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PubMedDate not supplied

Neurobehavioral effects of prenatal lamivudine (3TC) exposure in preweaning mice.

The present study provides a characterization of the behavioral changes induced in preweaning mice by prenatal exposure to lamivudine (3TC), an antiviral drug recently entered in the clinical practice to treat HIV patients. Pregnant CD1 mice were given per os bidaily either 3TC at different doses (125, 250, or 500 mg/kg) or vehicle solution (saline 0.9%) from pregnancy day 10 to delivery. Data on reproductive performance, such as gestation length, litter size, and offspring viability, were collected. Offspring were then examined for a series of different somatic and behavioral end points, including sensorimotor development, ontogenetic pattern of ultrasonic vocalization, passive avoidance learning, and locomotor activity. In the absence of gross changes in somatic and sensorimotor development, a slight change in ultrasound emission was found on postnatal day (PND) 3, with 125 and 500 mg/kg 3TC-treated offspring emitting a lower number of ultrasounds. Learning and retention performances of a passive-avoidance task on PND 20-21 were unaffected by 3TC treatment, while decreased habituation in an automated locomotor activity test was evident in male offspring exposed to 250 and 500 mg/kg 3TC.

Animals↗
PubMed1983

Considerations for functional training in adults after head injury.

Functional deficits in head-injured patients are a major concern to physical therapists involved in the rehabilitation process. Functional outcomes are affected by deficits in behavior, cognition, communication, and sensorimotor abilities. These deficits interact frequently and must be considered in planning and implementing treatment. The purpose of this paper is to describe the deficits affecting functional abilities, to discuss the rationale for functional assessment, and to provide treatment suggestions for functional retraining. The suggestions include retraining of protective and equilibrium responses and advanced locomotor skills and use of assistive devices or orthoses. Problems are identified in functional outcome reporting methods. Research endeavors are addressed for physical management during the recovery process and its relationship to functional outcomes.

Adult↗
PubMed2003

Stimulus-driven and voluntary saccades are coded in different coordinate systems.

We make fast, "saccadic" eye movements to view our surroundings, "voluntary" saccades when saccade targets are deliberately selected, and "stimulus-driven" saccades when a target suddenly appears. Saccades of patients with spatial neglect have been studied to identify the coordinate systems guiding such behavior. However, previous reports disagree on whether neglect involves an eye-centered deficit of (delayed and hypometric) saccades specifically when performed in the direction opposite the brain lesion or not. We show that this inconsistency is due to independent mechanisms underlying voluntary and stimulus-driven saccades. We used a new experimental procedure comparing identical saccades performed either during an exploratory search task or a stimulus-driven task, both of which required similar cognitive functions (Figure 1). Only the patients' stimulus-driven saccades showed the eye-centered deficit. The same saccades were intact when voluntarily performed. However, here the patients showed a head-centered deficit; their saccades ignored the left part of space. In none of our control subjects with or without brain lesions did the neglect patients' pattern of deficits occur. The results argue that the brain flexibly uses a system of distinct but interrelated neural circuits for visual orienting to optimally encode its sensorimotor functions in multiple behavioral situations.

Brain Injuries↗
PubMedDate not supplied

Long-term treatment of male F344 rats with deprenyl: assessment of effects on longevity, behavior, and brain function.

L-Deprenyl (selegiline) was chronically administered to male Fischer 344 rats via their drinking water beginning at 54 weeks of age (estimated daily dose: 0.5 mg/kg/day). Beginning at 84 weeks of age, the rats were behaviorally evaluated using a sensorimotor battery, a motor-learning task, and the Morris water maze. At 118 weeks of age, cerebellar noradrenergic function was evaluated in the surviving rats using in vivo electrochemistry. The rats were then sacrificed to measure brain monoamine oxidase activity and perform quantitative autoradiography to evaluate the effect of chronic deprenyl treatment on beta-adrenergic receptors in the cerebellum, alpha 2-adrenergic receptors several brain regions, and D1 and D2 dopamine receptors in the striatum. Deprenyl treatment reduced brain monoamine oxidase B activity by 85%, but had no effect on brain monoamine oxidase A. A clear effect of chronic deprenyl treatment upon longevity was not observed. Several measures of CNS function were altered in the deprenyl-treated animals: 1) spatial learning in the Morris water maze was improved; 2) electrochemical signals recorded following local application of NE were reduced, and the responsiveness to the reuptake blocker nomifensine was enhanced, in the cerebellum; 3) beta-adrenergic receptor binding affinity was increased in the cerebellum; 4) alpha 2-adrenergic receptor density was increased in the inferior colliculus; and 5) striatal D1 dopamine receptor density was reduced but binding affinity was enhanced. In contrast, chronic deprenyl treatment did not cause changes in: 1) sensorimotor function, as evaluated by balance beam, inclined screen, or wire hang tasks; 2) motor learning; 3) alpha 2-adrenergic receptor density in any region examined except for the inferior colliculus, or binding affinity in any region examined; or 4) striatal D2 dopamine receptor number or affinity. Thus, long-term oral administration of deprenyl extended the functional life span of rats with respect to cognitive, but not motor, performance.

Animals↗
PubMed2001

A comparison of long-term functional outcome after 2 middle cerebral artery occlusion models in rats.

BACKGROUND AND PURPOSE: Proven behavioral assessment strategies for testing potential therapeutic agents in rat stroke models are needed. Few studies include tasks that demand higher levels of sensorimotor and cognitive function. Because behavioral outcome and rate of recovery vary among ischemia models, there is a need to characterize and compare performance on specific tasks across models. METHODS: To this end, sensorimotor and cognitive deficits were assessed during a 5-week period after either permanent proximal middle cerebral artery occlusion (pMCAO) or permanent distal middle cerebral artery occlusion combined with a 90-minute occlusion of both common carotid arteries (dMCAO/tCCAO) in Sprague-Dawley rats. The EBST, hindlimb and forelimb placing, and cylinder tests were given at regular intervals postinjury to assess sensorimotor function. Cognitive function was assessed with a multitrial water navigation task. RESULTS: pMCAO, which caused both striatal and cortical damage, produced persistent sensorimotor and cognitive deficits. Limb placing responses and postural reflexes were impaired throughout the month of testing. A persistent bias for using the ipsilateral forelimb for wall movements in the cylinder test was observed as well as a bias for landing on the opposite forelimb. pMCAO rats were also impaired in the water navigation task. dMCAO/tCCAO, which caused only cortical damage, produced similar sensorimotor deficits, but these were greatly diminished by 2 weeks after injury. No impairment was found for water tank navigation. Correlations between forelimb placing (both models), water navigation performance (pMCAO model), and sensorimotor asymmetry (dMCAOtCCAO model) and infarct volume were observed. CONCLUSIONS: Based on the range of functions affected and stability of observed deficits, the pMCAO model appears to be preferable to the dMCAO/tCCAO model for use in assessing therapeutic agents for stroke.

Animals↗
PubMed2001

Structural and functional characteristics of neurons in the sensorimotor cortex of rats with different resistance to emotional stress.

Wistar rats behaviorally active in the open field test (resistant to emotional stress) are characterized by polymorphism of neurons in layer V of the sensorimotor cortex and the presence of hyperchromatic cells, which probably determines resistance to emotional stress in these rats. Atrophy of hyperchromatic neurons reflecting transient inhibition of cell activity was noted in Wistar rats subjected to stress. In the sensorimotor cortex of behaviorally passive animals (predisposed to emotional stress) groups of densely packed hyperchromatic cells and pronounced pericellular edema were revealed. In these rats stress caused irreversible changes in cortical neurons and death of some cells. The presence of ischemic cortical neurons in rats subjected to emotional stress suggests that cerebral hypoxia plays a role in structural and functional disorganization of the sensorimotor cortex during emotional stress.

Animals↗
PubMed2005

Activation of dopaminergic neurotransmission in the medial prefrontal cortex by N-methyl-d-aspartate stimulation of the ventral hippocampus in rats.

Many behavioral functions-including sensorimotor, attentional, memory, and emotional processes-have been associated with hippocampal processes and with dopamine transmission in the medial prefrontal cortex (mPFC). This suggests a functional interaction between hippocampus and prefrontal dopamine. The anatomical substrate for such an interaction is the intimate interconnection between the ventral hippocampus and the dopamine innervation of the mPFC. The present study yielded direct neurochemical evidence for an interaction between ventral hippocampus and prefrontal dopamine transmission in rats by demonstrating that subconvulsive stimulation of the ventral hippocampus with N-methyl-d-aspartate (NMDA; 0.5 mug/side) activates dopamine transmission in the mPFC. Postmortem measurements revealed that bilateral NMDA stimulation of the ventral hippocampus, resulting in locomotor hyperactivity, increased the homovanillic acid/dopamine ratio, an index of dopamine transmission, in the mPFC; indices of dopamine transmission in any of five additionally examined forebrain regions (amygdala, nucleus accumbens shell/core, lateral prefrontal cortex, caudate putamen) were unaltered. In vivo microdialysis measurements in freely moving rats corroborated the suggested activation of prefrontal dopamine transmission by demonstrating that unilateral NMDA stimulation of the ventral hippocampus increased extracellular dopamine in the ipsilateral mPFC. The suggested influence of the ventral hippocampus on prefrontal dopamine may be an important mechanism for hippocampo-prefrontal interactions in normal behavioral processes. Moreover, it indicates that aberrant hippocampal activity, as found in neuropsychiatric diseases, such as schizophrenia and mood disorders, may contribute to disruption of certain cognitive and emotional functions which are extremely sensitive to imbalanced prefrontal dopamine transmission.

Animals↗
PubMed2001

Evaluation of sensorimotor training in children with ADHD.

Reduced ability to regulate motor behavior seems to be an essential aspect of Attention-Deficit Hyperactivity Disorder (ADHD) and may reflect deficits in behavioral response inhibition. In this respect, pragmatic clinical experience over the last two decades, in daily practice, training of motor control has played an important role within multimodal treatment approaches, although an adequate proof of its efficacy is still lacking. Therefore, to examine the efficacy of sensorimotor training, 12 children with ADHD (two groups of six) were treated with both sensorimotor training and (as control) cognitive behavioral training using a within-subject cross-over design. Each treatment had a duration of 4 months (20 sessions), yielding a total of 40 sessions for the completed cross-over design. Results showed that Sensorimotor Training improved sensorimotor coordination slightly, while Cognitive Behavioral Training ameliorated cognitive impulse control. Hyperactivity and anxious-depressive/aggressive behavior were markedly reduced by Sensorimotor Training but not by Cognitive Behavioral Training. In conclusion, a combined treatment may be recommended since compensation and regulation of inhibitory deficits in ADHD come into play within the framework of both kinds of training.

Attention Deficit Disorder with Hyperactivity↗
PubMed2005

Alpha-2 adrenoceptor activation inhibits phencyclidine-induced deficits of spatial working memory in rats.

N-methyl-D-aspartate (NMDA)/glutamate receptor antagonists, such as phencyclidine (PCP), induce behavioral abnormalities (locomotor hyperactivity, sensorimotor gating deficits, impairments of cognition) in animals that are thought to model aspects of schizophrenia. The administration of PCP increases noradrenaline transmission in the rat prefrontal cortex, a brain structure required for normal cognitive processes. Noradrenaline, in turn, works through a set of receptors that have themselves been implicated directly in NMDA antagonist-induced deficits; we recently reported that the alpha-2 agonist, clonidine, is effective at preventing PCP-induced deficits of working memory and visual attention in rats. Here, we further investigated the role for alpha-2 adrenoreceptors in the effects of PCP on spatial working memory performance. The alpha-2 agonist clonidine (0.001-0.01 mg/kg, subcutaneously (s.c.)) produced a significant amelioration of PCP-induced working memory deficits; the effects of PCP (1.0 mg/kg, s.c.), but not clonidine, were reduced in noradrenaline-depleted rats. In addition, the alpha-2A-preferring agonist guanfacine (0.05-1.0 mg/kg, s.c.) dose-dependently prevented the deficits of spatial working memory performance produced by PCP. Although the highly selective alpha-2 receptor antagonist, atipamezole (ATI), failed to affect spatial working memory on its own, at the doses studied (0.1-0.5 mg/kg, s.c.), it dramatically enhanced the working memory deficit produced by PCP. These data indicate that alpha-2 adrenoreceptors tonically inhibit PCP-induced deficits of spatial working memory, suggesting an important role for these receptors in cognitive deficits associated with NMDA receptor hypofunction.

Adrenergic alpha-2 Receptor Agonists↗
PubMed2004

Regional and subcellular compartmentation of the dopamine transporter and tyrosine hydroxylase in the rat ventral pallidum.

The ventral pallidum (VP) is a major intermediary in the prefrontal cortical circuitry regulating sensorimotor gating and locomotor behavior, both of which are potently modulated by catecholamines. The VP catecholaminergic innervation is derived from midbrain dopaminergic neurons that differ in expression levels of the dopamine transporter (DAT) and from brainstem noradrenergic neurons without DAT. The preferentially low level of DAT in dopaminergic terminals in the prefrontal cortex and in striatal regions projecting more extensively to the VP medial (VPm) compared with VP lateral (VPl) compartment suggests possible region-specific differences in VP axonal distribution of DAT. To test this hypothesis, we examined the electron microscopic localization of DAT and the catecholamine-synthesizing enzyme, tyrosine hydroxylase (TH), in the VPm and VPl of rat brain. In both regions, DAT and TH were localized primarily in small unmyelinated axons and morphologically heterogeneous axon terminals. DAT-immunogold particles were few in number, but mostly located on the plasma membrane. In contrast, TH immunoreactivity was distributed in the cytoplasm of individual profiles, many of which were without detectable DAT. In comparison with TH, the mean area density of DAT-labeled axons was low throughout the VP. The mean area density of DAT-immunogold axon terminals, however, was significantly higher in VPl than in VPm, whereas that of TH-labeled axons was higher in VPm than in VPl. This dissociation suggests that, compared to the VPl, the VPm receives the greatest input from catecholaminergic afferents that are either nondopaminergic or characterized by having low levels or less terminal distributions of DAT.

Animals↗
PubMed1994

Tactile sensory input regulates basal and apomorphine-induced immediate-early gene expression in rat barrel cortex.

Clipping of mystacial vibrissae on one side of the rat's snout results in sensorimotor asymmetries in normal behavior and in behavior induced by the dopamine receptor agonist, apomorphine. Immediate-early gene expression, a marker for short-term changes in neuron function, was used to examine whether this sensory deprivation leads to functional changes in the somatosensory barrel cortex under experimental conditions which reveal behavioral asymmetries. The expression of c-fos and zif268 immediate-early genes was assessed with in situ hybridization histochemistry. Four hours after unilateral clipping of the mystacial vibrissae, the level of zif268 mRNA was reduced in the corresponding part of the contralateral barrel field. Injection of apomorphine (5 mg/kg) resulted in increased expression of both c-fos and zif268 immediate-early genes in cortex and striatum. This apomorphine-induced increase was blocked in the sensory-deprived somatosensory cortex. Laminar analysis of gene regulation showed that vibrissae removal affected immediate-early gene expression in all layers of the barrel cortex. These results demonstrate that: (1) basal zif268 gene expression in neurons of the somatosensory cortex is dependent on sensory input, (2) cortical immediate-early gene expression is increased after dopamine receptor activation, and (3) in the barrel cortex, this increase is also dependent on sensory input. We suggest that the observed reduction in gene expression after vibrissae removal reflects decreased activation of neurons in the barrel column by removal of sensory input.

Animals↗
PubMed1983

Parabrachial nuclei damage in infant rats produces residual deficits in gustatory preferences/aversions and sodium appetite.

Ten-day-old rats sustained bilateral electrolytic lesions of the parabrachial nuclei in the pons (PBN). Growth measures and tests of sensorimotor, feeding and drinking behaviors, sodium appetite, and gustatory capacities were made between ages 1 and 150 days. PBN rats displayed a transient period of attenuated suckling, as evidenced by body weight loss. When tested soon after weaning, PBN rats were hyperdipsic in response to cellular dehydration and during food deprivation. This effect, however, was temporary. When tested as adults, PBN rats were hypodipsic in response to extracellular fluid volume depletion, they displayed alterations in sodium appetite, showed "exaggerated" preferences and aversions to saccharin and NaCl solutions, and they displayed attenuated quinine aversions. These results are generally similar to the behaviors of rats sustaining more central gustatory pathway lesions as adults. The functional significance of the PBN in the developing rat for preference/aversion and sodium appetite behaviors are discussed.

Animals↗
PubMed1987

Involuntary grasping and groping responses to space-related visual stimuli.

Involuntary groping-grasping responses to visual stimuli were studied in relation to the location of the stimuli in the space surrounding the patient. The following space-related patterns of stimulus-response were observed in four patients: (a) responses were evoked only by visual stimuli in the hemispace ipsilateral to the arm involved; (b) responses were evoked only by visual stimuli within the reach of maximal arm extension; (c) responses were evoked only by visual stimuli in the space around the hand; (d) all such patterns were variously combined. These findings are discussed in relation to the general problem of specific correlations between sensorimotor subsystems and peripersonal behavioral space.

Adult↗
PubMed1992

Complex motor and sensorimotor functions of striatal and accumbens dopamine: involvement in instrumental behavior processes.

The suggestions that dopamine (DA) systems are involved in "motor control" and "reward" represent the classic working hypotheses on the behavioral functions of these systems. The research generated by these hypotheses has yielded results that are far more complicated than the simplest form of either hypothesis would indicate. Pharmacological or lesion-induced interference with DA function does not suppress all aspects of movement control, nor all aspects of reward, nor all aspects of motivation. The deficits produced by interference with DA systems are selective and dissociative in nature, affecting some aspects of motor or motivational function, but leaving others basically intact. In some sense the hypotheses that DA is involved in "motor" or "reward" or "motivational" processes are partly correct, but the processes to which these terms refer are too broad to offer an accurate and detailed description of the behavioral functions of brain DA. A review of the literature on the behavioral pharmacology of DA suggests that the behaviors most easily disrupted by DA antagonists are highly activated and complex learned instrumental responses that are elicited or supported by mild conditioned stimuli, and maintained for considerable periods of time. It is proposed that DA in accumbens and striatum modulates the ability of neocortical and limbic areas involved in sensory, associative, and affective processes to influence complex aspects of motor function, and also modulates the execution of complex motor acts organized by the neocortex. Thus, interference with DA systems produces a "subcortical apraxia", which dissociates complex stimulus processes from complex motor processes, but leaves aspects of those processes intact.

Animals↗
PubMed2005

Intrinsic connectivity of human superior colliculus.

The superior colliculus (SC) is believed to play an important role in sensorimotor integration and orienting behavior. It is classically divided into superficial layers predominantly containing visual neurons and deep layers containing multisensory and premotor neurons. Investigations of intrinsic connectivity within the SC in non-human species initially led to controversy regarding the existence of interlaminar connections between superficial and deep layers. It now seems more likely that such connections exist in a number of species, including non-human primates. In the latter, anatomical data concerning intrinsic SC connectivity are restricted to a limited number of intracellularly labeled neurons. No studies have been conducted to investigate the existence of intrinsic connections of human SC. In the present study, DiI (1,1'-dioctadecyl-3,3,3',3'- tetramethylindocarbocyanine perchlorate) and BDA (biotinylated dextran amine) were two tracers used in post-mortem human brains to examine intrinsic SC connections. Injections into the superficial layers revealed tangential connections within superficial layers and radial superficial-layer to deep-layer connections. Within superficial layers, horizontal connections were found over the entire rostro-caudal axis and were mostly directed laterally, i.e. toward the brachium of the inferior colliculus. Superficial-layer to deep-layer connections were more prominent in sections containing the injection site or located close to it. In these sections, an axon bundle having roughly the same diameter as the injection site crossed all deep layers, and individual axons displayed en passant or terminal boutons. The present results suggest that intrinsic connections within superficial layers and radial superficial-layers to deep-layers exist in human SC. The putative roles of these connections are discussed with regard to visual receptive field organization, as well as visuomotor and multisensory integration.

Aged↗
PubMed1996

Long-term effects of neonatal ischemic-hypoxic brain injury on sensorimotor and locomotor tasks in rats.

Perinatal ischemia and/or hypoxia in humans are major risk factors for neurologic injury that often manifest as sensorimotor and locomotor deficits throughout development and into maturity. In these studies, we utilized an established model of neonatal ischemic-hypoxia that creates unilateral striatal, cortical, and hippocampal damage (Rice III, J.E., Vanucci, R.C. and Brierley, J.B., Ann. Neurol., 9 (1981) 131-141) to investigate sensorimotor and locomotor deficits in these animals during development and as adults. Sensorimotor deficits were examined by measuring the amount of time that the animals were able to remain on a rotating treadmill. Locomotor abnormalities were assessed by measuring apomorphine-induced rotational asymmetry. Following the neonatal ischemic-hypoxic episode, at 3-9 weeks of age, animals were not able to remain on the treadmill as long as their normal littermate controls. In addition, these animals demonstrated an abnormal, ipsiversive rotational asymmetry in response to systemic administration of apomorphine. When these animals reached adulthood, the degree of atrophy in specific regions of the damaged hemisphere was quantified using measurements of cross-sectional area. The mean cross-sectional area of the striatum was decreased by 29%, the sensorimotor cortex area by 26%, and the dorsal hippocampus cross-sectional area was approximately 6% of its normal size. These data suggest that this rodent model of neonatal ischemic-hypoxic brain injury results in cerebral atrophy and long-lasting sensorimotor and locomotor deficits. These particular behavioral tasks may be used in future studies to assess locomotor and sensorimotor deficits following neonatal ischemic-hypoxic brain injury.

Animals↗
PubMed1998

Ascorbate modulates glutamate-induced excitations of striatal neurons.

To assess the role of ascorbate (AA), an antioxidant vitamin, in modulating striatal activity, single-unit recording was combined with iontophoresis in awake, unrestrained rats. Brief applications of AA (20 s, 5-80 nA) elicited few changes in either basal activity or activity evoked by continuous application of glutamate (GLU), but relatively high AA ejection currents (>40 nA) often inhibited fast-firing units. Comparable results were obtained with the antioxidant isomer, iso-AA, suggesting the AA-induced inhibition represents a high-dose, antioxidant effect. When applied for prolonged periods (2-4 min) at doses that failed to alter basal activity, AA either enhanced or attenuated the excitatory response to test pulses of GLU. The AA-induced enhancement occurred more frequently (16 vs. 6 applications) and was characterized by a more rapid (shorter onset and peak latencies) and more pronounced (greater peak magnitude) excitation to GLU without an evident change in offset latency. In most cases, further increases in AA ejection current attenuated the GLU response. Iso-AA, in contrast, had only inhibitory effects, which occurred at moderate- to high-dose applications. Collectively, these results suggest that AA, apart from its antioxidant effects, modulates phasic changes in striatal excitability induced by GLU. Because extracellular levels of striatal AA fluctuate in relation to behavioral activation, this neuromodulatory action of AA may contribute to behaviorally relevant changes in sensorimotor responsivity.

Animals↗
PubMed2000

Effects of sulpiride on the orienting movement evoked By acoustic stimulation in the Rat.

Drugs that selectively block D(2) receptors are known to provoke a rapid cell firing increase followed by A9 and A10 dopaminergic (DA) neuron inactivation (depolarization block). In this study, possible relationships between cell firing rapid increase and specific behavioral effects, linked to sensorimotor integration, were investigated in the rat. To this purpose, with the aid of a video camera apparatus and a frame-by-frame analysis, effects of sulpiride-induced blockade of DA D(2) receptors were analyzed on the orienting movement of the head induced by acoustic stimulation. In a control group of rats, during trials lasting 20 min, latency and duration of head turning (HT) were 186.15 +/- 51.66 ms and 266.87 +/- 47.49 ms, respectively. Sulpiride injection (20,40,100 mg/kg IP) provoked a dose-dependent increase of HT latency and duration; however, only latencies showed statistically significant variations. It is suggested that cell firing rapid increase, observed on A9 and A10 DA neurons, following sulpiride administration, may be correlated to rapid modifications of specific HT parameters linked to sensorimotor integration.

Acoustic Stimulation↗