Renshaw cell

Last updated
Renshaw cell
Details
Neurotransmitter Glycine
Identifiers
MeSH D066293
NeuroLex ID nifext_113
FMA 86787
Anatomical terms of neuroanatomy

Renshaw cells are inhibitory interneurons found in the gray matter of the spinal cord, and are associated in two ways with an alpha motor neuron.

Contents

In this way, the Renshaw cell action represents a negative feedback mechanism. A Renshaw cell may be supplied by more than one alpha motor neuron collateral and it may synapse on multiple motor neurons.

Function

Although during embryonic development the Renshaw cells lack synapses from the dorsal root, prenatal and postnatal stages show the development of dorsal root originating synapses, which are functional and stimulate action potentials. But these decrease during development while acetylcholine motor axons begin to synapse and proliferate with Renshaw cells, ultimately being primarily stimulated by the motor neurons. [1]

The Renshaw cells are ultimately excited by multiple antidromic motor neuron axons, where the majority of axons originate from synergist motor neurons, and in turn the Renshaw cell synapses with multiple neurons, eliciting IPSP in alpha motor, 1a inhibitory interneurons and gamma motor neurons. The antidromic collateral circuit back to the triggering motor neuron is known as “recurrent inhibition”. This homonymous inhibition is not universal. Whereas most initial experiments have been done on cats, it has been found that in man that proximal muscles of the hand and foot do not have homonymous inhibition. Heteronymous inhibition has been found to be dominant in the leg compared to the arm, where antagonist muscles work simultaneously. (Renshaw cells are activated by gamma motor neurons, but to a lesser extent). The Renshaw cells not only synapse with homonymous and heteronymous nerves, but also with the Ia interneurones, which are stimulated by the Ia afferents from the same muscle group activated by the motor neurons, which have an inhibitory effect on the antagonist muscle group. This “recurrent facilitation” causes reduced inhibition of the reciprocal inhibition of the Ia interneuron of the antagonist group (Baret et al.; 2003), which may in turn also be inhibited by signals from the corticospinal tract. [2] It has been shown that: [3] [4] [5]

The Renshaw cells may also be inhibited by both proprioceptive dorsal root afferents], [6] [7] antidromic ventral axons [8] as well as “descending” inhibition. [9] [10] The hyperpolarization of Renshaw cells by afferent and descending neurons have been shown to be caused by the release of glycine, but GABA may also hyperpolarize the Renshaw cell - for a prolonged time relative to glycine. It has also been shown that glycine is the inhibitory transmitter released by the Renshaw cells. [11] [12]

In essence the Renshaw cells regulate the firing of the alpha motor neuron leaving the ventral horn. Conceptually they remove “noise” by dampening the firing frequency of over-excited neurons with a negative feedback loop, which prevents weakly excited alpha motor neurons from firing. Descending spinal cord nerves in turn regulate the Renshaw cells.

The rate of discharge of the Renshaw cell is broadly proportional to the rate of discharge of the associated motor neuron(s), and the rate of discharge of the motor neuron(s) is broadly inversely proportional to the rate of discharge of the Renshaw cell(s). Renshaw cells thus act as "limiters," or "governors," on the alpha motor neuron system, thus helping to prevent muscular damage from tetanus.

Renshaw cells utilize the neurotransmitter glycine as an inhibitory substance that synapses on the alpha motor neurons.

Clinical significance

Renshaw cells are also the target of the toxin of Clostridium tetani , a Gram positive, spore-forming anaerobic bacterium that lives in the soil, and causes tetanus. When wounds are contaminated with C. tetani, the toxin travels to the spinal cord where it inhibits the release of glycine, an inhibitory neurotransmitter, from Renshaw cells. As a result, alpha motor neurons become hyperactive, and muscles constantly contract.

Strychnine poison also specifically acts on these cell’s ability to control alpha motor neuron firing by binding to the glycine receptors on the alpha motor neuron and thus muscles contiually contract and may prove fatal if the diaphragm is involved.

History

The concept of the Renshaw cells was postulated by Birdsey Renshaw (1911–1948), [13] when it was discovered that with antidromic signals from a motor neuron running collaterally back via the ventral root into the spinal cord, there were interneurons firing with a high frequency, resulting in inhibition. Later work by Eccles et al., [14] provided evidence that these interneurons, which they called “Renshaw Cells,” are stimulated by acetylcholine from motor neurons (nicotinic receptor). Previous work by Renshaw [15] and Lloyd [16] [17] had shown that this antidromic inhibition resembled direct inhibition from spinal nerves but resulted in relatively longer inhibition of 40-50 ms (compared to 15 ms). The antidromic stimulation of the nerve fiber also resulted in action potentials in the cell bodies of the motor neurons along with hyperpolarization of other groups of motor neurons. In the event where the initial stimulation of the motor neuron originated in a spinal tract the Renshaw cell spike occurred during the declining phase of the initial motor neuron soma spike giving an indication of the source and sequence of stimulation of the Renshaw cell.

Related Research Articles

In neuroscience, an F wave is one of several motor responses which may follow the direct motor response (M) evoked by electrical stimulation of peripheral motor or mixed nerves. F-waves are the second of two late voltage changes observed after stimulation is applied to the skin surface above the distal region of a nerve, in addition to the H-reflex which is a muscle reaction in response to electrical stimulation of innervating sensory fibers. Traversal of F-waves along the entire length of peripheral nerves between the spinal cord and muscle, allows for assessment of motor nerve conduction between distal stimulation sites in the arm and leg, and related motoneurons (MN's) in the cervical and lumbosacral cord. F-waves are able to assess both afferent and efferent loops of the alpha motor neuron in its entirety. As such, various properties of F-wave motor nerve conduction are analyzed in nerve conduction studies (NCS), and often used to assess polyneuropathies, resulting from states of neuronal demyelination and loss of peripheral axonal integrity.

Motor neuron Neuron whose cell body is located in the motor cortex, brainstem or the spinal cord, and whose axon projects to the spinal cord or outside of the spinal cord to directly or indirectly control effector organs, mainly muscles and glands

A motor neuron is a neuron whose cell body is located in the motor cortex, brainstem or the spinal cord, and whose axon (fiber) projects to the spinal cord or outside of the spinal cord to directly or indirectly control effector organs, mainly muscles and glands. There are two types of motor neuron – upper motor neurons and lower motor neurons. Axons from upper motor neurons synapse onto interneurons in the spinal cord and occasionally directly onto lower motor neurons. The axons from the lower motor neurons are efferent nerve fibers that carry signals from the spinal cord to the effectors. Types of lower motor neurons are alpha motor neurons, beta motor neurons, and gamma motor neurons.

Somatic nervous system Part of the peripheral nervous system

The somatic nervous system is the part of the peripheral nervous system associated with the voluntary control of body movements via skeletal muscles.

An inhibitory postsynaptic potential (IPSP) is a kind of synaptic potential that makes a postsynaptic neuron less likely to generate an action potential. IPSP were first investigated in motorneurons by David P. C. Lloyd, John Eccles and Rodolfo Llinás in the 1950s and 1960s. The opposite of an inhibitory postsynaptic potential is an excitatory postsynaptic potential (EPSP), which is a synaptic potential that makes a postsynaptic neuron more likely to generate an action potential. IPSPs can take place at all chemical synapses, which use the secretion of neurotransmitters to create cell to cell signalling. Inhibitory presynaptic neurons release neurotransmitters that then bind to the postsynaptic receptors; this induces a change in the permeability of the postsynaptic neuronal membrane to particular ions. An electric current that changes the postsynaptic membrane potential to create a more negative postsynaptic potential is generated, i.e. the postsynaptic membrane potential becomes more negative than the resting membrane potential, and this is called hyperpolarisation. To generate an action potential, the postsynaptic membrane must depolarize—the membrane potential must reach a voltage threshold more positive than the resting membrane potential. Therefore, hyperpolarisation of the postsynaptic membrane makes it less likely for depolarisation to sufficiently occur to generate an action potential in the postsynaptic neurone.

Muscle spindle Innervated muscle structure involved in reflex actions and proprioception

Muscle spindles are stretch receptors within the body of a muscle that primarily detect changes in the length of the muscle. They convey length information to the central nervous system via afferent nerve fibers. This information can be processed by the brain as proprioception. The responses of muscle spindles to changes in length also play an important role in regulating the contraction of muscles, for example, by activating motor neurons via the stretch reflex to resist muscle stretch.

Grey column mass of grey matter in the spinal cord

The grey column refers to a somewhat ridge-shaped mass of grey matter in the spinal cord. This presents as three columns: the anterior grey column, the posterior grey column, and the lateral grey column, all of which are visible in cross-section of the spinal cord.

Reflex arc neural pathway that controls a reflex

A reflex arc is a neural pathway that controls a reflex. In vertebrates, most sensory neurons do not pass directly into the brain, but synapse in the spinal cord. This allows for faster reflex actions to occur by activating spinal motor neurons without the delay of routing signals through the brain. The brain will receive the sensory input while the reflex is being carried out and the analysis of the signal takes place after the reflex action.

Reciprocal inhibition describes the process of muscles on one side of a joint relaxing to accommodate contraction on the other side of that joint. In some allied health disciplines this is known as reflexive antagonism. Joints are controlled by two opposing sets of muscles, extensors and flexors, which must work in synchrony for smooth movement. When a muscle spindle is stretched and the stretch reflex is activated, the opposing muscle group must be inhibited to prevent it from working against the resulting contraction of the homonymous muscle. This inhibition is accomplished by the actions of an inhibitory interneuron in the spinal cord.

Gamma motor neuron

A gamma motor neuron, also called gamma motoneuron, is a type of lower motor neuron that takes part in the process of muscle contraction, and represents about 30% of fibers going to the muscle. Like alpha motor neurons, their cell bodies are located in the anterior grey column of the spinal cord. They receive input from the reticular formation of the pons in the brainstem. Their axons are smaller than those of the alpha motor neurons, with a diameter of only 5 μm. Unlike the alpha motor neurons, gamma motor neurons do not directly adjust the lengthening or shortening of muscles. However, their role is important in keeping muscle spindles taut, thereby allowing the continued firing of alpha neurons, leading to muscle contraction. These neurons also play a role in adjusting the sensitivity of muscle spindles.

Motor unit recruitment refers to the activation of additional motor units to accomplish an increase in contractile strength in a muscle. A motor unit consists of one motor neuron and all of the muscle fibers it stimulates. All muscles consist of a number of motor units and the fibers belonging to a motor unit are dispersed and intermingle amongst fibers of other units. The muscle fibers belonging to one motor unit can be spread throughout part, or most of the entire muscle, depending on the number of fibers and size of the muscle. When a motor neuron is activated, all of the muscle fibers innervated by the motor neuron are stimulated and contract. The activation of one motor neuron will result in a weak but distributed muscle contraction. The activation of more motor neurons will result in more muscle fibers being activated, and therefore a stronger muscle contraction. Motor unit recruitment is a measure of how many motor neurons are activated in a particular muscle, and therefore is a measure of how many muscle fibers of that muscle are activated. The higher the recruitment the stronger the muscle contraction will be. Motor units are generally recruited in order of smallest to largest as contraction increases. This is known as Henneman's size principle.

Golgi cell Type of interneuron

In neuroscience, Golgi cells are inhibitory interneurons found within the granular layer of the cerebellum. They were first identified as inhibitory by Eccles et al. in 1964. It was also the first example of an inhibitory feed back network, where the inhibitory interneuron was identified anatomically. These cells synapse onto the dendrite of granule cells and unipolar brush cells. They receive excitatory input from mossy fibres, also synapsing on granule cells, and parallel fibers, which are long granule cell axons. Thereby this circuitry allows for feed-forward and feed-back inhibition of granule cells.

Alpha motor neuron

Alpha (α) motor neurons (also called alpha motoneurons), are large, multipolar lower motor neurons of the brainstem and spinal cord. They innervate extrafusal muscle fibers of skeletal muscle and are directly responsible for initiating their contraction. Alpha motor neurons are distinct from gamma motor neurons, which innervate intrafusal muscle fibers of muscle spindles.

The Mauthner cells are a pair of big and easily identifiable neurons located in the rhombomere 4 of the hindbrain in fish and amphibians that are responsible for a very fast escape reflex. The cells are also notable for their unusual use of both chemical and electrical synapses.

The Golgi tendon reflex (also called inverse stretch reflex, autogenic inhibition, tendon reflex) is an inhibitory effect on the muscle resulting from the muscle tension stimulating Golgi tendon organs (GTO) of the muscle, and hence it is self-induced. The reflex arc is a negative feedback mechanism preventing too much tension on the muscle and tendon. When the tension is extreme, the inhibition can be so great it overcomes the excitatory effects on the muscle's alpha motoneurons causing the muscle to suddenly relax. This reflex is also called the inverse myotatic reflex, because it is the inverse of the stretch reflex.

Uwe Windhorst is a German neuroscientist, systems scientist and cyberneticist, who was born in Bremen, Germany in 1946. Windhorst became known for his pioneer research in the use of diverse methods of correlation, spectral analysis as well as nonlinear systems analysis to describe the dynamic properties of signal transmission through small neuronal networks assessed in experimental animals.

Neural substrate of locomotor central pattern generators in mammals

Central pattern generators are biological neural networks organized to produce any rhythmic output without requiring a rhythmic input. In mammals, locomotor CPGs are organized in the lumbar and cervical segments of the spinal cord, and are used to control rhythmic muscle output in the arms and legs. Certain areas of the brain initiate the descending neural pathways that ultimately control and modulate the CPG signals. In addition to this direct control, there exist different feedback loops that coordinate the limbs for efficient locomotion and allow for the switching of gaits under appropriate circumstances.

Spinal interneuron

A spinal interneuron, found in the spinal cord, relays signals between (afferent) sensory neurons, and (efferent) motor neurons. Different classes of spinal interneurons are involved in the process of sensory-motor integration. Most interneurons are found in the grey column, a region of grey matter in the spinal cord.

James B. Preston

James B. Preston was an American born neurophysiologist whose research was fundamental to discovering how our brains control movement. Over the course of his career, he published over forty research based articles in his field. Preston was the chairman of numerous national committees and former President of the Association of Chairs of Departments of Physiology.

Presynaptic inhibition

Presynaptic inhibition is an inhibitory input to a neuron to make it less likely to fire an action potential and communicate with downstream neurons. Inhibition can be provided both at the postsynapse (IPSP) and the presynapse. Presynaptic inhibition occurs when an inhibitory neurotransmitter, like GABA, acts on GABA receptors on the axon terminal. Presynaptic inhibition is ubiquitous among sensory neurons.

An axo-axonic synapse is a type of synapse, formed by one neuron projecting its axon terminals onto another neuron’s axon.

References

  1. ↑ George Z. Mentis, Valerie C. Siembab, Ricardo Zerda, Michael J. O'Donovan, and Francisco J. Alvarez, Primary Afferent Synapses on Developing and Adult Renshaw Cells. The J.of Neuroscience, 2006, 26(51):13297-13310
  2. ↑ Mazzocchio R, Rossi A, Rothwell JC. Depression of Renshaw recurrent inhibition by activation of corticospinal fibres in human upper and lower limb. J Physiol (Lond) 1994; 481: 487–9
  3. ↑ H. Hultborn, E. Pierrot-Deseilligny.Changes in recurrent inhibition during voluntary soleus contractions in man studied by an H-Reflex Technique. J. Phyeiol. 1979, 297, pp. 229–251.
  4. ↑ Iles JF, Pardoe J. Changes in transmission in the pathway of heteronymous spinal recurrent inhibition from soleus to quadriceps motor neurons during movement in man. Brain 1999; 122: 1757–64
  5. ↑ Nielsen J, Pierrot-Deseilligny E. Evidence of facilitation of soleus-coupled Renshaw cells during voluntary co-contraction of antagonistic ankle muscles in man. J Physiol (Lond) 1996; 493: 603–11
  6. ↑ Wilson VJ, Talbot WH, Kato M Inhibitory convergence upon Renshaw cells. Journal of neurophysiology. 1964;27:1063-1079.
  7. ↑ R. W. Ryall, M. F. Piercey, and C. Polosa. Intersegmental and intrasegmental distribution of mutual inhibition of Renshaw cells. J Neurophysiol 34: 700-, 1971
  8. ↑ RYALL, R. W. Renshaw cell mediated inhibition of Renshaw cells: patterns of excitation and inhibition from impulses in motor axon collaterals. J.Neurophysiol. 1970, 33, 257-270
  9. ↑ R. Granit, J. Haase, and L. T. Rutledge. Recurrent inhibition in relation to frequency of firing and limitation of discharge rate of extensor motoneurones. J. Physiol. 1960 December; 154(2): 308–328.
  10. ↑ J Haase, J van der Meulen. Effects of supraspinal stimulation on Renshaw cells belonging to extensor motoneurones. Journal of neurophysiology. 10/1961; 24:510-20
  11. ↑ D R Curtis, C J Game, D Lodge, and R M McCulloch. A pharmacological study of Renshaw cell inhibition. J. Physiol. 1976 June; 258(1): 227–242
  12. ↑ Victor J. Wilson & William H. Talbot. Integration at an Inhibitory Interneurone: Inhibition of Renshaw Cells. Nature 1963 200, 1325–1327
  13. ↑ Renshaw B. Central effects of centripetal impulses in axons of spinal ventral roots. J Neurophysiol 1946 9:191–204
  14. ↑ Eccles JC, Fatt P, Koketsu K. Cholinergic and inhibitory synapses in a pathway from motor-axon collaterals to motoneurones. J. Physiol. 1954;126:524–562.
  15. ↑ Renshaw B. Influence of discharge of motoneurons upon excitation of neighboring motoneurons. J Neurophysiol 1941 4:167
  16. ↑ Lloyd, D. P. C.. Facilitation and inhibition of spinal motoneurons, J.Neurophysiol.,1946, 9,421.
  17. ↑ Lloyd, D. P. C., After-currents, after-potentials, excitability, and ventral root electrotonus in spinal motoneurons, J.gen. Physiol..,1951,35 ,289
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.