Non-spiking neuron
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.
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.
Discovery
Animal models
There are an abundance of
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
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Cell types
Many of the nonspiking neurons are found near neuromuscular junctions and exist as long fibers that help to
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
These interneurons are connected to one another via
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
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
See also
- Transduction (biophysics)
- EPSP (excitatory post-synaptic potential)
- IPSP(inhibitory post-synaptic potential)
References
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- ^ 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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- ^ 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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