals↗
PubMed1983

Recovery of function after mesotelencephalic dopaminergic injury in senescence.

After intracerebral 6-hydroxydopamine injections that extensively damage the ascending mesotelencephalic dopaminergic projection, young adult rats develop severe sensorimotor deficits, including an inability to orient toward somatosensory stimuli. Many rats with such damage recover their localization of touch, and this recovery depends on the survival of a small proportion of the neostriatal dopaminergic terminals. Behavioral recovery appears to be mediated by an increased dopamine synthesis and release within surviving terminals and an increased responsiveness to dopamine of neostriatal neurons. The ability of aged rodents to increase activity at neostriatal dopaminergic synapses following partial injury to these neurons is remarkably intact, despite the reduced basal level of transmission at these synapses in senescence. First, 27-28-month-old rats recovered somatosensory localization after injury as readily as did 4-5-month-old animals that had equivalent neostriatal dopamine depletions. Second, old and young rats developed a similar degree of behavioral supersensitivity to apomorphine (0.25 mg/kg, i.p.) after unilateral 6-hydroxydopamine injections, as measured by contralateral turning. Third, injury to these neurons produced an equivalent increase in [3H]spiroperidol binding in the neostriatum of old and young rats at 5-7 weeks. Old rats suffered more extensive neostriatal dopamine depletions after intracerebral 6-hydroxydopamine injections than did young adult animals, particularly when small quantities (2 micrograms) of the neurotoxin were injected. This enhanced susceptibility to 6-hydroxydopamine of dopaminergic neurons in old rats could not be attributed to age differences in the placement of the injection cannula or the extent of the non-specific damage at the injection site. The implications of this enhanced susceptibility to the neurotoxin are discussed.

Aging↗
PubMed1991

The expression of a deafferentation syndrome in the Sprague-Dawley rat: effects of frontoparietal cortical lesions.

Forelimb sensorimotor (SMI) cortical lesions in the rat have been found to suppress a deafferentation syndrome which follows C5-T2 ganglionectomy/avulsion whether the cortical lesions were made prior to, or several days after, the dorsal root lesions. None of the 6 rats with only frontoparietal lesions developed a deafferentation syndrome. These results may be influenced by the presence of a sensorimotor amalgam in the parietal cortex of the rat.

Afferent Pathways↗
PubMed2005

Primary neurologic screening and motor coordination of Dstdt-J mutant mice (dystonia musculorum) with spinocerebellar atrophy.

The autosomal recessive dystonia musculorum (Dst(dt-J)) mutation causes degenerative lesions of peripheral and central sensory pathways. A test battery of motor, sensory, postural, and autonomic functions was used to compare young control and homozygous Dst(dt-J) mice. The Dst(dt-J) mutants were severely impaired for muscle strength, limb coordination, and postural reflexes. As a result of a loss in motor control, the mutants were hypoactive in the open-field and fell quickly from the stationary beam. In sensory tests, the acoustic startle response was impaired, but not tactile reflexes and contact righting, attesting to preserved labyrinthine function and non-lemniscal pathways. Dst(dt-J) mutants were also distinguishable from controls on the basis of tremor, a paler skin, piloerection, and half-open eyes, as well as low body weight and fecal boli. Grooming episodes were less frequent in the mutants but without any reduction in grooming time. The neurologic screening battery delineated the functional integrity of some sensorimotor pathways in a spinocerebellar mutant whose severe phenotype prevents a more elaborate evaluation.

Analysis of Variance↗
PubMed1995

Mastery motivation and cognitive development in 4-year-old children born at various degrees of medical risk.

Although technology has enabled premature infants to survive, longitudinal assessments have primarily focused on IQ outcomes. The purpose of this study was to establish the usefulness of mastery assessment in establishing developmental outcome. Mastery motivation and cognition were examined in 167 preschool children born at various degrees of medical risk. Mastery motivation was measured by a videotaped toy sequence designed to tap sensorimotor practice, effect production, and problem solving. Patterns of correlations indicate that the relationship between mastery and IQ were complementary and not redundant. Three regression models showed that significant interactions between perinatal status and mastery motivation behaviors confirm mastery assessment worthy of consideration in biologically high-risk children.

Achievement↗
PubMed2005

Motor coding in floccular climbing fibers.

The climbing fibers (CFs) that project from the dorsal cap of the inferior olive (IO) to the flocculus of the cerebellar cortex have been reported to be purely sensory, encoding "retinal slip." However, a clear oculomotor projection from the nucleus prepositus hypoglossi (NPH) to the IO has been shown. We therefore studied the sensorimotor information that is present in the CF signal. We presented rabbits with visual motion noise stimuli to break up the tight relation between instantaneous retinal slip and eye movement. Strikingly, the information about the motor behavior in the CF signal more than doubled that of the sensory component and was time-locked more tightly. The contribution of oculomotor signals was independently confirmed by analysis of spontaneous eye movements in the absence of visual input. The motor component of the CF code is essential to distinguish unexpected slip from self-generated slip, which is a prerequisite for proper oculomotor learning.

Action Potentials↗