Showing papers on "Motor neuron published in 1983"

Associative conditioning of single sensory neurons suggests a cellular mechanism for learning

Abstract: A cellular analog of associative learning has been demonstrated in individual sensory neurons of the tail withdrawal reflex of Aplysia. Sensory cells activated by intracellular current injection shortly before a sensitizing shock to the animal's tail display significantly more facilitation of their monosynaptic connections to a tail motor neuron than cells trained either with intracellular stimulation unpaired to tail shock or with tail shock alone. This associative effect is acquired rapidly and is expressed as a temporally specific amplification of heterosynaptic facilitation. The results suggest that activity-dependent neuromodulation may be a mechanism underlying associative information storage and point to aspects of subcellular processes that might be involved in the formation of neural associations.

Motor neuron columns in the lumbar spinal cord of the rat

Abstract: The location in the rat spinal cord of motor neurons innervating 23 muscles or muscle groups of the hind limb has been determined by using retrograde transport of horseradish peroxidase. The motor neurons supplying a single muscle form a discrete longitudinal column in the lateral ventral horn. The columns extend through up to three adjacent spinal segments and their longitudinal location varies by as much as one segment in different animals. The relative positions of the columns supplying different muscles and their transverse location in the spinal cord are very consistent between individuals and a stereotaxic map has been constructed. This is briefly compared with descriptions from other species. Counts of the numbers of motor axons in seven different muscles nerves have been made with the aid of acetylcholinesterase histochemistry to identify the motor component. The numbers of motor neuron somata labelled with horseradish peroxidase are on average 70% of the axon counts.

Mechanoafferent neurons innervating tail of Aplysia. II. Modulation by sensitizing stimulation

Abstract: The tail-withdrawal reflex of Aplysia can be sensitized by weak stimulation of a site outside the site used to test the reflex or by repeatedly stimulating the test site itself. The sensitization of tail-withdrawal responses is associated with enhanced activation of the tail motor neurons and heterosynaptic facilitation of the monosynaptic connections between the tail sensory neurons and tail motor neurons. This synaptic facilitation can occur under conditions in which neither posttetanic potentiation nor generalized changes in postsynaptic input resistance contribute to the facilitation. In addition to producing monosynaptic excitatory postsynaptic potentials (EPSPs), action potentials in tail sensory neurons often recruit longer latency polysynaptic input to the tail motor neurons during sensitization. Strong, noxious tail shock similar in intensity to that used previously for sensitization and aversive classical conditioning of other responses in Aplysia produces more heterosynaptic facilitation than does weak sensitizing stimulation. Heterosynaptic facilitation builds up progressively with multiple trials and lasts for hours. Very strong shocks to the tail can change the response characteristics of tail sensory neurons so that a prolonged, regenerative burst of spikes is elicited by a brief intracellular depolarizing pulse. This bursting response produced by sensitizing stimulation has not been described previously in Aplysia sensory neurons and can greatly amplify the synaptic input to tail motor neurons from the sensory neurons. In addition, strong shocks to the tail increase the duration and magnitude of individual sensory neuron action potentials. Sensitizing tail stimulation usually produces long-lasting depolarization of the tail motor neurons and often long-lasting hyperpolarization of the tail sensory neurons. The tail motor and sensory neurons show both increases and decreases of input resistance following sensitizing stimulation. However, the small, occasional increases in input resistance of the motor neuron are insufficient to explain the heterosynaptic facilitation produced by sensitizing stimulation. Serotonin (5-HT) application can mimic many of the effects of sensitizing tail shock, including facilitation of both tail withdrawal and the monosynaptic connections between tail sensory and motor neurons, hyperpolarizing and depolarizing responses in the tail sensory neurons, and an increase in the duration and magnitude of the sensory neuron action potential. In the nearly isolated sensory neuron soma, 5-HT usually produces a slow, decreased conductance depolarizing response, suggesting that the 5-HT-induced hyperpolarizing response see

Amyotrophic lateral sclerosis: Alterations in neurotransmitter receptors

Abstract: Loss of motor neurons is the primary pathological hallmark of amyotrophic lateral sclerosis. Drug and neurotransmitter receptors are neuronal markers and can be indicators of neuronal connectivity. Knowledge of alterations in receptors in amyotrophic lateral sclerosis should contribute to our understanding of normal spinal cord neurotransmitter systems as well as of the pathophysiology of amyotrophic lateral sclerosis. We therefore used a sensitive, light microscopic in vitro labeling receptor autoradiographic technique to map and quantitate muscarinic cholinergic, glycinergic, and benzodiazepine receptors in three levels of spinal cord from six patients with amyotrophic lateral sclerosis and six age- and sex-matched control patients. In control tissues, the receptor distributions were similar in the three levels of spinal cord and also similar to those found in previous studies with animals. In amyotrophic lateral sclerosis, major reductions in receptor densities were noted in Rexed layer IX, the region containing motor neurons. Reductions were noted in other laminae as well, particularly for muscarinic receptors. The changes in muscarinic receptors were caused solely by changes in high-affinity agonist sites. Reductions in glycine and muscarinic receptors were highly correlated with the degree of motor neuron loss found in the amyotrophic lateral sclerosis patients. The findings in this study point out the usefulness of this receptor mapping technique in understanding the changes in neuronal populations that occur in the degenerative neurological diseases.

Dopamine elicits feeding motor program in Limax maximus

Abstract: A neural system within the cerebral and buccal ganglia of the terrestrial mollusc Limax maximus responds to lip chemostimulation by emitting a feeding motor program (FMP) in vivo and in vitro. We have analyzed chemically the cerebral and buccal ganglia of Limax for neurotransmitters involved in controlling expression of FMP. Dopamine was found in clusters of cells in and the neuropil of the cerebral ganglia at a concentration of 62 pmol/ganglion; a large proportion of such dopamine-containing cells projected to the lips. The buccal ganglia contained several small dopaminergic cells and large amounts of dopamine in the neuropil; the measured concentration was 10 pmol/ganglion. Exogenous dopamine applied to the cerebral and buccal ganglia in vitro between 10(-7) M and 3 X 10(-6) M excited an autoactive salivary duct motor neuron (FB) and inhibited an autoactive secretomotor neuron (BSN). Concentrations of dopamine between 3 X 10(- 6) M and 3 X 10(-5) M triggered FMP output, with an increased probability of triggering at higher concentrations of dopamine. ADTN and SKF none of the neuroleptics tested was effective. Thus, the Limax system shows agonist responses similar to the vertebrate D1 receptors, but its antagonist-binding properties appear to have requirements quite different from vertebrate receptors. The effects of exogenous serotonin differed from dopamine's effects; serotonin excited BSN and several buccal motor neurons, could not elicit synchronized motor program cycling, and was not efficiently blocked by ergonovine. These data suggest that dopamine is a good candidate as an endogenous triggering and sustaining transmitter for the Limax feeding motor program.

The innervation of skeletal muscles in chickens curarized during early development.

Abstract: Chicken embryos were treated with partially paralysing doses ofd-tubocurarine (dtc) from embryonic (E) days 6 to 10. The pattern of innervation of the lateral gastrocnemius (GL) muscle was examined both morphologically and physiologically just before hatching on day E20 or E21. There was a 70% increase in number of surviving motor neurons in the lateral motor column and a 50% increase in the number of myelinated axons in the nerve to GL. The GL muscle was significantly atrophic, with an average weight of 40% of normal. The atrophy was largely due to the reduced size of the muscle fibres. The mean size of the motor units was essentially unchanged or perhaps slightly increased. There was a striking increase in the level of polyneuronal innervation of the muscle fibres, both in terms of number of synaptic sites per fibre and number of axons innervating each site. Spontaneous miniature endplate potentials (mepps) indicated focal innervation of the fibres in the normal muscle. Most fibres in the dtc-treated muscles had mepps of widely varying time courses, and there was no simple relation between amplitude and rise time. Many of the slow mepps were not represented in the endplate potentials evoked by nerve stimulation. The quantal content of the endplate potential (epp) was generally increased in the dtc-treated muscles. The findings are discussed in terms of a retrograde signal from muscle to nerve and its dependence on muscle activity.

Degenerating compartment and functioning compartment of motor neurons in ALS: possible process of motor neuron loss.

Abstract: Using a morphometric method, we studied ventral spinal roots and anterior horn neurons of the fourth lumbar segment in 17 patients with ALS. Both populations of large myelinated fibers and anterior horn cells had significantly high correlations to muscle strength in the legs and duration of symptoms. However, active axonal degeneration was consistently, present in terms of either large myelinated fibers or anterior horn cells.

Neuronal control of locomotion in hydrozoan medusae

Abstract: 1. The swimming control systems of 13 hydromedusan species were examined electrophysiologically and morphologically. Despite obvious differences in the structure, behavior and life style of these medusae, the basic organization of swimming system components is similar. 2. Motor neurons that activate swimming muscles are located in the inner nerve-ring comprising electrically-coupled condensed networks (Figs. 2, 3). Individual neurons of these networks are of far larger diameter than other neurons of the nerve-rings (Figs. 4–6). 3. Spontaneous activity persists in the swim motor neuron networks in seawater containing excess Mg++ suggesting that the network may perform a pacemaker function. 4. The swimming muscle sheet includes circular, striated epitheliomuscular cells of the subumbrella and velum, and an interposed non-muscular epithelial region which overlies the inner nerve-ring (Fig. 1). Gap junctions are common throughout this tissue sheet (Figs. 13, 14, 18). Electrical(Fig. 10) and dye-coupling (Fig. 3) of cells in this sheet suggests that direct current spread between myocytes is important in transmission of excitation throughout the subumbrella. 5. Recordings from epithelial cells immediately adjacent to swim motor neurons reveal graded potentials presumably of synaptic origin (Figs. 2, 10). The synaptic potentials, and muscle action potentials, are blocked in seawater containing excess Mg++. Synaptic contacts were observed between swim motor neurons and overlying epithelial cells throughout the inner nerve-rings of all medusae examined (Figs. 19–21).

Death of motorneurons during the postnatal loss of polyneuronal innervation of rat muscles

Abstract: A study was made of the decline in the number of motor neurons and axons of the brachial spinal cord of the rat during postnatal development. The injection of horseradish peroxidase (HRP) into the biceps muscle showed that it was innervated by motor neurons located in the dorsolateral position of the lateral motor column in segments C5 and C6; HRP injections into the triceps muscle showed that it was innervated by motor neurons located in the ventrolateral position of the lateral motor column in segments C7 and C8. There was no change in the position of these motor neuron pools between birth and maturity. However, there was a decline in the number of neurons in each pool during the postnatal period; over 35% of the neurons present at birth had disappeared by maturity. This loss of neurons was uniform throughout the rostrocaudal extent of each pool. It was accompanied by a similar percentage loss in the number of axons in a ventral root at the branchial level (C8). Electrophysiological measurements showed that the disappearance of motor neurons was accompanied by a loss in the polyneuronal innervation of synaptic sites in the biceps muscle. The possibility that a decrease in the number of neurons contributes to the loss of polyneuronal innervation is discussed.

Which behavior does the lamprey central motor program mediate

Abstract: The isolated lamprey spinal cord, when bathed in 2 millimolar D-glutamic acid, will generate a pattern of motor neuron discharge that has generally been assumed to represent the central motor program for swimming. Motion pictures of behaving lampreys were analyzed by a computer algorithm to estimate undulatory movement parameters that could be directly compared with those generated during D-glutamate--induced undulations. The D-glutamate--induced movement parameters were significantly different from those observed during normal behaviors, including swimming, but accurately predicted the undulations produced by spinally transected adult lampreys.

Evidence for a presynaptic blockage of transmission in a temperature-sensitive mutant of Drosophila.

Abstract: In the temperature sensitive mutant of Drosophila, shibirets1 (shi), synaptic transmission in the dorsal longitudinal flight muscles (DLM) is normal at 19 degrees C, but is diminished progressively as the temperature is raised, and is blocked at 29 degrees C. The purpose of this paper is to determine whether this defect is located presynaptically, postsynaptically, or both. It is demonstrated here that the postsynaptic sensitivity to L-glutamate, the putative transmitter for this synapse, is not decreased at 29 degrees C. Furthermore, studies conducted with genetic mosaics of this mutant show that transmission is blocked when a mutant motor neuron synapses on a wild-type muscle fiber, but is not blocked when a wild-type motor neuron synapses on a mutant muscle fiber. Thus, the shi phenotype (temperature dependent transmission block) correlates with a shi motor neuron, not with a shi muscle fiber. The data, therefore, suggest that the defect is not postsynaptic, but presynaptic.

A dominantly inherited syndrome with continuous motor neuron discharges

Abstract: A distinct syndrome with continuous motor neuron discharges apparently developed in seven members of a single family, involving both sexes and spanning three generations. Persistent vermiform twitching and episodic stiffness predominantly in lower extremity muscles occurred in early childhood and tended to be less severe in adulthood. In 2 patients the clinical manifestations improved with oral phenytoin and carbamazepine but not with parenteral diazepam. Insertional activity was normal, and continuous, rhythmical, normal-appearing muscle discharges were observed on electromyography. The cerebrospinal fluid levels of homovanillic acid and 5-hydroxyindoleacetic acid were increased in the proband. The disappearance of continuous muscle discharges during spinal anesthesia and the lack of response to diazepam indicated generation of the discharges from the proximal portion of the motor unit.

Sprouting and regeneration of sensory axons after destruction of ensheathing glial cells in the leech central nervous system.

Abstract: To test the importance of glia during regeneration of mechanosensory neuron axons in the leech central nervous system, individual glial cells that ensheathed the axons were destroyed by intracellular protease injection. Recordings with intracellular microelectrodes showed that glial-desheathed axons re-established synaptic connections with their appropriate target cell, a motor neuron, as frequently and as selectively as control, glial-ensheathed axons. Intracellular staining with horseradish peroxidase showed that desheathed regenerating axons sprouted more than controls, and loss of the glial cell in some cases caused uninjured (intact) axons to sprout. Successful, accurate regeneration could occur whether axons grew along normal or along aberrant pathways. The distal stumps of some sensory axons severed from cell bodies and maintained in organ culture survived without their glial sheath for up to 3 weeks. These experiments show that, although loss of the glial cell affects sensory axon growth, the glial cell is not required for accurate axonal regeneration in the leech central nervous system.

Control of extrinsic feeding muscles in Aplysia.

Abstract: The extrinsic buccal muscles in Aplysia are responsible for the overall protraction and retraction of the buccal mass during feeding. The six pairs of extrinsic muscles are organized into two groups, consisting of three protractors and three retractors. Insights into how the extrinsic muscles are controlled were obtained by examining the organization of the motor neurons that innervated them. The extrinsic buccal muscles are innervated by cerebral ganglion nerves and neurons. All the muscles examined appear to be multiply innervated. Identified neurons in the cerebral B, E, and G clusters were found to be motor neurons for individual extrinsic muscles. Some extrinsic muscles had both excitatory and inhibitory innervation. Two synergistic muscles, the extrinsic ventrolateral protractor (ExVLP) and the extrinsic dorsal protractor (ExDP), had common excitatory innervation by identified neuron E5. Two antagonistic muscles, the ExVLP and the extrinsic ventral retractor (ExVR), also had common innervation. Identified neuron E1 appeared to be an inhibitory motor neuron for the ExVLP but an excitatory motor neuron for the ExVR. Common innervation provides a simple mechanism for coordinating synergistic and antagonistic extrinsic muscles. On the basis of these data, a model for the control of buccal mass protraction and retraction is proposed. Bursting by extrinsic buccal muscles was coordinated with cyclic activity in the intrinsic muscles of the buccal mass. Antagonistic extrinsic muscles burst antiphasically and synergistic extrinsic muscles burst in phase when the buccal mass was fully protracted and exhibited a series of rhythmic contractions. Additionally, cerebral E cluster neurons burst in phase with stereotyped rhythmic buccal motor neuron discharges recorded from buccal nerves. The cerebral E cluster motor neurons were coordinated by common synaptic input. No monosynaptic connections were observed; homologous neurons in each E cluster received synaptic input with similar but not identical timing, indicating that the interneurons that coordinate the homologous motor neurons are synchronized. The source of the rhythm that drives synaptically mediated cerebral extrinsic muscle motor neuron bursting was in the buccal ganglia. Cutting one cerebral-buccal connective eliminated E neuron bursting on that side but had no effect on homologous neurons on the intact side. This suggests that a single oscillator in the buccal ganglia may coordinate both the extrinsic and intrinsic buccal muscles during feeding.

Reciprocal excitation between identified flight motor neurons inDrosophila and its effect on pattern generation

Abstract: Intracellular recordings from the motor neurons innervating the dorsal longitudinal flight muscle (DLM) show that when one motor neuron fires, a response is transmitted to the other motor neurons (especially between the pairs innervating muscle fibers 1–2 and 3–4). The transmitted response often had a very similar waveform to the neuron's own response, consisting of a prepotential, spike-like component, and hyperpolarized phase. It is suggested that this response is transmitted electrically rather than chemically.

The identification of motor neurones innervating an abdominal ventilatory muscle in the locust

Abstract: Motor neurones to abdominal ventilatory muscles, with their axons innerve 6 of the metathoracic ganglion of the locust, have been identified by intracellular recording and staining. Three muscles are innervated by the larger branches of this nerve: nerve 6a contains six motor neurones innervating the ventral diaphragm; nerve 6b contains four motor neurones innervating the median internal ventral muscle, and nerve 6d contains five motorneurones innervating the longitudinal dorsal muscle. All motor neuronesinnervate muscles on one side of the body only. Both the median internalventral and the longitudinal dorsal muscles contract during the expiratoryphase of ventilation. Three excitatory motor neurones to the median internalventral muscles spike during expiration whilst the fourth, an inhibitorymotor neurone, is active during both expiration and inspiration. Two of theexcitatory motor neurones have cell bodies in the half of the ganglion ipsilateralto the muscle they innervate. Their neuropilar branches, however, are in both left and right halves of the ganglion. The third excitatory motorneurone has its cell body close to the midline and has most of its neuropilarbranches in the half of the ganglion ipsilateral to its axon. The inhibitorymotor neurone has its cell body just to the contralateral side of the midline, and three distinct areas of neuropilar branches, two contralateral and oneipsilateral to its axon.

A theory on the lability and stability of spinal motoneuron soma size and induction of synaptogenesis in the adult spinal cord.

Abstract: There exists a dynamic relationship between the soma size of a motoneuron and its motor unit size. Adult motoneuron soma size can be experimentally increased if the neuron is allowed to innervate more muscle fibers than it normally innervates. In postnatal mammals a transition from polyneuronal to mononeuronal innervation of limb muscle fibers occurs which is temporally related to a plastic change in the perikaryal size. This lability of postnatal motoneuron size is temporally related to growth of synaptic connections on the motoneuron. In adult mammal, regenerating motor axons polyneuronally innervate the muscle fibers for a transient period. This hypothesis proposes that a plastic change in soma size occurs in these adult motoneurons. This short-lived labile state may revive the embryonic properties and evoke growth of synaptic boutons. Experimentally induced labile state in motoneuron pools and spinal ganglion neurons in the adult mammal should offer a basis for the study of mechanisms of synaptogenesi...

Spinal cord stimulation as a tool for physiological research.

Abstract: The use of spinal cord stimulation for alleviation of disabilities due to motor neuron lesions has provided the opportunity to explore a new approach to measurement of spinal cord physiology. Externalized leads of epidural electrodes provide the possibility of recording evoked spinal cord activity, while both externalized or implanted leads can be used to study cortical evoked responses and twitches induced by spinal cord stimulation. The use of such electrophysiological techniques can be expected to expand greatly the applicability of the technique for alleviating motor disabilities, through a better definition of the degree, nature and extent of the lesion.

Myasthenia gravis immunoglobulin augments motor neuron survival without producing muscle paralysis.

Abstract: Effects of sera or immunoglobulins from patients with acquired myasthenia gravis on motor neuron survival during critical stages of embryonic development were investigated in the trochlear nucleus-superior oblique muscle system of white Peking duck embryos. A significant increase in motor neuron survival occurred following application of myasthenia gravis sera or myasthenic immunoglobulin during the period of embryonic death of motor neurons. There was no reduction in limb or extraocular muscle movement in treated embryos. Trochlear motor neuron survival persisted after sera or immunoglobulin treatment was discontinued. The total number of muscle fibers and acetylcholine receptors were unchanged following immunoglobulin treatment. Myasthenic immunoglobulin is therefore unique in preventing motor neuron death without producing muscle paralysis and in promoting a prolonged augmentation of motor neuron survival. It is concluded that factors other than muscle activity may also control neuron survival during embryogenesis. Previous studies of myasthenic sera in muscle have shown effects only postsynaptically. This is the first demonstration that myasthenic immunoglobulin affects structures in the central nervous system.

Morphological study on the hereditary neurogenic amyotrophic dogs: accumulation of lipid compound-like structures in the lower motor neuron

Abstract: A morphological study was performed on hereditary neurogenic amyotrophic dogs, the clinical features of which especially resembled spinal progressive muscular atrophy (SPMA), a human motor neuron disease. The skeletal muscles showed obvious neurogenic atrophy with endomysial fibrosis. The peripheral nerves revealed axonal degeneration mainly limited to the motor nerve. In the spinal cord, the number of anterior horn cells seemed normal but, interestingly enough, numerous accumulated granules were detected in these anterior horn cells. Histochemically, these granules were interpreted as a lipid compound. Under the electron microscope, the granules were disclosed as multi-lamellar structures, arranged concentrically or in parallel, resembling membranous cytoplasmic bodies (MCBs) or zebra bodies. This finding strongly suggests that hereditary abnormality of lipid metabolism may underlie SPMA in these dogs. However, unlike other metabolic disorders where accumulations of granules are diffusely distributed, in the dogs we examined accumulations were found only in the anterior horn cells of the spinal cord and in the hypoglossal and spinal accessory nuclei. We are unable to explain this occurrence at the present time. Further investigations should be made on dogs because they serve as an important animal model of human motor neuron disease.

Neurotrophic regulation of the phosphorylation of a soluble cytosolic protein in skeletal muscle

Abstract: Neural influences are exerted not only by propagation of nerve impulses, but also by trophic actions of the motor neuron upon its contiguous muscle cell. Previously, we found that the in vitro phosphorylation of soluble protein catalyzed by an endogenous protein kinase is increased in cytosolic fractions from denervated soleus muscles. This alteration occurred within several hours after the loss of some neural influence, but not as an immediate consequence of denervation (Squinto, S. P., J. A. McLane, and I. R. Held (1980) Neurosci. Lett. 20: 295–300; Squinto, S. P., J. A. McLane, and I. R. Held (1981) Neurochem. Res. 6: 203–211). In this paper, we further define the cytosolic protein substrates and demonstrate a nerve stump length-dependent phosphorylative modulation of the predominate substrate in rat soleus muscles which were denervated for 1, 3, and 6 hr and then at 6-hr intervals to 78 hr by unilaterally cutting the sciatic nerve to leave either a short (2 mm or less), intermediate (17 to 20 mm), or long (32 to 35 mm) distal nerve stump attached to the muscle. The results are compared with those obtained from sham- operated, contralateral solei and unoperated muscles. We found that the times of onset and of maximal increase of the in vitro phosphorylation of soluble cytosolic protein in denervated solei are directly related to the lengths of the distal nerve stumps; i.e., 1.4 hr/mm and 1.3 hr/mm, respectively, based upon linear regression analysis. Also, this alteration could be accounted for by an increased phosphorylation of a 56-kilodalton soluble cytosolic protein which was resolved as a minor protein-staining band after SDS slab PAGE. Although gel autoradiographs clearly showed that other soluble cytosolic proteins were also phosphorylated, approximately 80% of the incorporated 32P label was bound to the 56-kilodalton substrate. The transfer of 32PO4 from [gamma- 32P]ATP to the 56-kilodalton protein during the assay was markedly inhibited by cAMP, but was not affected by Ca2+, cGMP, or a specific inhibitor of cAMP-dependent protein kinase. The possibility that the 56- kilodalton protein substrate is the autophosphorylatable regulatory subunit of protein kinase type II is discussed. The temporal relationship of the increased phosphorylation of the 56-kilodalton protein with the denervation period and nerve stump length suggests this change is mediated by some neurotrophic regulation of skeletal muscle.

Reinnervation in Duchenne muscular dystrophy.

Abstract: Motor neuron abnormalities have been implicated in the pathogenesis of Duchenne muscular dystrophy. Evidence concerning the effect of injury on motor neurons of human Duchenne muscular dystrophy (DMD) is lacking. We report a DMD patient having, in addition, an obstetric paresis on his left arm. EMG and muscle histochemistry showed signs of reinnervation superimposed on myopathy in his left arm. This suggests that sprouting is preserved in DMD motor neurons and that muscle fibers retain the capability of accepting reinnervation.