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PubMedDate not supplied

Brain neuronal mechanisms of motivation and reinforcement: systemic organization of behavior.

The concept of systemic quantitation of behavior was used to study the interaction between dominant motivation and reinforcement on brain neurons. Feeding and escape were used as experimental models. Results showed that feeding and escape motivations are based on the mechanisms of ascending activating influences of lateral or ventromedial hypothalamic centers, respectively, on cortical neurons. Feeding and escape motivations evoked by electrical stimulation of hypothalamus, or the ones occurring naturally, modify the responses of single neurons of sensorimotor and insular cortex to sensory stimuli, to microiontophoretic application of neurotransmitters and neuropeptides, and especially to reinforcement. Dominant motivations are reflected in the burst-like activity and in a specific pattern of interpulse intervals of single units in various brain structures. Reinforcement transforms this activity into a regular pattern and also changes the neuronal responses of hypothalamic feeding and escape centers, to electrical stimulation and to microiontophoretic application of oligopeptides. Specific patterns of the unit responses to conditioned stimuli in the course of consecutive reinforcement was determined. After several instances of reinforcement, especially after repetitive reinforcement, the brain neurons influenced by the dominant motivation begin to produce specific protein molecules that are important for organization of an appropriate type of behavior. This process can be blocked by protein synthesis inhibitors.

Animals↗
PubMed2005

Evolutionary autonomous agents and the nature of apraxia.

BACKGROUND: Evolutionary autonomous agents are robots or robot simulations whose controller is a dynamical neural network and whose evolution occurs autonomously under the guidance of a fitness function without the detailed or explicit direction of an external programmer. They are embodied agents with a simple neural network controller and as such they provide the optimal forum by which sensorimotor interactions in a specified environment can be studied without the computational assumptions inherent in standard neuroscience. METHODS: Evolutionary autonomous agents were evolved that were able to perform identical movements under two different contexts, one which represented an automatic movement and one which had a symbolic context. In an attempt to model the automatic-voluntary dissociation frequently seen in ideomotor apraxia, lesions were introduced into the neural network controllers resulting in a behavioral dissociation with loss of the ability to perform the movement which had a symbolic context and preservation of the simpler, automatic movement. RESULTS: Analysis of the changes in the hierarchical organization of the networks in the apractic EAAs demonstrated consistent changes in the network dynamics across all agents with loss of longer duration time scales in the network dynamics. CONCLUSION: The concepts of determinate motor programs and perceptual representations that are implicit in the present day understanding of ideomotor apraxia are assumptions inherent in the computational understanding of brain function. The strength of the present study using EAAs to model one aspect of ideomotor apraxia is the absence of these assumptions and a grounding of all sensorimotor interactions in an embodied, autonomous agent. The consistency of the hierarchical changes in the network dynamics across all apractic agents demonstrates that this technique is tenable and will be a valuable adjunct to a computational formalism in the understanding of the physical basis of neurological disorders.

Apraxias↗
PubMed1996

Triphenyl phosphite and diisopropylphosphorofluoridate produce separate and distinct axonal degeneration patterns in the central nervous system of the rat.

This study compared the neurotoxic effects of triphenyl phosphite (TPP) in the rat with those seen after exposure to diisopropylphosphorofluoridate (DFP), a compound known to produce organophosphorus-induced delayed neurotoxicity (OPIDN). Animals received either three subcutaneous injections of TPP (1184 mg/kg body wt each dose) administered at 3-day intervals or a single subcutaneous injection of DFP (4 mg/kg body wt). TPP-induced clinical signs were initially observed 2 to 18 days after the last injection and included ataxia, flaccid paresis, stereotyped alternating side-to-side movements, and circling behavior. Axonal and terminal degeneration were present in the cerebellum, vestibular nuclear complex, cochlear nuclei, and superior and inferior colliculi. The subthalamic nucleus, substantia nigra, septal region, hypothalamus, thalamus, hippocampus, and cerebral cortex also contained degenerating axons and terminals. Degeneration was particularly evident in the sensorimotor cerebral cortex, mediodorsal, ventromedial, and medial geniculate thalamic nuclei and in the magnocellular preoptic and medial mammillary nuclei of the hypothalamus. Very light degeneration was present in the gracile fasciculus and nucleus. In contrast, rats injected with DFP showed moderate degeneration in the gracile fasciculus and nucleus but did not display degeneration in any other brain region. Injections of DFP did not produce delayed onset clinical signs. The results indicate that in the rat, different central nervous system cell groups are affected by these two organophosphorus compounds and that TPP affects nuclei and tracts at all levels of the neuraxis, including those associated with higher-order processing and cognitive functions. In addition, the distinct degeneration patterns produced by these two compounds support the view that TPP-induced neurotoxicity should not be considered as a type of OPIDN, but rather as a separate category of organophosphorus-induced neurotoxicity.

Animals↗
PubMed1996

Sensorimotor learning in three cerebellar mutant mice.

Cerebellar damage occurs during developmental stages in three mutant mice (staggerer, hot-foot, and lurcher), causing disturbances in posture and equilibrium. During three tests of motor coordination, the performances of staggerer mutants was inferior to that of normal mice and did not improve with extended practice for up to 7 days of training. The sensorimotor performance of hot-foot mutants and of lurcher mutants was also lower than that of normal mice. Nevertheless, hot-foot mutants showed evidence of learning in two of the three tests and lurcher mutants in all three tests. Cerebellar atrophy in the latter two mutants did not prevent sensorimotor learning, but instead impaired their ability to reach the same level of performance as that of normal mice.

Animals↗
PubMed1994

Inhibition of clonic seizure-like excitatory effects induced by intrathecal morphine using two NMDA receptor antagonists: MK-801 and ACEA-1011.

Microinjection of high doses of morphine into the spinal lumbar intrathecal (i.t.) space of mice produces dose-dependent clonic seizure-like excitatory effects. Naloxone, an opioid antagonist (10 mg/kg, i.p.), injected 5 min prior to i.t. morphine, did not reverse the seizure-like motor effects, suggesting that these effects of morphine are not mediated through opioid receptors. Systemic administration of MK-801, a non-competitive NMDA receptor antagonist (0.01-0.10 mg/kg, i.p.), or ACEA-1011, a novel NMDA receptor/glycine site antagonist (0.5-20.0 mg/kg, i.p.), attenuated the clonic seizure-like excitatory effects induced by i.t. morphine in a dose-dependent manner. Sensorimotor performance of the mice was evaluated using the rotarod test. Although both compounds (MK-801 and ACEA-1011) impaired the sensorimotor performance of mice in a dose-dependent fashion, there was no impairment of motor performance at doses employed to block the excitatory effects induced by i.t. morphine. These data suggest that NMDA receptors play a pivotal role in the clonic seizure-like behaviors induced by i.t. morphine.

Analgesics↗
PubMed1995

The cellular basis of classical conditioning in Aplysia californica--it's less simple than you think.

Classical conditioning of the withdrawal reflex of the marine snail Aplysia californica can be used as an important model system for investigating the neurobiology of associative learning. It results when weak tactile stimulation of the snail's mantle shelf or siphon is repeatedly paired with strong electrical shocks to the animal's tail. This learned behavioral change is thought to be mediated by a presynaptic neuronal mechanism-activity-dependent presynaptic facilitation of the connections between sensory and motor neurons in the CNS of Aplysia. Recent evidence suggests, however, that another type of synaptic plasticity-Hebbian potentiation of the sensorimotor connections-might contribute to classical conditioning in Aplysia. Additional evidence indicates that this relatively simple form of learning is likely to be mediated by multiple neuronal mechanisms.

Animals↗
PubMed2005

Prefrontal D1 and ventral hippocampal N-methyl-D-aspartate regulation of startle gating in rats.

BACKGROUND: Sensorimotor gating, as measured by prepulse inhibition of the startle reflex, is deficient in schizophrenia patients, and in rats after specific manipulations of limbic cortico-striato-pallido-thalamic circuitry. For example, prepulse inhibition in rats is disrupted after D1 blockade in the medial prefrontal cortex, and after N-methyl-D-aspartate infusion into the ventral hippocampus. In the present study, we examined whether these two substrates form part of an integrated circuit regulating sensorimotor gating, which might contribute to the loss of prepulse inhibition in patient populations. METHODS: Prepulse inhibition was assessed in male Sprague-Dawley rats after systemic or intra-medial prefrontal cortex administration of the D1 antagonist, SCH 23390. Separate rats received intra-medial prefrontal cortex infusion of the retrograde transported label Fluoro-Gold. In rats with sham or electrolytic lesions of the medial prefrontal cortex, prepulse inhibition was tested after infusion of N-methyl-D-aspartate or vehicle into ventral hippocampus regions that were determined to send projections to the medial prefrontal cortex. RESULTS: Prepulse inhibition was disrupted after systemic SCH 23390 treatment and after infusion of SCH 23390 into medial prefrontal cortex sites within the prelimbic and cingulate cortices. Fluoro-Gold infusion into these medial prefrontal cortex sites labeled cells in the ventral hippocampus complex, including regions CA1 and entorhinal cortex. N-methyl-D-aspartate infusions into these ventral hippocampus regions disrupted prepulse inhibition in rats after sham but not electrolytic lesions of the medial prefrontal cortex. CONCLUSIONS: Prepulse inhibition appears to be regulated by interacting substrates within the ventral hippocampus and MPFC. Specifically, NMDA activation of the ventral hippocampus appears to disrupt prepulse inhibition in a manner that is dependent on the integrity of infralimbic or cingulate cortical regions that also support a D1-mediated regulation of prepulse inhibition. Conceivably, dysfunction within these hippocampal-frontal circuits may contribute to sensorimotor gating deficits in schizophrenia.

Acoustic Stimulation↗
PubMedDate not supplied

Pragmatic ability and disability as emergent phenomena.

A holistic approach to pragmatic ability and disability is outlined which takes account both of the behaviour of individuals involved in the communicative process, and also of the underlying factors which contribute to such behaviour. Rather than being seen as resulting directly from a dysfunction in some kind of discrete pragmatic "module" or behavioural mechanism, pragmatic impairment and also normal pragmatic functioning are instead viewed as the emergent consequence of interactions between linguistic, cognitive and sensorimotor processes which take place both within and between individuals.

Adult↗
PubMed1991

Multiple representations contribute to body knowledge processing. Evidence from a case of autotopagnosia.

Body schema disturbances were studied in a 62-yr-old woman with Alzheimer's disease. She was severely impaired in verbal and nonverbal tasks requiring her to localize body parts (on her own body, the examiner's body or a doll's body) even though she correctly named the same parts when pointed at by the examiner. Pointing responses were misdirected mainly to parts contiguous with the target area and, to a lesser extent, to functionally equivalent body parts. We also found that the patient was able to define body part names functionally but not spatially. In another series of tasks, and in contrast to the above results, performances were normal when small objects, attached to the patient's body, served as pointing targets. Furthermore, on subsequent testing she pointed correctly at the remembered position of these objects. The fact that the same point in 'body space' is localized correctly when it corresponds to an external object and erroneously when it corresponds to a body part contradicts the idea of the body schema as a unitary function. Learning the position of objects on the body surface requires access to some form of body-reference system on which this information can be mapped. We argue that such a system can be available in autotopagnosia and is independent from the visuospatial representations of the body structure that are postulated to be damaged or inaccessible in this syndrome. An integrated account of the present results and of those reported by other authors suggests that multiple levels of representation (e.g., sensorimotor, visuospatial, semantic) are involved in the organization of body knowledge.

Agnosia↗
PubMedDate not supplied

Medical and social factors affecting behaviour patterns in patients with acquired brain damage: a study of patients living at home three years after the incident.

This study aimed to describe the consequence of stroke or brain trauma 3 years after the incident for individuals living at home, and how patterns of behaviour were influenced by determinants. One hundred and eighty-eight individuals in three age groups answered a questionnaire. Answers were classified according to WHO's ICIDH, and 11 areas of behaviour were distinguished. Diagnoses and locations of lesions were noted from medical records. Impairment and disability increased with increasing age at the time of the incident. Individuals working before but not after the incident indicated decreased life satisfaction and changed intellectual function, personal care, and domestic/housework/gardening activities, and inability to organize their time. Those who had resumed work but at different tasks indicated changed emotional and sensorimotor function and content in leisure activities. The influence of the localization and lateralization of the lesion is also discussed.

Activities of Daily Living↗
PubMed2002

Effects of transient focal inactivation of the basal ganglia in parkinsonian primates.

Ablative and chronic stimulation procedures targeting the internal pallidum (GPi) and the subthalamic nucleus (STN) have led to major advancements in the treatment of Parkinson's disease and other movement disorders. Although these procedures have evolved to primarily target the posterior ventrolateral sensorimotor portion of GPi and to less selectively target STN, centrally, the ideal targets within these structures remain to be fully established. In this study, we sought to identify the optimal targeting sites in GPi and STN for reversal of parkinsonian signs through a series of reversible injections of the GABA(A) agonist muscimol in these nuclei in parkinsonian primates. Akinesia and bradykinesia were strongly ameliorated by discrete inactivation within the centromedial extent of the sensorimotor territory in GPi and the lateral portion of the sensorimotor territory in STN. This suggests that akinesia and bradykinesia might, in fact, originate from abnormalities in the same, or at least overlapping, motor circuits in the parkinsonian state. Inactivation of areas outside of the motor territories did not improve parkinsonism but induced circling and behavioral abnormalities. The segregation of basal ganglia-thalamocortical circuits appears to be therefore maintained, at least to a large extent, in the parkinsonian state. These results underscore that inactivation of discrete regions in the central territory of GPi and the lateral portion of STN are sufficient to ameliorate parkinsonian motor signs and that extension of lesions into nonmotor territories may be deleterious. Surgical outcomes might therefore be optimized by placing more discrete lesions and by restricting the extent of chronic stimulation.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2005

Bi-hemispheric contribution to functional motor recovery of the affected forelimb following focal ischemic brain injury in rats.

In many recovering hemiparetic stroke patients, movement of the affected limb elicits ipsilateral activation of sensorimotor areas within the undamaged hemisphere, which is not observed in control subjects. Following middle cerebral artery occlusion, rats received intensive enriched-rehabilitation (ER) of the impaired forelimb for 4 weeks. Weekly assessments on a skilled reaching test demonstrated significant improvement in ischemic animals over 4 weeks of ER (P < 0.05). We hypothesized that if the undamaged forelimb motor cortex contributed to improved forelimb function, then inhibition of neural activity within this region should reinstate (at least some of) the initial motor impairment. After 3 and 4 weeks of ER, animals received a microinjection of lidocaine hydrochloride into the undamaged motor cortex and were re-assessed on reaching ability. The behavioral effect of lidocaine challenge was dependent on the size of the infarct: animals with large infarcts were rendered unable to retrieve any food pellets and had great difficulty even contacting a pellet with the affected forepaw. Small-infarct animals were only moderately affected (25% reduction in success) by lidocaine, an effect similar to that observed in control animals. Qualitative assessments of recovered reaching after 4 weeks of rehabilitation revealed that impairments in forelimb lift, advance and aim were exacerbated (P < 0.05) following lidocaine-inactivation of the undamaged motor cortex of animals with large ischemic infarcts. In animals with small infarcts, lidocaine challenge only impaired limb advance. Thus, recruitment of the undamaged hemisphere may depend on the functional integrity of the remaining sensorimotor system. These data suggest that, in the rat, the undamaged (ipsilateral) motor system may contribute to compensatory recovery of the affected forelimb.

Animals↗
PubMedDate not supplied

Behavioral performance of rats following transient forebrain ischemia.

Rats subjected to transient forebrain ischemic injury by the method of four vessel occlusion (4-VO) develop irreversible injury to select populations of vulnerable neurons which include pyramidal cells in the CA-1 region of the hippocampus. This brain area is thought to be crucial for learning and memory. Rats subjected to 30 minutes of 4-VO, and then cerebral reperfusion were tested on a radial 8-arm maze task after they had recovered. The data shows that both 4-VO and control animals improve their performance over trials, but that 4-VO rats are impaired on "working" and "reference" tasks. The data suggest that 4-VO rats' impaired "working" performance is permanent, compared to their transient "reference" impairment. Alterations in sensorimotor activity could not account for these performance deficits since control and 4-VO rats demonstrated equivalent choice time per maze arm. Performance deficits in rats following forebrain ischemic injury may be similar to some of the cognitive deficits found in humans survivors of cerebral hypoxia-ischemia.

Animals↗
PubMed2006

Blockade of mGluR glutamate receptors in the subthalamic nucleus ameliorates motor asymmetry in an animal model of Parkinson's disease.

It has been suggested that Group I metabotropic glutamate receptor antagonists could have potential therapeutic value in the treatment of Parkinson's disease. There is evidence that when given systemically, 2-methyl-6-(phenylethynyl)-pyridine (MPEP), a metabotropic glutamate receptor type 5 (mGluR5) antagonist, produces anti-parkinsonian effects in animal models, but the site of action has not been directly established. In the present study, we examined whether the subthalamic nucleus (STN) and its output structures may mediate such an effect using a unilateral rat model of Parkinson's disease. A battery of simple behavioral tests, reliably sensitive to dopamine depletion, was applied consecutively: (i) prior to surgery; (ii) 3 weeks following a unilateral 6-hydroxydopamine lesion of the substantia nigra pars compacta; (iii) at 1 h, 24 h and 4 days following a microinjection of MPEP, via an indwelling cannula, into the STN, entopeduncular nucleus (EP) or substantia nigra zona reticulata. Unilaterally dopamine-depleted animals typically had severe motor and sensorimotor asymmetries 3 weeks following surgery. Microinjection of 25 nmol MPEP into the STN of these animals significantly attenuated these asymmetries relative to vehicle. Further microinjections of lower doses (5 and 10 nmol) revealed a dose-response effect. Microinjection of MPEP into either the EP or substantia nigra zona reticulata was without effect. These data suggest that MPEP may act at the level of the STN to reduce glutamatergic overactivity and thereby induce anti-parkinsonian effects.

Animals↗
PubMed2005

Granulocyte colony-stimulating factor induces sensorimotor recovery in intracerebral hemorrhage.

Granulocyte colony-stimulating factor (G-CSF) has been used in the treatment of neutropenia in hematologic disorders. The neuroprotective and anti-inflammatory effects of G-CSF were reported in various neurological disease models. In this study, we examined whether G-CSF induces functional recovery after intracerebral hemorrhage (ICH). ICH was induced using collagenase injection in adult rats. Either G-CSF (50 microg/kg, i.p.) or saline was given from 2 h after ICH and every 24 h for 3 days. 72 h after ICH induction, the rats were sacrificed for histological analysis and measurement of brain edema. Behavioral tests were performed before and 1, 7, 14, 21, 28, and 35 days after ICH. We also measured the blood-brain barrier (BBB) permeability using Evans blue dye injection method. G-CSF-treated rats recovered better on rotarod and limb placing tests, starting from 14 days throughout 5 weeks after ICH. The brain water content and BBB permeability of G-CSF-treated group decreased in the lesioned hemispheres compared with those of ICH-only group. In G-CSF-treated group, the number of TUNEL+, myeloperoxidase+, and OX42+ cells was smaller than that of ICH-only group in the periphery of hematoma. These findings suggest that G-CSF induces long-term sensorimotor recovery after ICH with reduction of brain edema, inflammation, and perihematomal cell death.

Animals↗
PubMed2003

Patterns of functional activity associated with cocaine self-administration in the rat change over time.

RATIONALE: Although imaging studies in human addicts have been valuable for identifying the neural substrates of the effects of abused drugs, few studies have used this approach in animal models where conditions can be carefully controlled. OBJECTIVE: To define the substrates that mediate the effects of cocaine in a rodent model of cocaine self-administration using the 2-[(14)C]deoxyglucose method and to assess changes in these patterns over the course of drug exposure. METHODS: Male Sprague-Dawley rats self-administered cocaine (0.75 mg/kg per injection; FR2; 21 injections/session) and control rats received saline infusions in the same pattern as the cocaine rats for 5 or 30 days. Metabolic mapping was applied immediately after the final session. RESULTS: Following 5 days of self-administration, rates of glucose utilization were decreased in the nucleus accumbens, and increased in autonomic brainstem structures and in sensorimotor regions. After 30 days of cocaine exposure, self-administration reduced glucose utilization throughout the dorsal and ventral striatum, central nucleus of the amygdala, medial forebrain bundle, and infralimbic and prelimbic prefrontal cortices. In addition, at this time point glucose utilization was no longer elevated in any autonomic or sensorimotor brain regions. CONCLUSIONS: These data demonstrate that the distribution of functional activity associated with self-administered cocaine undergoes considerable change over the course of drug exposure. While increases in metabolic rates were largely found in autonomic and sensorimotor structures after short-term cocaine access, decreases were prominent in mesocorticolimbic regions after prolonged exposure. These differences in the patterns of brain activity that develop with long-term cocaine self-administration may play a role in the transition to habitual drug seeking behavior.

Animals↗
PubMed1998

Differential effects of GDNF treatment on rotational asymmetry, skilled forelimb use deficits and sensory neglect in unilateral 6-OHDA-lesioned rats.

The ability of a single intranigral infusion of glial cell line-derived neurotrophic factor (GDNF) to reverse deficits in skilled paw usage and sensorimotor orientation and to ameliorate apomorphine-induced rotational asymmetry in unilateral 6-hydroxydopamine-lesioned rats was examined. After lesioning, all rats developed sensory inattention on the side contralateral to the lesion, rotational asymmetry in response to apomorphine administration and significant deficits in successfully performing a forelimb reaching task dependent upon the use of somatosensory and proprioceptive feedback. A single intranigral injection of GDNF (300 micro g) made 4 wks. after the 6-OHDA lesion, significantly decreased the number of drug-induced rotations at 1 and 2 wks. after GDNF administration. At the same time however, no improvements were noted in performance of the paw reaching task or in sensorimotor orienting. Post mortem analyses showed that the GDNF treatment did not cause any increase in striatal dopamine levels but did increase tyrosine hydroxylase-positive immunohistochemical staining in the substantia nigra on the side of the GDNF infusion. These results demonstrate the need for multiple behavioral measures of efficacy when evaluating treatments for parkinsonism in the unilateral 6-hydroxydopamine lesion model in the rat.

Journal Article↗
PubMed2006

Spatial updating in virtual reality: the sufficiency of visual information.

Robust and effortless spatial orientation critically relies on "automatic and obligatory spatial updating", a largely automatized and reflex-like process that transforms our mental egocentric representation of the immediate surroundings during ego-motions. A rapid pointing paradigm was used to assess automatic/obligatory spatial updating after visually displayed upright rotations with or without concomitant physical rotations using a motion platform. Visual stimuli displaying a natural, subject-known scene proved sufficient for enabling automatic and obligatory spatial updating, irrespective of concurrent physical motions. This challenges the prevailing notion that visual cues alone are insufficient for enabling such spatial updating of rotations, and that vestibular/proprioceptive cues are both required and sufficient. Displaying optic flow devoid of landmarks during the motion and pointing phase was insufficient for enabling automatic spatial updating, but could not be entirely ignored either. Interestingly, additional physical motion cues hardly improved performance, and were insufficient for affording automatic spatial updating. The results are discussed in the context of the mental transformation hypothesis and the sensorimotor interference hypothesis, which associates difficulties in imagined perspective switches to interference between the sensorimotor and cognitive (to-be-imagined) perspective.

Adolescent↗