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PubMed1999

Central neuronal loss and behavioral impairment in mice lacking neurotrophin receptor p75.

The neurotrophin receptor p75 is a low-affinity receptor that binds neurotrophins. To investigate the role of p75 in the survival and function of central neurons, p75 null-mutant and wild type litter mate mice were tested on behavioral tasks. Null mutants showed significant performance deficits on water maze, inhibitory avoidance, motor activity, and habituation tasks that may be attributed to cognitive dysfunction or may represent a global sensorimotor impairment. The p75 null-mutant and wild type litter mate mice were assessed for central cholinergic deficit by using quantitative stereology to estimate the total neuronal number in basal forebrain and striatum and for subpopulations expressing the high-affinity tyrosine receptor kinase A (trkA) neurotrophin receptor and choline acetyltransferase (ChAT). In the adult brain, cholinergic neurons of the basal forebrain receive target-derived trophic support, whereas cholinergic striatal neurons do not. Adult p75 null-mutant mice had significant reduction of basal forebrain volume by 25% and had a corresponding significant loss of 37% of total basal forebrain neurons. The basal forebrain population of ChAT-positive neurons in p75-deficient mice declined significantly by 27%, whereas the trkA-positive population did not change significantly. There was no significant change in striatal volume or in striatal neuronal number either in total or by cholinergic subpopulation. These results demonstrate vulnerability to the lack of p75 in adult central neurons that are neurotrophin dependent. In addition, the loss of noncholinergic central neurons in mice lacking p75 suggests a role for p75 in cell survival by an as yet undetermined mechanism. Possible direct and indirect effects of p75 loss on neuronal survival are discussed.

Analysis of Variance↗
PubMed2001

Anatomical evidence for brainstem circuits mediating feeding motor programs in the leopard frog, Rana pipiens.

Using injections of small molecular weight fluorescein dextran amines, combined with activity-dependent uptake of sulforhodamine 101 (SR101), brainstem circuits presumed to be involved in feeding motor output were investigated. As has been shown previously in other studies, projections to the cerebellar nuclei were identified from the cerebellar cortex, the trigeminal motor nucleus, and the vestibular nuclei. Results presented here suggest an additional pathway from the hypoglossal motor nuclei to the cerebellar nucleus as well as an afferent projection from the peripheral hypoglossal nerve to the Purkinje cell layer of the cerebellar cortex. Injections in the cerebellar cortex combined with retrograde labeling of the peripheral hypoglossal nerve demonstrate anatomical convergence at the level of the medial reticular formation. This suggests a possible integrative region for afferent feedback from the hypoglossal nerve and information through the Purkinje cell layer of the cerebellar cortex. The activity-dependent uptake of SR101 additionally suggests a reciprocal, polysynaptic pathway between this same area of the medial reticular formation and the trigeminal motor nuclei. The trigeminal motor neurons innervate the m adductor mandibulae, the primary mouth-closing muscle. The SR101 uptake clearly labeled the ventrolateral hypoglossal nuclei, the medial reticular formation, and the Purkinje cell layer of the cerebellar cortex. Unlike retrograde labeling of the peripheral hypoglossal nerve, stimulating the hypoglossal nerve while SR101 was bath-applied labeled trigeminal motor neurons. This, combined with the dextran labeling, suggests a reciprocal connection between the trigeminal motor nuclei and the cerebellar nuclei, as well as the medulla. Taken together, these data are important for understanding the neurophysiological pathways used to coordinate the proper timing of an extremely rapid, goal-directed movement and may prove useful for elucidating some of the first principles of sensorimotor integration.

Action Potentials↗
PubMed2005

Neurotransmission- and cellular stress-related gene expression associated with prepulse inhibition in mice.

Prepulse inhibition (PPI) is a cross-species measure of sensorimotor gating. PPI deficits have been associated with a number of neuropsychiatric disorders, including schizophrenia. Differential PPI has been demonstrated also across various inbred mouse strains; however, the molecular mechanisms underlying these differences in sensorimotor gating remain unclear. Here, we sought to identify gene expression in the medial prefrontal cortex (mPFC) of mice associated with PPI using a laser microdissection and microarray analysis-based approach. C57BL/6 mouse substrains were used for the study as they have dramatically different PPI. Transcriptional analysis of closely related substrains was predicted to reduce the detection of genetic variation incidental to the phenotype. Microarray analysis comparing the mPFC of C57BL/6J to C57BL/6NHsd mice revealed neurotransmission- and cellular stress-related transcriptional responses associated with lower PPI. Down-regulation of metabotropic glutamate receptor 5, phospholipase C, and inositol monophosphatase 1 gene expression suggest altered phosphoinositide signaling, while decreased expression of a gamma-amino-butyric acid (GABA)A receptor subunit implies changes in GABAergic signaling. Genes involved in neuronal excitation and protection were also differentially expressed, including up-regulation of five immediate early genes and anti-apoptotic/survival factors as Bcl2-associated athanogene 3 and brain-derived neurotrophic factor. These data support previous findings of genetic influences on PPI, and provide novel insights into the molecular mechanisms regulating sensorimotor gating.

Animals↗
PubMed2003

Reduced G(i) and G(o) protein function in the rat nucleus accumbens attenuates sensorimotor gating deficits.

Prepulse inhibition of the acoustic startle response (PPI) is a cross-species measure of sensorimotor gating, which is severely disrupted in patients with schizophrenia. PPI deficits can be produced in experimental animals by administration of selective D(2)-like dopamine receptor agonists in the nucleus accumbens (NAc). G proteins coupled to these receptors reportedly are altered in the NAc of patients with schizophrenia. Therefore, we sought to determine whether experimental inactivation of intracellular G proteins in the NAc alters PPI. In adult male Sprague-Dawley rats, baseline PPI was determined by presenting acoustic pulse stimuli (120 dB) alone or preceded 100 ms earlier by prepulse stimuli (3, 6 or 12 dB above 70 dB ambient noise). PPI disruption was assessed in the presence of quinpirole (0.0, 0.05, 0.1, 0.5 mg/kg, sc), and pertussis toxin (PTX; 0.05 microg/side) was then infused into the NAc bilaterally. Ten days later, quinpirole-mediated disruption of PPI was significantly reduced; neither PTX alone, nor heat-inactivated PTX had any effect on quinpirole-induced PPI reductions. PPI was significantly higher after PTX infusion upon moderate quinpirole challenge, suggesting that D(2)-like receptors were less effective. PTX treatment significantly reduced basal and dopamine-stimulated [35S]GTPgammaS binding in the NAc core and shell, and reduced G(i)(alpha) protein immunoreactivity in the NAc. The results suggest that PPI disruption mediated by D(2)-like receptor activation in the NAc depends on coupling to G(i) and G(o) proteins, alteration of which could cause sensorimotor gating deficits in schizophrenia.

Acoustic Stimulation↗
PubMed1999

Progressive and gender-dependent cognitive impairment in the APP(SW) transgenic mouse model for Alzheimer's disease.

To determine if early cognitive sensorimotor deficits exist in APP(SW) transgenic mice overexpressing human amyloid precursor protein (APP). Tg+ and Tg- animals at both 3 and 9 months of age (3M and 9M, respectively) were evaluated in a comprehensive battery of measures. The performance of all Tg+ mice at both ages was no different from all Tg- controls in Y-maze alternations, water maze acquisition, passive avoidance, and active avoidance testing. By contrast, results from other tasks revealed substantive cognitive deficits in Tg+ mice that were usually gender-dependent and sometimes progressive in nature. Between 3M and 9M, a progressive impairment was observed in circular platform performance by Tg+ males, as was a progressive deficit in visible platform testing for all Tg+ animals. Other transgenic effects included both impaired water maze retention and circular platform performance in 3M Tg+ females; this later effect was responsible for an overall (males + females) Tg+ deficit in circular platform performance at 3M. Sensorimotor testing revealed several Tg+ effects, most notably an increased activity of Tg+ males in both open field and Y-maze at 3M. Significant correlations between a number of behavioral measures were observed, although factor analysis suggests that each task measured components of sensorimotor/cognitive function not measured by other tasks. Finally, Tg+ mice had lower survivability than Tg- animals through 9M (85 vs. 96%). In summary, these results demonstrate the presence of gender-related and progressive cognitive deficits in APP(SW) transgenic mice at a relatively early age (i.e., prior to overt, beta-amyloid deposition in the brain), suggesting a pathophysiologic role for elevated levels of 'soluble' beta-amyloid in such impairments.

Alzheimer Disease↗
PubMed1985

Microstimulation of the primate neostriatum. II. Somatotopic organization of striatal microexcitable zones and their relation to neuronal response properties.

Sensorimotor response properties of neostriatal neurons were characterized in conjunction with assessments of the motor effects of intrastriatal microstimulation in unanesthetized rhesus monkeys. Neuronal activity and microexcitability were assessed at 250- to 500-micron intervals and, in some cases, at 25- to 100-micron intervals. The results are based on the functional characterization of 878 putamen and 224 caudate neurons and analysis of the effects of microstimulation at each of these recording sites. Recording/stimulation sites were located between stereotaxic planes A6 and A22 in 81 microelectrode tracks from three monkeys. A total of 443 (50.4%) putamen neurons showed discrete responses to the sensorimotor examination. Of neurons with sensorimotor responses, 232 (52.4%) showed increased rates of discharge in relation to both active and passive movements of specific body parts. An additional 193 (43.6%) cells increased their rates of discharge only during the monkey's active movements of specific body parts. The remaining 18 (4.0%) cells appeared to respond exclusively to passive somatosensory stimulation. The sensorimotor response areas of putamen neurons ranged in size from an entire limb to a single joint. Putamen neurons were somatotopically organized throughout the rostrocaudal extent of the nucleus. Neurons with sensorimotor response areas involving the leg were located in the dorsolateral putamen, those with orofacial representations were located ventromedially, and those with arm representations were located in an intermediate position. Microstimulation evoked discrete movements of individual body parts at 21.6% of the 878 putamen sites. Over 95% (181/190) of the effective sites were located within the central half of the rostrocaudal extent of the putamen, between stereotaxic planes A10 and A17. The pattern of somatotopic organization revealed by microstimulation was the same as that derived from sensorimotor response properties of putamen neurons. Moreover, a close correspondence was observed between the movements evoked from a given SMZ and the functional properties of local neurons. In contrast to the results obtained in the putamen, none of the 224 stimulation sites in the caudate nucleus was microexcitable, and only 17 (7.6%) of the caudate neurons had definable sensorimotor response properties. This is consistent with the view that the primate putamen, by virtue of its anatomic connections with the sensorimotor and premotor cortical fields, is more directly involved in motor functions, whereas the caudate nucleus, by virtue of its connections with cortical "association" areas, is involved in more complex behavioral functions.

Animals↗
PubMed1994

Synaptic plasticity in the thalamo-cortical pathway as one of the neurobiological correlates of forelimb flexion conditioning: electrophysiological investigation in the cat.

1. In a previous study, using a chronic cat preparation subjected to an associative conditioning procedure, we described the plasticity of the thalamo-cortical pathway by qualitatively and quantitatively analyzing the motor responses induced by stimulating each of the relays on the cerebello-thalamo-cortical pathway. In the present study, it was proposed to analyze the effects on the synapses located between thalamic endings and cortical neurones, using a twofold behavioral and electrophysiological approach, with a view to correlating the patterns of synaptic plasticity with the changes in the motor responses recorded. 2. For this purpose, a reduced, functionally organized sensorimotor circuit, which can be taken to be a neuronal analog of associative conditioning, was studied in an awake chronic animal preparation. This circuit was defined on the basis of the sites at which conditioned (CS) and unconditioned stimuli (UCS) were applied: the CS was applied at a site on the cerebellar interpositus nucleus which activated the forepaw musculature so as to induce flexion movements and the UCS was applied to the skin of the distal part of that paw so as to induce reflex flexion movements. By repetitively activating the central nervous pathways by the associated CS and UCS according to a predefined temporal pattern, the efficiency of the thalamo-cortical pathway's contribution to the movement production was enhanced, and its capacity to convey the cerebellar inputs to neurons in the motor cortex increased. 3. The associative nature of the conditioning was tested using previously established criteria. The setting up of motor and central changes in response to the repetitive presentation of paired CS and UCS, the fact that these changes were reversible because they could be abolished by applying extinction procedures, and the consistency of their occurrence whenever the CS was applied repeatedly alone for several days to naive animals, all showed that the stimuli of both kinds (CS and UCS) had to be applied together for the plasticity of the thalamo-cortical pathway to be expressed. 4. By determining whether the waves constituting the cerebello-cortical responses were excitatory or inhibitory, the nature of the changes in the transmission of the cerebellar impulses to neurons in the motor cortex was established.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMedDate not supplied

[Local disinhibition with bicuculline does not break the trained relationship between afferent input and efferent output in cat motor cortex].

Neurons of the cat motor cortex related to the lifting-withdrawal phase of forepaw placing reaction are preferentially activated by tactile stimulation of the dorsal surface of the forepaw. The placing reaction was altered in such a way that the innate "dorsal placing" was subjected to extinction and was substituted for the newly acquired conditioned reaction in response to the ventral side stimulation. This alteration of placing reaction led to the inversion of the innate input-output relationship in the motor cortex. The neurons related to forepaw lifting-withdrawal began to be activated by tactile stimulation of the ventral rather than dorsal forepaw surface. Local cortical disinhibition by bicuculline application at the recording site qualitatively changed neither normal input-output relationships nor inverse relationships after placing reaction alteration. This suggests that alteration of the sensorimotor coordination in cat motor cortex is underlain by changes in excitatory rather than inhibitory connections.

Animals↗
PubMed1990

Effects of temperature on nervous system: implications for behavioral performance.

Temperature change has a major impact on the function of the nervous system and its components, including altering synaptic gain and changing synaptic and conduction delays. Although many animals are subject to changes in body temperature, the degree of temperature change actually experienced by many poikilotherms is not well documented. The fact that many animals continue to exhibit coordinated sensorimotor function during changes in body temperature indicates that some form of temperature compensation has occurred within the nervous system. Compensations may occur automatically (opposing effects of temperature offsetting each other), they may be an inherent property of closed-loop systems, or they may be effected by more sophisticated control mechanisms such as those of the vertebrate cerebellum.

Action Potentials↗
PubMed2001

Group I metabotropic glutamate antagonist reduces acute neuronal degeneration and behavioral deficits after traumatic brain injury in rats.

Recent studies indicate that acute activation of Group I mGluRs following traumatic brain injury (TBI) contributes to the ensuing pathophysiology. The present study examined the effects of post-TBI administration of the selective mGluR1 antagonist (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA) on acute neuronal degeneration in the hippocampus and long-term sensorimotor and learning/memory outcome. In Experiment 1, 26 rats received 0.4, 2.0, or 10.0 nmol AIDA or artificial CSF vehicle infusion into the hippocampus starting 5 min postinjury. At 24 h after TBI characteristic pyramidal cell degeneration was observed in Fluoro-Jade-stained coronal sections of the CA2/3 sectors of the dorsal hippocampus. The mean (+/-SEM) number of Fluoro-Jade-positive neurons in the 10 nmol AIDA group (184 +/- 32) was significantly less (P < 0.05) than the vehicle group (310 +/- 47). In Experiment 2, 20 rats were trained on sensorimotor and memory tasks prior to parasagittal fluid percussion TBI. Rats were administered 10 nmol AIDA or vehicle as in Experiment 1. Rats were assessed on beam walking and radial arm maze (RAM) performance weekly for 6 weeks after TBI. Acquisition of a Morris water maze (MWM) task was assessed on days 11-15 after TBI. The AIDA-treated group had significantly reduced deficits in beam walk, MWM, and RAM performance compared to the vehicle-treated group. These data indicate that injury-induced acute activation of mGluR1 receptors contributes to both the cellular pathology and the behavioral morbidity associated with TBI.

Animals↗
PubMed1999

Avian behavioural neuroscience: past, present and future perspectives.

A survey of avian brain-behavior conference reports of the last 25 years reveals that neither the avian species studied nor the types of scientific questions asked have changed very much since the first such conference report in 1974. The birds studied tend, for the most part, to be pigeons, chickens, quail, and canaries. Because of the growing interest in avian vocalization and its neural control, one recent conference featured studies of canaries, zebra finches, and budgerigars. The topics of investigation at these conferences largely have involved sensory systems, mostly sensory and sensorimotor mechanisms with a heavy emphasis on vision and audition, as well as studies of learning and memory. Future research should expand the range of orders and species of birds studied so as to shed light on evolutionary trends within Aves as a whole. The scope of behavioral questions asked also should be broadened to include topics of neuroethological interest.

Animals↗
PubMed2004

Effect of brain-derived neurotrophic factor treatment and forced arm use on functional motor recovery after small cortical ischemia.

BACKGROUND AND PURPOSE: Both the administration of growth factors and physical therapy such as forced arm use (FAU) are promising approaches to enhance recovery after stroke. We explored the effects of these therapies on behavioral recovery and molecular markers of regeneration after experimental ischemia. METHODS: Rats were subjected to photothrombotic ischemia: sham (no ischemia), control (ischemia), brain-derived neurotrophic factor (BDNF; ischemia plus BDNF, 20 microg), and FAU (ischemia plus FAU, 1-sleeve plaster cast ipsilateral limb). Animals survived 1 or 6 weeks and underwent behavioral testing (Rotarod, beam balance, adhesive removal, plantar test, neuroscore). After the rats were killed, brain sections were immunostained for semiquantitative analysis of MAP1B, MAP2, synaptophysin, GFAP expression, and quantification of infarct volumes. RESULTS: Infarct volumes were not different between the groups 1 or 6 weeks after ischemia. BDNF-treated animals had better functional motor recovery (Rotarod, beam balance, neuroscore) compared with all other groups (P<0.05). There was no significant adverse effect of early FAU treatment on motor recovery, although sensorimotor function (adhesive removal test) was impaired (P<0.05). There were no differences between groups as measured by nociception of the left and right forepaw (plantar test). BDNF treatment transiently induced MAP1B expression in the ischemic border zone and synaptophysin expression within the contralateral cortex 6 weeks after ischemia (P<0.05). Both BDNF and FAU reduced astrogliosis compared with controls (P<0.05). CONCLUSIONS: Postischemic intravenous BDNF treatment improves functional motor recovery after photothrombotic stroke and induces widespread neuronal remodeling. Early FAU treatment after stroke does not increase infarct size, impairs sensorimotor function, but leaves motor function unchanged. Postischemic astrogliosis was reduced by both treatments.

Animals↗
PubMed1985

Systems model for pupil size effect. II. Feedback model.

The human pupillary control system has been the subject of interest to biologists and engineers as an example of a sensorimotor reflex which can be embedded in a control system paradigm. We present a nonlinear feedback model whose compact structure allows us to hypothesize possible physiological mechanisms which generate the proper behavior of the pupil system. The important pupil responses, including pupil size effect, asymmetry, and response the high-frequency stimuli, are defined. This model was simulated on a digital computer and comparisons to the paradigm experimental responses were performed, demonstrating a fit to each of the observed conditions. Improvements on previous models are discussed.

Feedback↗
PubMed1986

Mechanisms contributing to sparing of function following neonatal damage to spinal pathways.

When spinal pathways are damaged in newborn animals and their behavior is examined in adulthood, motor function is superior to that seen in animals in which the same lesion was made in adulthood. This is the infant lesion effect. After neonatal sensorimotor cortex ablation, spinal hemisection, or spinal transection, sparing of contact placing is observed; in adults, all three lesions abolish contact placing permanently. The anatomical correlates of the infant lesion effect are different in each case. After neonatal unilateral cortical ablation, an exuberant crossed corticorubral pathway from the other cortex fails to retract (as it does normally), giving the remaining cortex a path for mediating contact placing. After neonatal spinal hemisection, late-developing corticospinal axons take an aberrant course around the lesion and mediate contact placing. After neonatal transection, the spinal inhibitory GABA-ergic system fails to develop to a normal extent. This may result in abnormal enhancement of spinal reflex pathways, especially since some dorsal roots increase their input after that lesion. Thus, a number of factors may influence the outcome of damage to the developing nervous system.

Age Factors↗
PubMed1993

The ontogeny of repetitive firing and its modulation by norepinephrine in rat neocortical neurons.

The postnatal ontogeny of electrical properties was studied in rat sensorimotor cortical neurons (P6 to adult) using intracellular recording in an in vitro slice preparation. Many action potential properties and input resistance changed during the first 4 postnatal weeks. Repetitive firing behavior also changed during the first postnatal month. Spike-frequency adaptation was much stronger in immature neurons. At 1 week postnatal, the majority of cortical neurons would only fire for less than 200 ms regardless of the intensity of long depolarizing current injections. These cells were normal in other parameters and could fire throughout a depolarizing current injection in the presence of inorganic calcium channel blockers or norepinephrine (NE), suggesting that the inability to fire was not due to injury. The frequency with which we encountered cells with this extreme adaptation decreased with age. Spike-frequency adaptation in immature neurons appears to be primarily controlled by Ca-dependent K+ conductances as in mature neurons. In mature and immature neurons, three afterhyperpolarizations (AHPs) could be distinguished by their rate of decline. The fast AHP followed repolarization of a single spike and was only partially Ca- and K-dependent. The medium duration AHP was Ca-dependent and apamin-sensitive and the slow AHP was partially Ca-dependent and not blocked by apamin. NE decreased the slow Ca-dependent AHP via beta-adrenergic receptors. This effect of NE on AHPs appeared qualitatively similar throughout postnatal development. NE had a proportionately greater effect in younger neurons, however, due to their relatively larger slow AHP. The quantitative differences of NE's action on the slow AHP (sAHP) led to a qualitative difference in NE's effect on firing behavior. The effects of NE on firing behavior may therefore be greater during times critical for cortical maturation.

Action Potentials↗
PubMed2004

Changes in rolandic mu rhythm during observation of a precision grip.

We recorded 128-channel EEG from 16 participants while they observed, imitated, and self-initiated the precision grip of a manipulandum. Mu rhythm amplitudes were significantly lower during observation of a precision grip than during observation of a simple hand extension without object interaction. Scalp topographies for subtractions of observation, imitation, and execution conditions from the control condition showed a high degree of congruence, supporting the notion of a human observation-execution matching system. Surface Laplacian transformations suggest that the decrease in mu amplitude during precision grip observation reflects desynchronization of mu rhythm generators in the sensorimotor cortex. These results support the hypothesis that sensorimotor cortex is a neural substrate involved in the representation of both self- and other-generated actions and show the mu rhythm is sensitive to subtle changes in observed motor behavior.

Adult↗
PubMed2001

Activity-dependent factors affecting poststroke functional outcomes.

Over the last several years, there has been increasing recognition of the potential for central nervous system (CNS) recovery after brain damage. One commonality across the recovery and brain plasticity literature is that practice induces plastic, dynamic changes in the CNS. However, more than simply repetition, it is the manipulation of specific practice variables that appears to drive these dynamic processes in the CNS. The experimental manipulations used in the studies on neuroplasticity largely derive from the concept that in the undamaged or healthy brain neuronal connections and cortical maps are continuously remodeled by experience and by the performance of specific, intensive, and complex movements used to solve motor problems and attain goals. Intervention designed to promote recovery rather than compensation after stroke would then manipulate these same practice variables that have consistently promoted behavioral recovery and neuroplasticity in laboratory settings. Three current intervention strategies that incorporate these practice variables are reviewed. Preliminary results provide evidence that manipulation of task intensity and specificity and the sensorimotor experience of the task training are the necessary ingredients for maximizing the tremendous potential for recovery in patients with stroke.

Journal Article↗