Motoneuron

CGRP has a wide distribution in the nervous system (19) and was the first peptide to be localized to motoneurons (124). It is also found in primary sensory neurons where it is colocalized with substance P (125). CGRP is derived from a precursor stmcturaHy related to the calcitonin precursor. The latter precursor produces two products, calcitonin itself and katacalcin, while the CGRP precursor produces one copy of CGRP (123). Like other peptides, CGRP is cleaved from its precursor by tryptic breakdown between double basic amino acid residues. 

Neuromuscular junction (NMJ) is the synapse or junction of the axon terminal of motoneurons with the highly excitable region of the muscle fibre s plasma membrane. Neuronal signals pass through the NMJ via the neurotransmitter ACh. Consequent initiation of action potentials across the muscle s cell surface ultimately causes the muscle contraction. 

CNTF supports survival and differentiation of selected neuron populations including sensory, sympathetic, and motoneurons. Also, nonneuronal cells, such as... 

The neurons from which NTs are released number more than 7 billion in the human brain. Each (Fig. 1.2) consists of a cell body, the soma or perikaryon, with one major cytoplasmic process termed the axon, which projects variable distances to other neurons, e.g. from a cortical pyramidal cell to adjacent cortical neurons, or to striatal neurons or to spinal cord motoneurons. Thus by giving off a number of branches from its axon one neuron can influence a number of others. All neurons, except primary sensory neurons with cell bodies in the spinal dorsal root ganglia, have a number of other, generally shorter, projections running much shorter distances among neighbouring neurons like the branches of a tree. These processes are the dendrites. Their... 

Nevertheless, useful information can be deduced from patterns of distribution. Glycine is concentrated more in the cord than cortex and in ventral rather than dorsal grey or white matter. This alone would be indicative of a NT role for glycine in the ventral horn, where it is now believed to be the inhibitory transmitter at motoneurons. GABA, on the other hand, is more concentrated in the brain than in the cord and in the latter it is predominantly in the dorsal grey so that although it is an inhibitory transmitter like glycine it must have a different pattern of activity. 

Figure 2.13 Relation between the action potential recorded intracellularly from a cat spinal motoneuron following antidromic stimulation (int.) and the local field potential recorded with an extracellular electrode (ext.). (Adapted from Terzuolo, AC and Araki, T (1961) Ann. NY Acad. Sci. 94 547-558). Published by NYAS...

Since ACh is the transmitter at the skeletal neuromuscular junction one might also expect it to be released from any axon collaterals arising from the motor nerve to it. Such collaterals innervate (drive) an interneuron (the Renshaw cell) in the ventral horn of the spinal cord, which provides an inhibitory feedback onto the motoneuron. Not... 

Glycine is the simplest of all amino acids. It is involved in many metabolic pathways, is an essential component of proteins, and is found throughout the brain. A neurotransmitter role for glycine was first identified in the spinal cord, where it was found to be differentially distributed between dorsal and ventral regions and shown to cause hyperpolarisation of motoneurons (Werman et al. 1967). This inhibitory action of glycine is distinct from its... 

O Brien, JA and Berger, AJ (1999) Cotransmission of GABA and glycine to brain stem motoneurons. J. Neurophysiol. 82 1638-1641. 

Werman, R, Davidoff, RA and Aprison, MH (1967) Inhibition of motoneurones by iontophoresis of glycine. Nature 214 681-683. 

The dendrites of neurons adjacent to those which degenerate also show extensive growth and sprouting which could facilitate abnormal and disorganised synaptic transmission and cause hyperactivity. It is also known that the dendrites of cells around an alumina focus in monkeys, as well as in human epileptic brain, lose their spinous processes, which might contribute to the paroxysmal discharge by facilitating the spread of depolarisation to the neuron soma. Certainly an increase in the number of Na+ channels on the dendrites of spinal motoneurons, which would facilitate the occurrence of reactive dendritic Na+ spikes, has been seen after axotomy. 

Morales, F. R. Chase, M. H. (1978). Intracellular recording of lumbar motoneuron membrane potential during sleep and wakefulness. Exp. Neurol. 62, 821-7. 

Rye D. (2003). Modulation of normal and pathologic motoneuron activity during sleep. In Chokroverty S., Hening W., Walters A., editors. Sleep and Movement Disorders. Philadelphia, PA Butterworth-Heinemann pp. 94-119. 

FIGURE 6-1 Path of excitation in a simplified spinal reflex that mediates withdrawal of the leg from a painful stimulus. In each of the three neurons and in the muscle cell, excitation starts with a localized slow potential and is propagated via an action potential (a.p.). Slow potentials are generator potential (g.p.) at the skin receptor the excitatory postsynaptic potentials (e.p.s.p.) in the interneuron and the motoneuron and end-plate potential (e.p.p.) at the neuromuscular junction. Each neuron makes additional connections to other pathways that are not shown. 

Neurotransmission in autonomic ganglia is more complex than depolarization mediated by a single transmitter 190 Muscarinic receptors are widely distributed at postsynaptic parasympathetic effector sites 190 Stimulation of the motoneuron releases acetylcholine onto the muscle endplate and results in contraction of the muscle fiber 191 Competitive blocking agents cause muscle paralysis by preventing access of acetylcholine to its binding site on the receptor 191... 

Stimulation of the motoneuron releases acetylcholine onto the muscle endplate and results in contraction of the muscle fiber. Contraction and associated electrical events can be produced by intra-arterial injection of ACh close to the muscle. Since skeletal muscle does not possess inherent myogenic tone, the tone of apparently resting muscle is maintained by spontaneous and intermittent release of ACh. The consequences of spontaneous release at the motor endplate of skeletal muscle are small depolarizations from the quantized release of ACh, termed miniature endplate potentials (MEPPs) [15] (seeCh. 10). Decay times for the MEPPs range between l and 2 ms, a duration similar to the mean channel open time seen with ACh stimulation of individual receptor molecules. Stimulation of the motoneuron results in the release of several hundred quanta of ACh. The summation of MEPPs gives rise to a postsynaptic excitatory potential (PSEP),... 

Oppenheim, R. W. Neurotrophic survival molecules for motoneurons an embarrassment of riches. Neuron 17 195-7,1996. 

Oppenheim, R. W., Wiese, S. and Prevette, D. et al. Cardiotrophin-1, a muscle-derived cytokine, is required for the survival of subpopulations of developing motoneurons. /. Neurosci. 21 1283-91, 2001. 

Lambrechts, D., Storkebaum, E., Morimoto, M. et al. VEGF is a modifier of amyotrophic lateral sclerosis in mice and humans and protects motoneurons against ischemic death. Nat. Genet. 34 383-394, 2003. 

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