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At least 829 records · Page 46Linked to original sources
PubMed2002

Relative potency of synthetic analogs of Ptychodiscus brevis toxin in depressing synaptic transmission evoked in neonatal rat spinal cord in vitro.

Effects of Ptychodiscus brevis toxin (PbTx) analogs on the spinal synaptic transmission in neonatal rats in vitro were evaluated. PbTx1/PbTx2 had aromatic groups and PbTx3/PbTx4 had aliphatic groups. All the analogs depressed monosynaptic reflex (MSR) and polysynaptic reflex (PSR) in a concentration-dependent manner. The maximal depression of MSR (75% from initial) and PSR (96%) was at 84 microM for PbTx1. Concentration to produce 25% inhibition from initial (IC25) by PbTx1 for MSR and PSR was < or =2.8 microM. The maximal depression of MSR (80%) was at 96 microM and PSR (100%) was at 32 microM by PbTx2. IC25 for MSR and PSR were 5.5 microM and <3.2 microM, respectively. PbTx3 decreased MSR by 25% maximally (=IC25) at 36 microM. The depression of PSR fluctuated and was maximal (75%) at 108 microM and IC25 was 6.2 microM. PbTx4 depressed MSR and PSR at the maximum of 35% at 32 microM and IC25 for MSR was 8.3 microM and for PSR was 35 microM. Rank order of potency of toxins for depressing MSR was PbTx1>PbTx2>>PbTx4>PbTx3; and for PSR it was PbTx2>PbTx1>PbTx3>>PbTx4. Results indicate that the toxins having aromatic groups exhibited greater neurotoxicity.

Animals↗
PubMed1997

Mental simulation of an action modulates the excitability of spinal reflex pathways in man.

The question of whether mental simulation of an action has an effect on the spinal reflex circuits was examined in normal humans. Subjects were instructed either to exert or to mentally simulate a strong or a weak pressure on a pedal with the left or the right foot. Changes in the H- and T-reflexes activated by electrical and mechanical stimuli were measured on both legs during motor performance as well as during mental simulation of the same task. Asynchronous EMG activity of the soleus muscles was simultaneously recorded. Reflex excitability increased during performance of the pressure. It was larger when the H-reflex was triggered in the muscle involved in the task as compared to the contralateral side. Because actual performance modified the tension of the tendon and the location of the stimulus, ipsilateral changes of T-reflex amplitude could not be evaluated. Mental simulation of foot pressure in this condition resulted in a large increase of spinal reflex excitability, which was only slightly weaker than the reflex facilitation associated with the actual performance. Changes in T-reflex amplitude, but not in H-reflex amplitude, depended upon the lateralization and force of the simulated pressure, being larger in the leg involved in the simulation than in the contralateral leg, and larger for a strong than for a weak simulated movement. EMG activity was found to be weakly increased during mental imagery. This increase was significantly, although slightly, modulated by the lateralization and intensity of the imagined movement. However, no correlation was found across subjects between reflex amplitude and the amplitude of EMG activity.

Adult↗
PubMedDate not supplied

Phylogenesis and regulated expression of the RUNT domain transcription factors RUNX1 and RUNX3.

The RUNX transcription factors are key regulators of lineage specific gene expression in developmental pathways. The mammalian RUNX genes arose early in evolution and maintained extensive structural similarities. Sequence analysis suggested that RUNX3 is the most ancient of the three mammalian genes, consistent with its role in neurogenesis of the monosynaptic reflex arc, the simplest neuronal response circuit, found in Cnidarians, the most primitive animals. All RUNX proteins bind to the same DNA motif and act as activators or repressors of transcription through recruitment of common transcriptional modulators. Nevertheless, analysis of Runx1 and Runx3 expression during embryogenesis revealed that their function is not redundant. In adults both Runx1 and Runx3 are highly expressed in the hematopoietic system. At early embryonic stages we found strong Runx3 expression in dorsal root ganglia neurons, confined to TrkC sensory neurons. In the absence of Runx3, knockout mice develop severe ataxia due to the early death of the TrkC neurons. Other phenotypic defects of Runx3 KO mice including abnormalities in thymopoiesis are also being investigated.

Animals↗
PubMed2000

Voluntary teeth clenching facilitates human motor system excitability.

OBJECTIVE: Voluntary contraction of the teeth is a common maneuver used to facilitate peripheral monosynaptic reflexes. It was the aim of this study to determine the site along the neuraxis where this effect occurs. METHODS: Focal transcranial magnetic stimulation (TMS) was used to measure recruitment curves, motor thresholds and intracortical inhibition and facilitation from the right first dorsal interosseus (FDI) and tibialis anterior (TA) muscles in seven normal volunteers. Changes in excitability in subcortical structures during teeth clenching were studied using F waves, H reflexes, and brainstem magnetic stimulation. RESULTS: Recruitment curves of FDI and TA showed significant facilitation during voluntary teeth clenching indicating an overall enhancement in the motor system excitability. Teeth clenching additionally resulted in decreased intracortical inhibition in the FDI but not in TA, pointing to an intracortical site of enhancement for the hand. Motor evoked potentials (MEPs) following stimulation at the brainstem level and F waves in FDI and soleus H reflex amplitude were also facilitated by teeth clenching, indicating a subcortical site for this effect for the upper and lower extremity. M wave amplitudes did not change. CONCLUSIONS: The teeth clenching maneuver had a similar facilitatory effect on upper and lower extremities. Cortical and subcortical sites contribute to this effect in a hand muscle while only subcortical sites were identified in this facilitatory effect on the lower extremity.

Adult↗
PubMed1987

The physiology of idiopathic dystonia.

Dystonia is mysterious and its pathophysiology is uncertain. The fundamental motor abnormality is an abnormality of muscle command signals, such that the wrong agonists may be activated for too long, there is abnormal co-contraction of agonist and antagonists, and there is excessive and misdirected action of synergists and postural fixators. The result is action dystonia. In addition, muscle spasms may occur spontaneously. The peripheral motor apparatus, the corticomotoneurone pathway, and (as far as is known) the proprioceptive feedback machinery, are all intact in primary dystonia. However, a defect of interneuronal machinery has been identified in both the brainstem and spinal cord. In blepharospasm there is hyperexcitability of the lower brainstem interneurones responsible for the R2 component of the blink reflex. In the dystonic arm there is loss of the later phases of Ia reciprocal inhibition from extensors to flexors. Both deficits may be due to loss of normal basal ganglia inputs onto interneurones. The known sites of focal lesions that may cause symptomatic dystonia all impair basal ganglia output. However, whether such abnormal interneuronal function is sufficient to explain dystonia is not known. Among many unanswered questions are 1) are the cortical instructions for movement specified correctly, and 2) what is responsible for the spontaneous dystonic spasms?

Dystonia↗
PubMed2004

Parallel processing in an identified neural circuit: the Aplysia californica gill-withdrawal response model system.

The response of the gill of Aplysia calfornica Cooper to weak to moderate tactile stimulation of the siphon, the gill-withdrawal response or GWR, has been an important model system for work aimed at understanding the relationship between neural plasticity and simple forms of non-associative and associative learning. Interest in the GWR has been based largely on the hypothesis that the response could be explained adequately by parallel monosynaptic reflex arcs between six parietovisceral ganglion (PVG) gill motor neurons (GMNs) and a cluster of sensory neurons termed the LE cluster. This hypothesis, the Kupfermann-Kandel model, made clear, falsifiable predictions that have stimulated experimental work for many years. Here, we review tests of three predictions of the Kupfermann-Kandel model: (1) that the GWR is a simple, reflexive behaviour graded with stimulus intensity; (2) that central nervous system (CNS) pathways are necessary and sufficient for the GWR; and (3) that activity in six identified GMNs is sufficient to account for the GWR. The available data suggest that (1) a variety of action patterns occur in the context of the GWR; (2) the PVG is not necessary and the diffuse peripheral nervous system (PNS) is sufficient to mediate these action patterns; and (3) the role of any individual GMN in the behaviour varies. Both the control of gill-withdrawal responses, and plasticity in these responses, are broadly distributed across both PNS and CNS pathways. The Kupfermann-Kandel model is inconsistent with the available data and therefore stands rejected. There is, no known causal connection or correlation between the observed plasticity at the identified synapses in this system and behavioural changes during non-associative and associative learning paradigms. Critical examination of these well-studied central pathways suggests that they represent a 'wetware' neural network, architecturally similar to the neural network models of the widely used 'Perceptron' and/or 'Back-propagation' type. Such models may offer a more biologically realistic representation of nervous system organisation than has been thought. In this model, the six parallel GMNs of the CNS correspond to a hidden layer within one module of the gill-control system. That is, the gill-control system appears to be organised as a distributed system with several parallel modules, some of which are neural networks in their own right. A new model is presented here which predicts that the six GMNs serve as components of a 'push-pull' gain control system, along with known but largely unidentified inhibitory motor neurons from the PVG. This 'push-pull' gain control system sets the responsiveness of the peripheral gill motor system. Neither causal nor correlational links between specific forms of neural plasticity and behavioural plasticity have been demonstrated in the GWR model system. However, the GWR model system does provide an opportunity to observe and describe directly the physiological and biochemical mechanisms of distributed representation and parallel processing in a largely identifiable 'wetware' neural network.

Animals↗
PubMed1969

An effect of postsynaptic neurons upon presynaptic terminals.

Centrifugal ("antidromic") discharges in cat sensory fibers are observed consistently in a variety of experimental preparations and with many different surgical and recording techniques. As is well known, they can be either "spontaneous" or induced by afferent volleys in other sensory fibers. In addition, it is shown here that they can be elicited by antidromic motoneuron activation when the latter is conditioned by natural sensory stimuli or by shocks to the dorsal roots. The latency of the centrifugal dorsal root response to ventral root stimulation is shorter than that of the monosynaptic reflex mediated by the same fibers. An "antidromic" coupling, probably of an electrical nature, between motoneurons and presynaptic terminals is postulated.

Animals↗
PubMed1993

Diazepam dependence prevented by glutamate antagonists.

Long-term treatment leads to tolerance to and dependence on benzodiazepines. Abrupt termination of benzodiazepine administration triggers the expression of signs of dependence. Mice withdrawn from chronic treatment with diazepam showed a time-related evolution of anxiety, muscle rigidity, and seizures between days 4 and 21 after treatment discontinuation. A period between withdrawal days 1 and 3 was symptom-free. Surprisingly, during this "silent phase" the susceptibility of mice to alpha-amino-3-hydroxy-5-tert-butyl-4-isoxazolepropionate (ATPA) and kainate seizures and the magnitude of monosynaptic reflexes mediated by non-N-methyl-D-aspartate (NMDA) mechanisms were enhanced. In apparent contrast, the "active phase", between withdrawal days 4 and 21, was characterized by increased susceptibility to NMDA seizures and enhanced magnitude of polysynaptic reflexes, which are NMDA dependent. Treatment of mice with alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) antagonists 1-(4-aminophenyl)-4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine (GYKI 52466) or 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo(f)quinoxaline but not with the NMDA antagonist 3-[(+/-)-2-carboxypiperazin-4-yl]-propyl-1-phosphonate (CPP) during the silent phase prevented signs of dependence. In contrast, treatment with CPP but not with GYKI 52466 during the active phase prevented the symptoms. The development of tolerance to and dependence on diazepam was prevented by concurrent treatment of mice with CPP but was not prevented by GYKI 52466. These data indicate that NMDA-dependent mechanisms contribute to the development of tolerance to diazepam and to the expression of signs of dependence in mice after termination of long-term treatment with diazepam. Nevertheless, the non-NMDA-mediated silent phase is essential for triggering the symptoms. Therefore, AMPA antagonists may offer a therapeutic approach for preventing dependence on benzodiazepines that is an alternative to NMDA antagonism.

Animals↗
PubMed1987

Neuromuscular control of posture in the infant and child: is vision dominant?

This study explored the effects of vision and maturation on the characteristics of neuromuscular responses underlying balance control in both seated and standing children of five age groups (3 1/2-5 months, 8-14 months, 2-3 years, 4-6 years, and 7-10 years). A platform was used to unexpectedly disturb the child's balance in the anterior or posterior direction. Responses of the leg, trunk, and neck muscles were recorded using surface electromyograms. Vision was not required for the activation of these responses in any of the age groups tested. However, comparison of the muscle response latencies of standing children to posterior platform translation in the two visual conditions showed a significant reduction in latency for neck flexors in the 2- to 3-year-olds with vision removed and ann increase in the total number of monosynaptic reflexes. No reduction in latency was found in the older age groups. The hypothesis of a shift from an early long latency visual dominance to a shorter latency proprioceptive one during childhood is discussed. Postural control showed a cephalo-caudal developmental gradient with postural responses appearing first in the neck, then trunk, and finally, legs, as children developed from 3 to 14 months of age. A wide variety of response patterns was seen in the 3- to 5-month-olds, indicating that postural responses are not functional prior to experience with stabilizing the center of mass.

Journal Article↗
PubMed1995

Selective effects of alfentanil on nociceptive-related neurotransmission in neonatal rat spinal cord.

We have examined the effects of alfentanil on nociceptive-related neurotransmission in isolated neonatal rat spinal cord, with particular attention to acute tolerance. Electrical stimulation of a lumbar dorsal root was used to evoke the monosynaptic reflex (MSR), a slow ventral root potential (sVRP), and the dorsal root potential (DRP). Alfentanil (0.5 nmol litre-1 to 1 mumol litre-1) depressed sVRP area by a maximum of 85%; EC50 was approximately 2 nmol litre-1. The effects of alfentanil were selective for very slow, metabotropically mediated sVRP components compared with faster NMDA receptor-mediated components. The MSR was unaffected. Alfentanil depressed DRP area by a maximum of 50% at 1 mumol litre-1. Naloxone antagonized all alfentanil effects. Morphine depressed sVRP area with an approximate EC50 of 90 nmol litre-1, giving an alfentanil:morphine potency ratio of 45:1. The effects of alfentanil on sVRP showed no biphasic time dependence up to 60 min. Naloxone administered after alfentanil produced a significant rebound in sVRP area to a level of 143 (SD 21.3)% above control. Thus, in this study there was no evidence for acute tolerance, as measured by a decrease in effectiveness over time, but there was evidence as measured by rebound following naloxone.

Alfentanil↗
PubMed1975

Vibratory stimulation. Part II. Vibratory stimulation as an evaluation tool.

Phasic neural mechanisms are heavily involved in volitional movements, where as tonic mechanisms support postural adjustments. Yet, the two systems are so intimately related that any disturbance in one will exert profound effects on the other. Whether one system or the other is involved preferentially in different neural disorders is not known; hence, tests are needed to evaluate phasic and tonic functions independently. In this article, the classical applications of the tendon jerk reflex and H-response for assessing phasic mechanisms are first reviewed. Following this review, the tonic stretch reflex and tonic vibration reflex (TVR) are analyzed and compared. The effects of experimentally ablating or stimulating precise brain regions are described as a means of revealing the role of supraspinal mechanisms in the TVR. Finally, the responses to vibratory stimulation in specific motor disorders are examined and discussed as to their usefulness in prognosis and diagnosis.

Cerebellar Diseases↗
PubMed1977

Spasticity: its physiology and management. Part I. Neurophysiology of spasticity: classical concepts.

Spasticity, seen so frequently in clinical situations, presents motor signs resembling those produced experimentally by transecting the brain stem of a cat at the intercollicular level. This paper reviews experimental results which elucidate the roles of different brain regions in the genesis of classical decerebrate rigidity and demonstrate the function of the gamma motor system in the maintenance of the rigidity. Interruption of the gamma-spindle loop of a muscle (i.e. interrupting the monosynaptic reflex arc subserving the stretch reflexes) abolishes rigidity in that muscle. This reflex-mediated gamma support of decrebrate rigidity is also a prominent feature of clinical spasticity, making classical decerebrate rigidity a useful model for studying the neural mechanisms underlying spasticity. Not all rididities, however, are gamma dependent. Those rigidities surviving dorsal root rhizotomy are called alpha rigidity. Alpha rigidity results when a brain lesion disrupts descending systems which normally exert a net inhibitory effect upon alpha motoneurons.

Animals↗