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PubMed1996

Acute behavioral effects of MK-801 in the mouse.

The acute effects of 0.05 mg/kg MK-801 on spatial learning and memory in male mice were studied using a modified hole board food search task. Dose-response sensorimotor and activity tests suggested that this dose of MK-801 did not induce significant nonassociative effects. Mice were trained on the hole board using a massed trials protocol to learn the location of a hole baited with a food reward among four corner holes. Retention was tested 24 h later. Mice were split into two groups matched according to acquisition scores. The following week, mice injected with 0.05 mg/kg MK-801 30 min before being trained to a different baited hole were significantly impaired in acquiring a new baited hole location compared to saline-treated mice, although retention performance was unaffected. The same result was found in another experiment in which treatments were crossed over, and a different version of the task was used. However, in another experiment, 0.05 mg/kg MK-801 did not impair performance when the hole board task was well learned.

Animals↗
PubMed1985

Profound disturbances of spontaneous and learned behaviors following lesions of the nucleus basalis magnocellularis in the rat.

It has been shown that a marked decline in the cortical activity of the cholinergic synthesizing enzyme choline-acetyltransferase (ChAT), accompanied by a severe neuronal loss in the nucleus basalis magnocellularis of Meynert occurs in the brains of patients with senile dementia of the Alzheimer type. However, the functional role of these neurons is largely unknown. In fact, very few studies have been done in animals. In this paper we report the behavioral effects of the lesion of the nucleus basalis magnocellularis in the rat either by radiofrequency current or by ibotenic acid injection at the level of the cell bodies. The two kinds of lesion lead to a profound disturbance of spontaneous and learned behaviors. There is a complete disorganization of behavior which is evidenced by an enhanced locomotor activity, an alteration in alimentary and hoarding behavior. In addition, we observed a deterioration of spatial memory and an incapacity to reverse a previously learned response. Biochemical assay showed that radiofrequency and ibotenic acid lesions produced a decrease of ChAT activity in the prefrontal and sensorimotor cortices and in amygdala without affecting the hippocampus or striatum. Ibotenic acid lesions seem to specifically destroy the cell bodies of the nucleus basalis magnocellularis since the dopaminergic and noradrenergic fibers of passage remained intact as measured by the unchanged level of endogenous catecholamine concentration in the terminal region in the prefrontal cortex. Presently, it cannot be said that the behavioral syndrome results solely from the lesion of the cholinergic neurons. Also, it is likely that the lesion of the nucleus basalis magnocellularis in the rat does not exactly reproduce the behavioral syndrome observed in Alzheimer's disease in man. However, this experimental approach in leading to a better knowledge of the functioning of these neurones could improve our understanding of this disease.

Animals↗
PubMed2005

Functional somatotopy in sensorimotor cortex.

In an effort to understand the highly distributed somatotopy of primary motor cortex, this review draws on principles derived from studies of auditory, visual and somatosensory cortical areas. In each case, a behaviorally important feature or function is overlaid in multiple locations on an underlying topographic map of the peripheral sensory surface. Recent studies of hand muscle synergies suggest the types of two-dimensional functional axes that might reasonably be mapped to the two-dimensional surface of the primary motor cortex. However, other research emphasizes that even a functional somatotopy must be extremely flexible.

Animals↗
PubMed2001

Expression of the melanin-concentrating hormone (MCH) receptor mRNA in the rat brain.

The melanin-concentrating hormone (MCH) system is thought to be an important regulator of food intake. Recently the orphan G protein-coupled receptor SLC-1 was identified as the MCH receptor (MCHR). Preliminary analyses of MCHR mRNA distribution have supported a role for the MCH system in nutritional homeostasis. We report here a complete anatomical distribution of the MCHR mRNA. We have found high levels of expression of MCHR mRNA in most anatomical areas implicated in control of olfaction, with the exception of the main olfactory bulb. Dense labeling was also detected in the hippocampal formation, subiculum, and basolateral amygdala, all of which are important in learning and memory, and in the shell of the nucleus accumbens, a substrate for motivated behavior and feeding. Within the hypothalamus, MCHR mRNA was moderately expressed in the ventromedial nucleus, arcuate nucleus, and zona incerta, all of which serve key roles in the neuronal circuitry of feeding. In the brainstem, strong expression was observed in the locus coeruleus, which is implicated in arousal, as well as in nuclei that contribute to orofacial function and mastication, including the facial, hypoglossal, motor trigeminal, and dorsal motor vagus nuclei. In most regions there was a good correspondence between MCHR mRNA distribution and that of MCH-immunoreactive fibers. Taken together, these data suggest that MCH may act at various levels of the brain to integrate various aspects of feeding behavior. However, the extensive MCHR distribution throughout the brain suggests that this receptor may play a role in other functions, most notably reinforcement, arousal, sensorimotor integration, and autonomic control.

Amygdala↗
PubMed1995

Neonatal excitotoxic hippocampal damage in rats causes post-pubertal changes in prepulse inhibition of startle and its disruption by apomorphine.

Neonatal excitotoxic hippocampal damage in the rat results in postpubertal onset of a variety of abnormal behaviors related to excessive dopaminergic transmission in the mesolimbic/nigrostriatal system, and thus may be considered an animal model of some aspects of schizophrenia. Because sensorimotor gating is impaired in adult patients with schizophrenia and in rats with experimentally induced mesolimbic dopamine hyperactivity, the present experiments investigated the effects of neonatal (postnatal day 7, PD7) ibotenic acid (3 micrograms) lesions of the ventral hippocampus (VH) on the amplitude and prepulse inhibition (PPI) of acoustic startle in prepubertal (PD35) and postpubertal (PD56) rats. Startle was elicited using 105 and 118-dB pulses alone or preceded by 4, 8, or 16 dB above-background prepulses in rats treated with vehicle or apomorphine (APO; 0.025 or 0.1 mg/kg SC). At PD35, PPI in VH-lesioned rats did not differ significantly from these measures in sham operated rats. Apomorphine significantly increased startle amplitude and reduced PPI in both sham operated and VH-lesioned rats at PD35. At PD56, startle amplitude in VH-lesioned rats was not significantly different from controls, but PPI was reduced significantly compared to controls. Ventral hippocampus lesioned rats also exhibited an exaggerated reduction in PPI after treatment with APO. These findings provide further evidence of postpubertal impairments that may be related to increased mesolimbic dopamine transmission and receptor sensitivity in rats with neonatal hippocampal damage, and provide further support for the fidelity of this animal model of schizophrenia.

Animals↗
PubMed1990

"On-line" measurement of acetylcholinesterase release from the substantia nigra of the freely-moving guinea-pig.

Acetylcholinesterase is released from dopaminergic cells within the substantia nigra. The functional significance of this phenomenon has been studied in the freely-moving animal by a novel system for measuring acetylcholinesterase release from the substantia nigra "on-line" and in vivo. In the unanaesthetized guinea-pig the amount of acetylcholinesterase released was significantly greater than during anaesthesia, and release occurred in a more pulsatile manner. In addition, release of acetylcholinesterase could be evoked by either pharmacological or physiological manipulations, i.e. (1) a depolarizing concentration of potassium ions administered locally; (2) metamphetamine, administered systematically, which also resulted in increased locomotor activity; (3) drinking behaviour, elicited by presentation of a water bottle. Although all three treatments were accompanied by an increase in acetylcholinesterase release within the substantia nigra, potassium-evoked release did not cause any detectable change in behaviour. It is therefore suggested that release of the protein acetylcholinesterase within the substantia nigra is not necessarily a direct cause of locomotor activity: rather, it reflects diverse sensorimotor events.

Acetylcholinesterase↗
PubMed1994

N-methyl-D-aspartate receptor blockade impairs behavioural performance of rats in a reaction time task: new evidence for glutamatergic-dopaminergic interactions in the striatum.

The effects of blocking glutamate transmission at the N-methyl-D-aspartate receptor subtype were studied in rats performing a conditioned reaction time motor task. Rats were trained to release a lever after the onset of a visual stimulus within a time limit to obtain food reward. The results showed that the performances of the groups receiving the N-methyl-D-aspartate receptor antagonists dizocilpine maleate (0.1 mg/kg) injected systemically or DL-2-amino-5-phosphonovaleric acid at the highest dose tested (5.0 micrograms/microliter/side) injected locally into the striatum changed significantly as compared to controls. The effects of these antagonists, consisting of an increase in the number of lever releases occurring before the visual stimulus onset ("anticipated responses"), were similar to those induced by injecting dopamine into the same striatal location. Both dizocilpine maleate and DL-2-amino-5-phosphonovaleric acid (5.0 micrograms/microliter) reversed the motor deficits, resulting in an increase in the number of lever releases after the time limit ("delayed responses") that were induced by the D2 dopamine receptor antagonist raclopride. Although these results partly confirm the existence of a functional antagonism between the glutamatergic and the dopaminergic systems in the striatum, opposite findings were obtained with the group that received intrastriatal DL-2-amino-5-phosphonovaleric acid at the lowest dose (0.5 micrograms/microliter/side). When given alone, 0.5 micrograms/microliter DL-2-amino-5-phosphonovaleric acid had no behavioural effects, but when jointly administered with dopamine or raclopride, it was found to reverse the effects of dopamine and to potentiate the motor deficits induced by raclopride. These opposite effects on the reaction time task observed after the intrastriatal injection of DL-2-amino-5-phosphonovaleric acid, depending on the dose tested, occurred only after a combined treatment with a dopaminergic agonist or antagonist and suggest that the level of the striatal dopaminergic activity may play a critical role in regulating the glutamate transmission via the N-methyl-D-aspartate receptors during the performance of complex sensorimotor tasks of this kind.

2-Amino-5-phosphonovalerate↗
PubMed2004

Consequences of forced disuse of the impaired forelimb after unilateral cortical injury.

Extreme over-reliance on the impaired forelimb following unilateral lesions of the forelimb representation area of the rat sensorimotor cortex (FL-SMC) leads to exaggeration of injury when overuse is begun during the first week, but not later periods, after injury. Behavioral impairment is partially worsened by the additional tissue loss. In the present study, we show that complete disuse of the impaired forelimb during the first post-operative week renders surviving tissue vulnerable to later overuse of the same limb, in effect extending the window of vulnerability in which use-dependent exaggeration of brain injury can occur. Behavioral recovery is disrupted by complete disuse, but the degree of impairment is variable depending on the nature of the behavioral test employed. Our results uphold the idea that mild rehabilitative training early after injury is beneficial, while either extreme overuse or complete disuse may disrupt functional recovery.

Animals↗
PubMedDate not supplied

Effects of subanesthetic doses of ketamine on sensorimotor information processing in healthy subjects.

Ketamine, an antagonist N-Methyl-D-Aspartate receptor, induces a broad range of anomalies in healthy subjects similar to those observed in psychosis. Previous studies have shown that information sensorimotor processing was impaired in patients with schizophrenia. The aim of the study was to assess the effects of subanesthetic doses of ketamine on behavior symptoms and information processing in healthy volunteers. A double-blind, crossover, placebo-controlled study was performed with eight subjects. Brief Psychiatric Rating Scale, Scale for the Assessment of Negative Symptoms, and Scale for the Assessment of Positive Symptoms assessed behavior changes. Information processing was assessed using a choice reaction time. Three experimental factors (stimulus intensity, stimulus response compatibility, and foreperiod duration) chosen to affect a different stage of information processing were manipulated. Our study has demonstrated that administration of ketamine produced significant effects on Brief Psychiatric Rating Scale, Scale for the Assessment of Negative Symptoms, and Scale for the Assessment of Positive Symptoms scores. Results on choice reaction time demonstrated a significant longer reaction time under ketamine. Effects of stimulus intensity and compatibility stimulus response were similar under ketamine and under placebo. Moreover, there was a specific interaction between ketamine and foreperiod. This interaction indicated that foreperiod's effect was more prolonged under ketamine (29 ms) than under placebo (17 ms). These results showed that the clinical effects of ketamine were associated with schizophrenic-like impairments on choice reaction time in healthy subjects.

Adult↗
PubMed2002

Differential involvement of parietal and precentral regions in movement preparation and motor intention.

Flexible goal-oriented behavior relies on spatial coordinate transformations and motor control mechanisms, but also on the capability to take advantage of contextual information for steering the sensorimotor machinery. Although accurate performance of a sensorimotor task requires parietal and frontal regions, their differential contribution and functional relationship with other associative regions remains obscure. We have used event-related functional magnetic resonance imaging to measure human cerebral activity associated with motor cognitive processes in the context of delayed performance of an associative visuomotor task. Movement instruction (specified by visual cues) and motor performance (specified by an auditory cue) were separated by a variable delay period. By manipulating the predictive value of the instruction cue, we distinguished delay-related activity influenced by response probabilities (motor preparation and motor inhibition) from delay-related activity unaffected by the likelihood of providing a motor response (motor intention). We found delay-related activity distributed across a cerebral network involving not only frontal circuitry, but also extrastriate and mediotemporal regions. Areas showing motor intentions and preparatory responses were spatially intermingled. Posterior parietal cortex deviated from this pattern, showing delay-related activity regardless of movement probability, but no specific preparatory responses. These results suggest that posterior parietal cortex and dorsal precentral cortex play different strategic roles in handling associative visuomotor problems. While parietal regions cover a range of potential responses defined by the task setting, precentral regions focus on a likely movement. Temporo-prefrontal regions might incorporate contextual information in the visuomotor process by defining potential and probable responses on the basis of the task contingencies.

Acoustic Stimulation↗
PubMed1981

Relationship between language and sensorimotor development of Down syndrome and nonretarded children.

The relationship between sensorimotor and language development of Down syndrome and nonretarded children was investigated. The Ordinal Scales of Psychological Development (Uzgiris & Hunt, 1975) and the Receptive and Expressive Emergent Language (REEL) scale (Bzoch & League, 1970) were administered to 18 Down syndrome and 18 nonretarded children who had matched developmental ages of approximately 17 months. Comparison of the resulting scores indicated that although there were no differences between the groups on four subscales of the Uzgiris-Hunt, there were significant differences in favor of the nonretarded children on the Vocal Imitation subscale of the Uzgiris-Hunt and on Receptive and Expressive measures of the REEL. These results indicate that Down's syndrome children are delayed in their language development compared to nonretarded children of the same developmental age. This language delay appears to be related to deficiencies in vocal imitation skills but is not related to general sensorimotor functioning.

Child, Preschool↗
PubMed2006

Neonatal exposure to epidermal growth factor induces dopamine D2-like receptor supersensitivity in adult sensorimotor gating.

RATIONALE: Abnormality in the neurotrophic factor for dopamine neurons, epidermal growth factor (EGF), is associated with schizophrenia. Thus, rats treated with EGF as neonates are used as a putative animal model for schizophrenia showing impaired prepulse inhibition (PPI) and other cognitive deficits in the adult stage. OBJECTIVES: To elucidate the abnormal behavioral traits of this animal model, the EGF effects on the dopaminergic system were analyzed pharmacologically and biochemically at the adult stage. RESULTS: We examined the effects of subthreshold doses of dopamine agonists on PPI in this model. A non-selective dopamine agonist, apomorphine (0.1 mg/kg), decreased PPI in EGF-treated rats, but not in controls. Further, a D(2)-like receptor agonist, quinpirole (0.01 and 0.03 mg/kg), similarly decreased PPI in EGF-treated rats but had no effect in the control animals. In contrast, a D(1)-like receptor agonist, SKF38393 (3 and 10 mg/kg), had no effect on PPI in both groups. To explore the molecular mechanism underlying the change in sensorimotor gating, we assessed D(1) and D(2) receptors expression in the prefrontal cortex, striatum and hippocampus and their downstream signaling. Although there were no significant differences in basal receptor levels, quinpirole administration significantly enhanced phosphorylation of extracellular signal-regulated kinase (ERK) and cAMP response element binding protein (CREB) in the striatum of EGF-treated rats. CONCLUSION: These results suggest that circulating EGF in the early development substantially influences D(2) receptor-dependent regulation of sensorimotor gating.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1998

Insulin-like growth factor-1 ameliorates age-related behavioral deficits.

Insulin-like growth factor-1 has been found to be involved in the regulation of several aspects of brain metabolism, neural transmission, neural growth and differentiation. Because decreased insulin-like growth factor-1 and/or its receptors are likely to contribute to age-related abnormalities in behavior, the strategy of replacing this protein is one potential therapeutic alternative. The present study was designed to assess whether cognitive deficits with ageing may be partially overcome by increasing the availability of insulin-like growth factor-1 in the brain. Fischer-344 x Brown Norway hybrid (F1) male rats of two ages (four-months-old and 32-months-old) were preoperatively trained in behavioral tasks and subsequently implanted with osmotic minipumps to infuse the insulin-like growth factor-1 (23.5 microg/pump) or a vehicle, i.c.v. Animals were retested at two weeks and four weeks after surgery. Insulin-like growth factor-1 improved working memory in the repeated acquisition task and in the object recognition task. An improvement was also observed in the place discrimination task, which assesses reference memory. Insulin-like growth factor-1 had no effect on sensorimotor skills nor exploration, but mildly reversed some age-related deficits in emotionality. These data indicate a potentially important role for insulin-like growth factor-1 in the reversal of age-related behavioral impairments in rodents.

Aging↗
PubMed2006

Annotation: Tourette syndrome: a relentless drumbeat--driven by misguided brain oscillations.

OBJECTIVE: This annotation reviews recent evidence that points to the likely role of aberrant neural oscillations in the pathogenesis of Tourette syndrome (TS). METHODS: The available anatomic and electrophysiological findings in TS are reviewed in the context of an emerging picture of the crucial role that neural oscillations play in maintaining normal central nervous system (CNS) function. RESULTS: Neurons form behavior-dependent oscillating networks of various sizes and frequencies that bias input selection and facilitate synaptic plasticity, mechanisms that cooperatively support temporal representation as well as the transfer and long-term consolidation of information. Coherent network activity is likely to modulate sensorimotor gating as well as focused motor actions. When these networks are dysrhythmic, there may be a loss of control of sensory information and motor action. The known electrophysiological effects of medications and surgical interventions used to treat TS likely have an ameliorative effect on these aberrant oscillations. Similarly, a strong case can be made that successful behavioral treatments involve the willful training regions of the prefrontal cortex to engage in tic suppression and the performance of competing motor responses to unwanted sensory urges such that these prefrontal regions become effective modulators of aberrant thalamocortical rhythms. CONCLUSIONS: A deeper understanding of neural oscillations may illuminate the complex, challenging, enigmatic, internal world that is TS.

Basal Ganglia↗
PubMed2005

Behavioral and histological effects of chronic antipsychotic and antidepressant drug treatment in aged rats with focal ischemic brain injury.

Psychotropic drugs are commonly used in the elderly, including those who may sustain ischemic attacks. Concomitant CNS medication may interfere with functional recovery. The present study evaluated the effect of risperidone, an atypical neuroleptic, and fluoxetine, a selective serotonin reuptake inhibitor, on histological and functional outcome after experimental stroke in aged rats, which might be more vulnerable to brain insults. Aged Wistar rats were treated with risperidone at a dose of 1 mg/kg (i.p., once a day), fluoxetine at a dose of 5 mg/kg (i.p., once a day), or their combination. Drug treatment was started 7 days before focal cortical photothrombosis (Rose Bengal, 20 mg/kg) and continued for 28 days thereafter. Sensorimotor recovery was assessed by a new beam-walking test and spatial learning by the Morris water-maze before cortical stroke, immediately after stroke, and at the end of follow-up. Infarct volumes were measured from nitroblue tetrazolium-stained sections at the end of follow-up. The high slip ratio for the contralateral hindlimb in ischemic rats treated with risperidone indicated sensorimotor impairment when tested 2 h after drug administration. Sensorimotor impairment was not observed, however, when the rats were tested 24 h after risperidone administration. Similarly, water-maze performance was impaired 2 h after risperidone. Fluoxetine did not affect sensorimotor or water-maze performance. Cortical infarct volumes were not different in ischemic controls and ischemic rats treated with antipsychotic drugs. The present study showed that an atypical neuroleptic, risperidone, acutely impairs behavioral performance, but does not affect histological or functional outcome in aged rats subjected to cortical photothrombosis.

Affect↗
PubMed1995

The role of the basal ganglia in nociception and pain.

The involvement of the basal ganglia in motor functions has been well studied. Recent neurophysiological, clinical and behavioral experiments indicate that the basal ganglia also process non-noxious and noxious somatosensory information. However, the functional significance of somatosensory information processing within the basal ganglia is not well understood. This review explores the role of the striatum, globus pallidus and substantia nigra in nociceptive sensorimotor integration and suggests several roles of these basal ganglia structures in nociception and pain. Electrophysiological experiments have detailed the non-nociceptive and nociceptive response properties of basal ganglia neurons. Most studies agree that some neurons within the basal ganglia encode stimulus intensity. However, these neurons do not appear to encode stimulus location since the receptive fields of these cells are large. Many basal ganglia neurons responsive to somatosensory stimulation are activated exclusively or differentially by noxious stimulation. Indirect techniques used to measure neuronal activity (i.e., positron emission tomography and 2-deoxyglucose methods) also indicate that the basal ganglia are activated differentially by noxious stimulation. Neuroanatomical experiments suggest several pathways by which nociceptive information may reach the basal ganglia. Neuroanatomical studies have also indicated that the basal ganglia are rich in many different neuroactive chemicals that may be involved in the modulation of nociceptive information. Microinjection of opiates, dopamine and gamma-aminobutyric acid (GABA) into the basal ganglia have varied effects on pain behavior. Administration of these neurochemicals into the basal ganglia affects supraspinal pain behaviors more consistently than spinal reflexive behaviors. The reduction of pain behavior following electrical stimulation of the substantia nigra and caudate nucleus provides additional evidence for a role of the basal ganglia in pain modulation. Some patients with basal ganglia disease (e.g., Parkinson's disease, Huntington's disease) have alterations in pain sensation in addition to motor abnormalities. Frequently, these patients have intermittent pain that is difficult to localize. Collectively, these data suggest that the basal ganglia may be involved in the (1) sensory-discriminative dimension of pain, (2) affective dimension of pain, (3) cognitive dimension of pain, (4) modulation of nociceptive information and (5) sensory gating of nociceptive information to higher motor areas. Further experiments that correlate neuronal discharge activity with stimulus intensity and escape behavior in operantly conditioned animals are necessary to fully understand how the basal ganglia are involved in nociceptive sensorimotor integration.

Afferent Pathways↗
PubMed2001

Progressive neuronal and motor dysfunction in mice overexpressing the serine protease inhibitor protease nexin-1 in postmitotic neurons.

Perturbation of the homeostasis between proteases and their inhibitors has been associated with lesion-induced or degenerative neuronal changes. Protease nexin-1 (PN-1), a secreted serine protease inhibitor, is constitutively expressed in distinct neuronal cell populations of the adult CNS. In an earlier study we showed that transgenic mice with ectopic or increased expression of PN-1 in postnatal neurons have altered synaptic transmission. Here these mice are used to examine the impact of an extracellular proteolytic imbalance on long-term neuronal function. These mice develop disturbances in motor behavior from 12 weeks on, with some of the histopathological changes described in early stages of human motor neuron disease, and neurogenic muscle atrophy in old age. In addition, sensorimotor integration, measured by epicranial multichannel recording of sensory evoked potentials, is impaired. Our results suggest that axonal dysfunction rather than cell death underlies these phenotypes. In particular, long projecting neurons, namely cortical layer V pyramidal and spinal motor neurons, show an age-dependent vulnerability to PN-1 overexpression. These mice can serve to study early stages of in vivo neuronal dysfunction not yet associated with cell loss.

Amyloid beta-Protein Precursor↗