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Motor Circuits (motor + circuit)
Selected AbstractsDecreased dopamine D2 receptor binding in essential blepharospasmACTA NEUROLOGICA SCANDINAVICA, Issue 1 2009C. Horie Objectives ,, The purpose of this study was to investigate whether dopamine D2 receptor binding was altered in the striatum of essential blepharospasm patients. Methods ,, Striatal dopamine D2 receptor binding was measured with positron emission tomography and [11C]raclopride. We studied eight drug-naive patients with bilateral blepharospasm and eight age-matched normal controls. Results ,, The uptake indices in the blepharospasm group were significantly reduced by 11.7% in the caudate (P < 0.005), 11.6% in the anterior putamen (P < 0.0001), and 10.3% in the posterior putamen (P < 0.005) relative to the control group. Conclusions ,, This study indicates decreased dopamine D2 receptor binding in the entire striatal region of blepharospasm patients. The findings suggest that decreased dopamine D2 receptor binding might be one of the predisposing factors that leads to the dysfunction of the motor circuit, resulting in the loss of broad inhibition of unwanted movements during an intended movement in blepharospasm patients. [source] NaV1.6a is required for normal activation of motor circuits normally excited by tactile stimulationDEVELOPMENTAL NEUROBIOLOGY, Issue 7 2010Sean E. Low Abstract A screen for zebrafish motor mutants identified two noncomplementing alleles of a recessive mutation that were named non-active (navmi89 and navmi130). nav embryos displayed diminished spontaneous and touch-evoked escape behaviors during the first 3 days of development. Genetic mapping identified the gene encoding NaV1.6a (scn8aa) as a potential candidate for nav. Subsequent cloning of scn8aa from the two alleles of nav uncovered two missense mutations in NaV1.6a that eliminated channel activity when assayed heterologously. Furthermore, the injection of RNA encoding wild-type scn8aa rescued the nav mutant phenotype indicating that scn8aa was the causative gene of nav. In-vivo electrophysiological analysis of the touch-evoked escape circuit indicated that voltage-dependent inward current was decreased in mechanosensory neurons in mutants, but they were able to fire action potentials. Furthermore, tactile stimulation of mutants activated some neurons downstream of mechanosensory neurons but failed to activate the swim locomotor circuit in accord with the behavioral response of initial escape contractions but no swimming. Thus, mutant mechanosensory neurons appeared to respond to tactile stimulation but failed to initiate swimming. Interestingly fictive swimming could be initiated pharmacologically suggesting that a swim circuit was present in mutants. These results suggested that NaV1.6a was required for touch-induced activation of the swim locomotor network. © 2010 Wiley Periodicals, Inc. Develop Neurobiol 70:508,522, 2010 [source] Differences between the effects of three plasticity inducing protocols on the organization of the human motor cortexEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2006Karin Rosenkranz Abstract Several experimental protocols induce lasting changes in the excitability of motor cortex. Some involve direct cortical stimulation, others activate the somatosensory system and some combine motor and sensory stimulation. The effects usually are measured as changes in amplitude of the motor-evoked-potential (MEP) or short-interval intracortical inhibition (SICI) elicited by a single or paired pulses of transcranial magnetic stimulation (TMS). Recent work has also tested sensorimotor organization within the motor cortex by recording MEPs and SICI during short periods of vibration applied to single intrinsic hand muscles. Here sensorimotor organization is focal: MEPs increase and SICI decreases in the vibrated muscle, whilst the opposite occurs in neighbouring muscles. In six volunteers we compared the after effects of three protocols that lead to lasting changes in cortical excitability: (i) paired associative stimulation (PAS) between a TMS pulse and an electrical stimulus to the median nerve; (ii) motor practice of rapid thumb abduction; and (iii) sensory input produced by semicontinuous muscle vibration, on MEPs and SICI at rest and on the sensorimotor organization. PAS increased MEP amplitudes, whereas vibration changed sensorimotor organization. Motor practice had a dual effect and increased MEPs as well as affecting sensorimotor organization. The implication is that different protocols target different sets of cortical circuits. We speculate that protocols that involve repeated activation of motor cortical output lead to lasting changes in efficacy of synaptic connections in output circuits, whereas protocols that emphasize sensory inputs affect the strength of sensory inputs to motor circuits. [source] Central control of thermogenesis in mammalsEXPERIMENTAL PHYSIOLOGY, Issue 7 2008Shaun F. Morrison Thermogenesis, the production of heat energy, is an essential component of the homeostatic repertoire to maintain body temperature in mammals and birds during the challenge of low environmental temperature and plays a key role in elevating body temperature during the febrile response to infection. The primary sources of neurally regulated metabolic heat production are mitochondrial oxidation in brown adipose tissue, increases in heart rate and shivering in skeletal muscle. Thermogenesis is regulated in each of these tissues by parallel networks in the central nervous system, which respond to feedforward afferent signals from cutaneous and core body thermoreceptors and to feedback signals from brain thermosensitive neurons to activate the appropriate sympathetic and somatic efferents. This review summarizes the research leading to a model of the feedforward reflex pathway through which environmental cold stimulates thermogenesis and discusses the influence on this thermoregulatory network of the pyrogenic mediator, prostaglandin E2, to increase body temperature. The cold thermal afferent circuit from cutaneous thermal receptors ascends via second-order thermosensory neurons in the dorsal horn of the spinal cord to activate neurons in the lateral parabrachial nucleus, which drive GABAergic interneurons in the preoptic area to inhibit warm-sensitive, inhibitory output neurons of the preoptic area. The resulting disinhibition of thermogenesis-promoting neurons in the dorsomedial hypothalamus and possibly of sympathetic and somatic premotor neurons in the rostral ventromedial medulla, including the raphe pallidus, activates excitatory inputs to spinal sympathetic and somatic motor circuits to drive thermogenesis. [source] Sensory functions in dystonia: Insights from behavioral studies,,MOVEMENT DISORDERS, Issue 10 2009Michele Tinazzi MD Abstract The pathophysiology of primary dystonia is thought to involve dysfunction of the basal ganglia cortico-striatal-thalamo-cortical motor circuits. In the past, emphasis was placed on the role of the basal ganglia in controlling movements; in more recent times, however, it has also become clear that they play an important part in sensory as well as cognitive functions. Here, we review evidence for dysfunction of sensory processing in patients with dystonia, and speculate that this may lead to abnormalities in a crucial role of the basal ganglia that links sensory information to appropriate motor output. Sensory function, particularly in the somatosensory domain, has been shown to be compromised in patients with primary dystonia, both in adult onset focal dystonia and in genetically characterized DYT1 dystonia. Given that nonaffected DYT1 gene carriers may show similar abnormalities to clinically affected individuals, sensory deficits could constitute a subclinical endophenotypic trait of disease that precedes overt clinical manifestations. Whether they can trigger primary dystonia or are an epiphenomenon is an issue warranting further study, but the fact that a number of different neurorehabilitative approaches explicitly manipulate somatosensory inputs to improve motor function suggests there may be a causal link between them. We believe that in future, randomized, blind and controlled studies in large patient populations should address this issue, providing efficient strategies to aid functional recovery, particularly in focal hand dystonia, where the available medical treatments offer little benefit. © 2009 Movement Disorder Society [source] Deep brain stimulation for Parkinson's disease dissociates mood and motor circuits: A functional MRI case studyMOVEMENT DISORDERS, Issue 12 2003Taresa Stefurak MD Abstract Behavioral disturbances have been reported with subthalamic (STN) deep brain stimulation (DBS) treatment in Parkinson's disease (PD). We report correlative functional imaging (fMRI) of mood and motor responses induced by successive right and left DBS. A 36-year-old woman with medically refractory PD and a history of clinically remitted depression underwent uncomplicated implantation of bilateral STN DBS. High-frequency stimulation of the left electrode improved motor symptoms. Unexpectedly, right DBS alone elicited several reproducible episodes of acute depressive dysphoria. Structural and functional magnetic resonance imaging (fMRI) imaging was carried out with sequential individual electrode stimulation. The electrode on the left was within the inferior STN, whereas the right electrode was marginally superior and lateral to the intended STN target within the Fields of Forel/zona incerta. fMRI image analysis (Analysis of Functional NeuroImages, AFNI) contrasting OFF versus ON stimulation identified significant lateralized blood oxygen level-dependent (BOLD) signal changes with DBS (P < 0.001). Left DBS primarily showed changes in motor regions: increases in premotor and motor cortex, ventrolateral thalamus, putamen, and cerebellum as well as decreases in sensorimotor/supplementary motor cortex. Right DBS showed similar but less extensive change in motor regions. More prominent were the unique increases in superior prefrontal cortex, anterior cingulate (Brodmann's area [BA] 24), anterior thalamus, caudate, and brainstem, and marked widespread decreases in medial prefrontal cortex (BA 9/10). The mood disturbance resolved spontaneously in 4 weeks despite identical stimulation parameters. Transient depressive mood induced by subcortical DBS stimulation was correlated with changes in mesolimbic cortical structures. This case provides new evidence supporting cortical segregation of motor and nonmotor cortico-basal ganglionic systems that may converge in close proximity at the level of the STN and the adjacent white matter tracts (Fields of Forel/zona incerta). © 2003 Movement Disorder Society [source] Role of the somatosensory system in primary dystoniaMOVEMENT DISORDERS, Issue 6 2003Michele Tinazzi MD Abstract The pathophysiology of dystonia is still not fully understood, but it is widely held that a dysfunction of the corticostriatal,thalamocortical motor circuits plays a major role in the pathophysiology of this syndrome. Although the most dramatic symptoms in dystonia seem to be motor in nature, marked somatosensory perceptual deficits are also present in this disease. In addition, several lines of evidence, including neurophysiological, neuroimaging and experimental findings, suggest that both motor and somatosensory functions may be defective in dystonia. Consequently, abnormal processing of the somatosensory input in the central nervous system may lead to inefficient sensorimotor integration, thus contributing substantially to the generation of dystonic movements. Whether somatosensory abnormalities are capable of triggering dystonia is an issue warranting further study. Although it seems unlikely that abnormal somatosensory input is the only drive to dystonia, it might be more correlated to the development of focal hand than generalized dystonia because local somesthetic factors are more selectively involved in the former than in the latter where, instead it seems to be a widespread deficit in processing sensory stimuli of different modality. Because basal ganglia and motor areas are heavily connected not only with somatosensory areas, but also with visual and acoustic areas, it is possible that abnormalities of other sensory modalities, such as visual and acoustic, may also be implicated in the pathophysiology of more severe forms of primary dystonia. Further studies have to be addressed to the assessment of the role of sensory modalities and their interaction on the pathophysiology of different forms of primary dystonia. © 2003 Movement Disorder Society [source] Human neural stem cell grafts in the spinal cord of SOD1 transgenic rats: Differentiation and structural integration into the segmental motor circuitryTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 4 2009Leyan Xu Abstract Cell replacement strategies for degenerative and traumatic diseases of the nervous system depend on the functional integration of grafted cells into host neural circuitry, a condition necessary for the propagation of physiological signals and, perhaps, targeting of trophic support to injured neurons. We have recently shown that human neural stem cell (NSC) grafts ameliorate motor neuron disease in SOD1 transgenic rodents. Here we study structural aspects of integration of neuronally differentiated human NSCs in the motor circuitry of SOD1 G93A rats. Human NSCs were grafted into the lumbar protuberance of 8-week-old SOD1 G93A rats; the results were compared to those on control Sprague-Dawley rats. Using pre-embedding immuno-electron microscopy, we found human synaptophysin (+) terminals contacting the perikarya and proximal dendrites of host , motor neurons. Synaptophysin (+) terminals had well-formed synaptic vesicles and were associated with membrane specializations primarily in the form of symmetrical synapses. To analyze the anatomy of motor circuits engaging differentiated NSCs, we injected the retrograde transneuronal tracer Bartha-pseudorabies virus (PRV) or the retrograde marker cholera toxin B (CTB) into the gastrocnemius muscle/sciatic nerve of SOD1 rats before disease onset and also into control rats. With this tracing, NSC-derived neurons were labeled with PRV but not CTB, a pattern suggesting that PRV entered NSC-derived neurons via transneuronal transfer from host motor neurons but not via direct transport from the host musculature. Our results indicate an advanced degree of structural integration, via functional synapses, of differentiated human NSCs into the segmental motor circuitry of SOD1-G93A rats. J. Comp. Neurol. 514:297,309, 2009. © 2009 Wiley-Liss, Inc. [source] Ventromedial medulla: Pain modulation and beyondTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 1 2005Peggy Mason Abstract The midbrain periaqueductal gray (PAG) and ventromedial medulla (VMM) are generally viewed as the core of an endogenous descending modulatory system. However, available data demonstrate that PAG and VMM do not specifically target nociceptive transmission and that activation of either structure affects numerous homeostatic physiological processes. Pseudorabies virus (PRV) is a useful tracer that is retrogradely and transynaptically transported. PRV injections into homeostatic effector organs invariably label VMM neurons, both serotonergic and nonserotonergic. Studies in anesthetized rats have implicated two types of nonserotonergic VMM neurons in nociceptive modulation: ON cells are thought to facilitate nociception and OFF cells to inhibit nociception. Yet, in the unanesthetized animal, the discharge of VMM neurons changes in response to innocuous stimuli and during situations unrelated to nociception. In particular, VMM cells appear to modulate the timing of micturition, with ON cells promoting the initiation of voiding and OFF cells promoting urine storage. VMM cells also modulate sensory transmission. During both micturition and sleep, OFF cells discharge and sensory responsiveness is depressed. In sum, the VMM is hypothesized to modulate spinal sensory, autonomic, and motor circuits in order to maintain homeostasis. J. Comp. Neurol. 493:2,8, 2005. © 2005 Wiley-Liss, Inc. [source] | |||||||||||||