Non-spiking neuron

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Non-spiking neurons are neurons that are located in the central and peripheral nervous systems and function as intermediary relays for sensory-motor neurons. They do not exhibit the characteristic spiking behavior of action potential generating neurons.

Characteristic spiking behavior of neuron
Qualities Spiking neurons Nonspiking neurons
Location Peripheral and central Peripheral and central
Behavior Action potential Fewer sodium channel proteins

Non-spiking neural networks are integrated with spiking neural networks to have a synergistic effect in being able to stimulate some sensory or motor response while also being able to modulate the response.

Neural synapse

Discovery

Animal models

There are an abundance of

spiking networks in animals, a neuron that did not exhibit characteristic spiking behavior was discovered. These neurons use a graded potential to transmit data as they lack the membrane potential that spiking neurons possess. This method of transmission has a huge effect on the fidelity, strength, and lifetime of the signal. Non-spiking neurons were identified as a special kind of interneuron and function as an intermediary point of process for sensory-motor systems. Animals have become substantial models for understanding more about non-spiking neural networks and the role they play in an animal’s ability to process information and its overall function. Animal models indicate that the interneurons modulate directional and posture coordinating behaviors.[1][2]
retina amacrine cell
of the eye.

Physiology

Definition

A non-spiking neuron is a neuron that transmits a signal via graded potential. The rate of subsequent neurotransmitter release is linearly correlated with the magnitude and sign of summed inputs which allows them to preserve specific features of the eliciting stimulus, such as light quanta information by photoreceptors.[4] They are a fundamental component of visual processing in the retina.[5] They can be more susceptible to noise. Studies show that these neurons may offer a contribution to learning and modulation of motor neuron networks.

Spiking neurons and non-spiking neurons are usually integrated into the same neural network, but they possess specific characteristics. The major difference between these two neuron types is the manner in which encoded information is propagated along a length to the central nervous system or to some locus of interneurons, such as a neuromuscular junction. Non-spiking neurons propagate messages without eliciting an action potential. This is most likely due to the chemical composition of the membranes of the non-spiking neurons. They lack protein channels for sodium and are more sensitive to certain neurotransmitters. They function by propagating graded potentials and serve to modulate some neuromuscular junctions. Spiking neurons are noted as traditional action potential generating neurons.[4]

Identification

"

GABA, a neurotransmitter for muscle tone. They also have different staining responses permitting quick and qualified classification.[6]

A retinal amacrine cell

Cell types

Many of the nonspiking neurons are found near neuromuscular junctions and exist as long fibers that help to

innervate
certain motor nerves such as the thoracic-coxal muscle receptor organ (TCMRO) of a crab.[4] They function in a modulatory role by helping to establish posture and directional behavior. This was intensely modeled in the crustacean and in insects showing how appendages are oriented via these nonspiking neural pathways.[2] Amacrine cells are another major type of non-spiking neuron and their lifetime involves the conversion to a non-spiking neuron from a spiking neuron once the retina obtains maturity. They are one of the first cells to differentiate during prenatal development. Upon the opening of the eyes, these cells begin to shed their sodium ion channels and become non-spiking neurons. It was hypothesized that the reason for its establishment as a spiking neuron was to help with the maturation of the retina by the usage of action potentials themselves, and not necessarily the information the action potential carried. This was supported with the occurrence of synchronous firing by the starburst amacrine cells during the initial stages of development. This study used a rabbit model.[7] However, spiking wide field amacrine cells have been identified in the adult rabbit retina. These cells extend processes spanning >1mm across the retina and actively propagate dendritic spikes to and from the soma[8] Additionally, a spiking GABAergic nitric oxide producing amacrine cell type (nNOS-1 AC) has been identified in mice and is thought to play a role in precise feature extraction from light through a range of noisy background luminance.[9]

Physiological characteristics

Some studies have indicated that even with the volatility of signal transmission with these particular neurons, they still perform very well in maintaining signal strength. Studies show that the ratio of signal to noise in experimental settings of some signals are at least 1000 and upwards to 10000 over 5-7mm of propagation length by

nerves.[4]

Effect of noise on non-spiking neuron transmission

These interneurons are connected to one another via

postsynaptic cell even after being inhibited. Signal amplitude was used to determine the effects of the modulation on the signal transmission.[10]

The speed of signal transmission at 200 Hz, the most conserved bandwidth of signal transmission for non-spiking neurons, was approximately 2500 bits/second in which there was a 10-15% decrease in speed as the signal propagated down the axon. A spiking neuron compares at 200bits/ second, but reconstruction is greater and there is less influence by noise. There are other non-spiking neurons that exhibit conserved signal transmission at other bandwidths.[4]

Cell Type Characteristics
Arthropod Orienting motor control
Rabbit amacrine cell Eyes, establishment of function
Crustacean Orienting motor control; 2500 bit/s; bandwidth of 200 Hz

While some non-spiking neurons are specifically involved in neuromuscular modulation, studying amacrine cells has created opportunities to discuss the role of non-spiking neurons in neuroplasticity. Since amacrine cells, which are a type of non-spiking neurons, undergo a transformation from spiking to non-spiking cells, there have been many studies that try to identify the functional reasons for such a transformation. Starburst amacrine cells use action potentials during retinal development, and once the retina is mature, these cells transform into non-spiking neurons. The change from a cell that can generate action potentials to solely functioning off of a graded potential is drastic, and may provide insight into why the two kinds of neural networks exist. The cells lose sodium channels. The loss of the sodium channels is triggered by the opening of the eye correlating to the possibility of the environment playing a crucial role in determination of neural cell types. The rabbit animal model was used to develop this particular study. This transition is not quite understood but heavily concludes that the spiking and non-spiking statuses occupied by the starburst amacrine cells are vital to the maturation of the eyes.[7]

Functions

Modulation

By using known neurotransmitters that affect non-spiking neurons, modeled neural networks may be modified to either ease neuromuscular hyperactivity, or cells themselves may be transformed to be able to provide stronger signals. A

protein channels have on the overall fidelity and firing capacity of the non-spiking neurons.[11] Since most of the propagated messages are based on a proportionality constant, meaning, there is not a temporal or spatial significance to the presynaptic firing, these signals literally "repeat what they have been told". When it comes down to chemical systems in the body, a non-spiking neural network is definitely an area of exploration.[12] The amacrine cell study poses new and exciting components to the study of altering the chemical and mechanical properties of the non-spiking neural networks.[7]

Memory and learning

Very little is known about the application of these networks to memory and learning. There are indications that spiking and nonspiking networks both play a vital role in memory and learning.[13][14] Research has been conducted with the use of learning algorithms, microelectrode arrays, and hybrots. By studying how neurons transfer information, it becomes more possible to enhance those model neural networks and better define what clear information streams could be presented. Perhaps, by conjoining this study with the many neurotrophic factors present, neural networks could be manipulated for optimal routing, and consequently optimal learning.[15]

Device production

By studying the nonspiking neuron, the field of neuroscience has benefited by having workable models that indicate how information is propagated through a neural network. This allows for the discussion of the factors that influence how networks work, and how they may be manipulated. Non-spiking neurons seem to be more sensitive to interference given that they exhibit graded potentials. So for non-spiking neurons, any stimulus will elicit a response, whereas spiking neurons exhibit action potentials which function as an "all or none" entity.[4]

In

VS Ramachandran on phantom limbs and other optical applications, and other devices that simulate electrical impulses for sensory signal transduction. By continuing to achieve a workable model of the non-spiking neural network, its applications will become evident.[16]

See also

References

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  5. ^ Purves, Dale; Augustine, George J.; Fitzpatrick, David; Katz, Lawrence C.; LaMantia, Anthony-Samuel; McNamara, James O.; Williams, S. Mark (2001). Phototransduction.
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  7. ^ a b c Zhou, ZJ; Cheney M; Fain GL (1996). "Starburst amacrine cells change from spiking to non-spiking neurons during visual development". Investigative Ophthalmology & Visual Science. 37 (3): 5263–5263.
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