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Biological neuron model

Biological neuron models, also known as spiking neuron models, are mathematical descriptions of the conduction of electrical signals in neurons. Neurons are electrically excitable cells within the nervous system, able to fire electric signals, called action potentials, across a neural network. These mathematical models describe the role of the biophysical and geometrical characteristics of neurons on the conduction of electrical activity.

Biological background, classification, and aims of neuron models
Non-spiking cells, spiking cells, and their measurement Not all the cells of the nervous system produce the type of spike that defines the scope of the spiking neuron models. For example, cochlear hair cells, retinal receptor cells, and retinal bipolar cells do not spike. Furthermore, many cells in the nervous system are not classified as neurons but instead are classified as glia. Neuronal activity can be measured with different experimental techniques, such as the "Whole cell" measurement technique, which captures the spiking activity of a single neuron and produces full amplitude action potentials. With extracellular measurement techniques, one or more electrodes are placed in the extracellular space. Spikes, often from several spiking sources, depending on the size of the electrode and its proximity to the sources, can be identified with signal processing techniques. Extracellular measurement has several advantages: • It is easier to obtain experimentally; • It is robust and lasts for a longer time; • It can reflect the dominant effect, especially when conducted in an anatomical region with many similar cells. Overview of neuron models Neuron models can be divided into two categories according to the physical units of the interface of the model. Each category could be further divided according to the abstraction/detail level: • Electrical input–output membrane voltage models – These models produce a prediction for membrane output voltage as a function of electrical stimulation given as current or voltage input. The various models in this category differ in the exact functional relationship between the input current and the output voltage and in the level of detail. Some models in this category predict only the moment of occurrence of the output spike (also known as "action potential"); other models are more detailed and account for sub-cellular processes. The models in this category can be either deterministic or probabilistic. • Natural stimulus or pharmacological input neuron models – The models in this category connect the input stimulus, which can be either pharmacological or natural, to the probability of a spike event. The input stage of these models is not electrical but rather has either pharmacological (chemical) concentration units, or physical units that characterize an external stimulus such as light, sound, or other forms of physical pressure. Furthermore, the output stage represents the probability of a spike event and not an electrical voltage. Although it is not unusual in science and engineering to have several descriptive models for different abstraction/detail levels, the number of different, sometimes contradicting, biological neuron models is exceptionally high. This situation is partly the result of the many different experimental settings, and the difficulty to separate the intrinsic properties of a single neuron from measurement effects and interactions of many cells (network effects). Aims of neuron models Ultimately, biological neuron models aim to explain the mechanisms underlying the operation of the nervous system. However, several approaches can be distinguished, from more realistic models (e.g., mechanistic models) to more pragmatic models (e.g., phenomenological models). Modeling helps to analyze experimental data and address questions. Models are also important in the context of restoring lost brain functionality through neuroprosthetic devices. == Electrical input–output membrane voltage models ==
Electrical input–output membrane voltage models {{anchor|ElectricalModels}}
The models in this category describe the relationship between neuronal membrane currents at the input stage and membrane voltage at the output stage. This category includes (generalized) integrate-and-fire models and biophysical models inspired by the work of Hodgkin–Huxley in the early 1950s using an experimental setup that punctured the cell membrane and allowed to force a specific membrane voltage/current.). Hodgkin–Huxley The Hodgkin–Huxley model (H&H model) is a model of the relationship between the flow of ionic currents across the neuronal cell membrane and the membrane voltage of the cell. it is also possible to extend it to take into account the evolution of the concentrations (considered fixed in the original model). Perfect Integrate-and-fire One of the earliest models of a neuron is the perfect integrate-and-fire model (also called non-leaky integrate-and-fire), first investigated in 1907 by Louis Lapicque. A neuron is represented by its membrane voltage which evolves in time during stimulation with an input current according :I(t)=C \frac{d V(t)}{d t} which is just the time derivative of the law of capacitance, . When an input current is applied, the membrane voltage increases with time until it reaches a constant threshold , at which point a delta function spike occurs and the voltage is reset to its resting potential, after which the model continues to run. The firing frequency of the model thus increases linearly without bound as input current increases. The model can be made more accurate by introducing a refractory period that limits the firing frequency of a neuron by preventing it from firing during that period. For constant input the threshold voltage is reached after an integration time after starting from zero. After a reset, the refractory period introduces a dead time so that the total time until the next firing is . The firing frequency is the inverse of the total inter-spike interval (including dead time). The firing frequency as a function of a constant input current, is therefore :\,\! f(I)= \frac{I} {C_\mathrm{} V_\mathrm{th} + t_\mathrm{ref} I}. A shortcoming of this model is that it describes neither adaptation nor leakage. If the model receives a below-threshold short current pulse at some time, it will retain that voltage boost forever - until another input later makes it fire. This characteristic is not in line with observed neuronal behavior. The following extensions make the integrate-and-fire model more plausible from a biological point of view. Leaky integrate-and-fire The leaky integrate-and-fire model, which can be traced back to Louis Lapicque, The model can also be used for inhibitory neurons. The most significant disadvantage of this model is that it does not contain neuronal adaptation, so that it cannot describe an experimentally measured spike train in response to constant input current. This disadvantage is removed in generalized integrate-and-fire models that also contain one or several adaptation-variables and are able to predict spike times of cortical neurons under current injection to a high degree of accuracy. Adaptive integrate-and-fire Neuronal adaptation refers to the fact that even in the presence of a constant current injection into the soma, the intervals between output spikes increase. An adaptive integrate-and-fire neuron model combines the leaky integration of voltage with one or several adaptation variables (see Chapter 6.1. in the textbook Neuronal Dynamics) : \tau_\mathrm{m} \frac{d V_\mathrm{m} (t)}{d t} = R I(t)- [V_\mathrm{m} (t) - E_\mathrm{m} ]- R \sum_k w_k : \tau_k \frac{d w_k (t)}{d t} = - a_k [V_\mathrm{m} (t) - E_\mathrm{m} ]- w_k + b_k \tau_k \sum_f \delta (t-t^f) where \tau_m is the membrane time constant, is the adaptation current number, with index k, \tau_k is the time constant of adaptation current , is the resting potential and is the firing time of the neuron and the Greek delta denotes the Dirac delta function. Whenever the voltage reaches the firing threshold the voltage is reset to a value below the firing threshold. The reset value is one of the important parameters of the model. The simplest model of adaptation has only a single adaptation variable and the sum over k is removed. File:Spike Time Prediction with Generalized Integrate-and-Fire model.jpg|thumb|Spike times and subthreshold voltage of cortical neuron models can be predicted by generalized integrate-and-fire models such as the adaptive integrate-and-fire model, the adaptive exponential integrate-and-fire model, or the spike response model. In the example here, adaptation is implemented by a dynamic threshold which increases after each spike. Moreover, adaptive integrate-and-fire neurons with several adaptation variables are able to predict spike times of cortical neurons under time-dependent current injection into the soma. An advantage of this model is that it can capture adaptation effects with a single variable. The model has the following form spike generation is exponential, following the equation: : \frac{dV}{dt} - \frac{R} {\tau_m} I(t)= \frac{1} {\tau_m} \left[ E_m-V+\Delta_T \exp \left( \frac{V - V_T} {\Delta_T} \right) \right]. where V is the membrane potential, V_T is the intrinsic membrane potential threshold, \tau_m is the membrane time constant, E_m is the resting potential, and \Delta_T is the sharpness of action potential initiation, usually around 1 mV for cortical pyramidal neurons. In numerical simulation the integration is stopped if the membrane potential hits an arbitrary threshold (much larger than V_T) at which the membrane potential is reset to a value . The voltage reset value is one of the important parameters of the model. Importantly, the right-hand side of the above equation contains a nonlinearity that can be directly extracted from experimental data. the above exponential nonlinearity of the voltage equation is combined with an adaptation variable w : \tau_m \frac{dV}{dt} = R I(t) + \left[ E_m-V+\Delta_T \exp \left( \frac{V - V_T} {\Delta_T} \right) \right] - R w : \tau \frac{d w (t)}{d t} = - a [V_\mathrm{m} (t) - E_\mathrm{m} ]- w + b \tau \delta (t-t^f) , v_{th}, gradually returns to its steady state value depending on the threshold adaptation time constant \tau_{\theta}. This is one of the simpler techniques to achieve spike frequency adaptation. The expression for the adaptive threshold is given by: v_{th}(t) = v_{th0} + \frac{\sum \theta(t - t_f)}{f} = v_{th0} + \frac{\sum \theta_0 \exp\left[-\frac{(t - t_f)}{\tau_{\theta}}\right]}{f} where \theta(t) is defined by: \theta(t) = \theta_0 \exp\left[-\frac{t}{\tau_{\theta}}\right] When the membrane potential, u(t), reaches a threshold, it is reset to v_{rest}: u(t) \geq v_{th}(t) \Rightarrow v(t) = v_{\text{rest}} A simpler version of this with a single time constant in threshold decay with an LIF neuron is realized in to achieve LSTM like recurrent spiking neural networks to achieve accuracy nearer to ANNs on few spatio temporal tasks. Double Exponential Adaptive Threshold (DEXAT) The DEXAT neuron model is a flavor of adaptive neuron model in which the threshold voltage decays with a double exponential having two time constants. Double exponential decay is governed by a fast initial decay and then a slower decay over a longer period of time. This neuron used in SNNs through surrogate gradient creates an adaptive learning rate yielding higher accuracy and faster convergence, and flexible long short-term memory compared to existing counterparts in the literature. The membrane potential dynamics are described through equations and the threshold adaptation rule is: v_{th}(t) = b_{0} + \beta_{1}b_{1}(t) + \beta_{2}b_{2}(t) The dynamics of b_{1}(t) and b_2(t) are given by b_{1}(t + \delta t) = p_{j1}b_{1}(t) + (1 - p_{j1})z(t)\delta(t), b_{2}(t + \delta t) = p_{j2}b_{2}(t) + (1 - p_{j2})z(t)\delta(t), where p_{j1} = \exp\left[-\frac{\delta t}{\tau_{b1}}\right] and p_{j2} = \exp\left[-\frac{\delta t}{\tau_{b2}}\right]. Further, multi-time scale adaptive threshold neuron model showing more complex dynamics is shown in. == Stochastic models of membrane voltage and spike timing ==
Stochastic models of membrane voltage and spike timing
The models in this category are generalized integrate-and-fire models that include a certain level of stochasticity. Cortical neurons in experiments are found to respond reliably to time-dependent input, albeit with a small degree of variations between one trial and the next if the same stimulus is repeated. Stochasticity in neurons has two important sources. First, even in a very controlled experiment where input current is injected directly into the soma, ion channels open and close stochastically and this channel noise leads to a small amount of variability in the exact value of the membrane potential and the exact timing of output spikes. Second, for a neuron embedded in a cortical network, it is hard to control the exact input because most inputs come from unobserved neurons somewhere else in the brain. or (ii) the process of spike generation is noisy. In both cases, the mathematical theory can be developed for continuous time, which is then, if desired for the use in computer simulations, transformed into a discrete-time model. The relation of noise in neuron models to the variability of spike trains and neural codes is discussed in Neural Coding and in Chapter 7 of the textbook Neuronal Dynamics. Stein's neuron model and variants thereof have been used to fit interspike interval distributions of spike trains from real neurons under constant input current. This is important because the frequency-current relation (f-I-curve) is often used by experimentalists to characterize a neuron. The leaky integrate-and-fire with noisy input has been widely used in the analysis of networks of spiking neurons. Noisy input is also called 'diffusive noise' because it leads to a diffusion of the subthreshold membrane potential around the noise-free trajectory (Johannesma, The theory of spiking neurons with noisy input is reviewed in Chapter 8.2 of the textbook Neuronal Dynamics. First, input current I is filtered by a first filter k. Second the sequence of output spikes S(t) is filtered by a second filter η and fed back. The resulting membrane V(t) potential is used to generate output spikes by a stochastic process ρ(t) with an intensity that depends on the distance between membrane potential and threshold. The spike response model (SRM) is closely related to the Generalized Linear Model (GLM). The function F is often taken as a standard sigmoidal F(x) = 0.5[1 + \tanh(\gamma x)] with steepness parameter \gamma, The membrane voltage at time t is V(t)= \sum_f \eta(t-t^f) + \int\limits_0^\infty \kappa(s) I(t-s)\,ds + V_\mathrm{rest} where is the firing time of spike number f of the neuron, is the resting voltage in the absence of input, is the input current at time t-s and \kappa(s) is a linear filter (also called kernel) that describes the contribution of an input current pulse at time t-s to the voltage at time t. The contributions to the voltage caused by a spike at time t^f are described by the refractory kernel \eta(t-t^f). In particular, \eta(t-t^f) describes the reset after the spike and the time course of the spike-afterpotential following a spike. It therefore expresses the consequences of refractoriness and adaptation. The estimation of parameters of probabilistic neuron models such as the SRM using methods developed for Generalized Linear Models is discussed in Chapter 10 of the textbook Neuronal Dynamics. is a stochastic neuron model related to time-dependent nonlinear renewal theory and a simplification of the Spike Response Model (SRM). The main difference to the voltage equation of the SRM introduced above is that in the term containing the refractory kernel \eta(s) there is no summation sign over past spikes: only the most recent spike (denoted as the time \hat{t}) matters. Another difference is that the threshold is constant. The model SRM0 can be formulated in discrete or continuous time. For example, in continuous time, the single-neuron equation is : V(t)= \eta(t-\hat{t}) + \int_0^\infty \kappa(s) I(t-s) \, ds + V_\mathrm{rest} and the network equations of the SRM0 are : V_i(t\mid\hat{t}_i) = \eta_i(t-\hat{t}_i) + \sum_j w_{ij} \sum_f \varepsilon_{ij}(t-\hat{t}_i,t-t^f) + V_\mathrm{rest} where \hat{t}_i is the last firing time neuron i. Note that the time course of the postsynaptic potential \varepsilon_{ij} is also allowed to depend on the time since the last spike of neuron i to describe a change in membrane conductance during refractoriness. The instantaneous firing rate (stochastic intensity) is : f(V-\vartheta) = \frac{1}{\tau_0} \exp[\beta(V-V_{th})] where V_{th} is a fixed firing threshold. Thus spike firing of neuron i depends only on its input and the time since neuron i has fired its last spike. With the SRM0, the interspike-interval distribution for constant input can be mathematically linked to the shape of the refractory kernel \eta . Moreover the stationary frequency-current relation can be calculated from the escape rate in combination with the refractory kernel \eta. With an appropriate choice of the kernels, the SRM0 approximates the dynamics of the Hodgkin-Huxley model to a high degree of accuracy. Moreover, the PSTH response to arbitrary time-dependent input can be predicted. == Didactic toy models of membrane voltage ==
Didactic toy models of membrane voltage
The models in this category are highly simplified toy models that qualitatively describe the membrane voltage as a function of input. They are mainly used for didactic reasons in teaching but are not considered valid neuron models for large-scale simulations or data fitting. FitzHugh–Nagumo Sweeping simplifications to Hodgkin–Huxley were introduced by FitzHugh and Nagumo in 1961 and 1962. Seeking to describe "regenerative self-excitation" by a nonlinear positive-feedback membrane voltage and recovery by a linear negative-feedback gate voltage, they developed the model described by :\begin{align}{rcl} \dfrac{d V}{d t} &= V-V^3/3 - w + I_\mathrm{ext} \\ \tau \dfrac{d w}{d t} &= V-a-b w \end{align} where we again have a membrane-like voltage and input current with a slower general gate voltage and experimentally-determined parameters . Although not derivable from biology, the model allows for a simplified, immediately available dynamic, without being a trivial simplification. The experimental support is weak, but the model is useful as a didactic tool to introduce dynamics of spike generation through phase plane analysis. See Chapter 7 in the textbook Methods of Neuronal Modeling. Morris–Lecar In 1981, Morris and Lecar combined the Hodgkin–Huxley and FitzHugh–Nagumo models into a voltage-gated calcium channel model with a delayed-rectifier potassium channel represented by :\begin{align} C\frac{d V}{d t} &= -I_\mathrm{ion}(V,w) + I \\ \frac{d w}{d t} &= \varphi \cdot \frac{w_\infty - w}{\tau_{w}} \end{align} where I_\mathrm{ion}(V,w) = \bar{g}_\mathrm{Ca} m_\infty \cdot(V-V_\mathrm{Ca}) + \bar{g}_\mathrm{K} w\cdot(V-V_\mathrm{K}) + \bar{g}_\mathrm{L}\cdot(V-V_\mathrm{L}). in the textbook Methods of Neuronal Modeling. a model of neuronal activity described by three coupled first-order differential equations: :\begin{align} \frac{d x}{d t} &= y+3x^2-x^3-z+I \\ \frac{d y}{d t} &= 1-5x^2-y \\ \frac{d z}{d t} &= r\cdot (4(x + \tfrac{8}{5})-z) \end{align} with , and so that the variable only changes very slowly. This extra mathematical complexity allows a great variety of dynamic behaviors for the membrane potential, described by the variable of the model, which includes chaotic dynamics. This makes the Hindmarsh–Rose neuron model very useful, because it is still simple, allows a good qualitative description of the many different firing patterns of the action potential, in particular bursting, observed in experiments. Nevertheless, it remains a toy model and has not been fitted to experimental data. It is widely used as a reference model for bursting dynamics. The standard formulation of the theta model is : \frac{d\theta(t)}{d t} = (I-I_0) [1+ \cos(\theta)] + [1- \cos(\theta)] The equation for the quadratic integrate-and-fire model is (see Chapter 5.3 in the textbook Neuronal Dynamics ) : \tau_\mathrm{m} \frac{d V_\mathrm{m} (t)}{d t} = (I-I_0) R + [V_\mathrm{m} (t) - E_\mathrm{m} ][V_\mathrm{m} (t) - V_\mathrm{T} ] The equivalence of theta model and quadratic integrate-and-fire is for example reviewed in Chapter 4.1.2.2 of spiking neuron models. For input I(t) that changes over time or is far away from the bifurcation point, it is preferable to work with the exponential integrate-and-fire model (if one wants to stay in the class of one-dimensional neuron models), because real neurons exhibit the nonlinearity of the exponential integrate-and-fire model. == Sensory input-stimulus encoding neuron models ==
{{anchor|NaturalModels}} Sensory input-stimulus encoding neuron models
The models in this category were derived following experiments involving natural stimulation such as light, sound, touch, or odor. In these experiments, the spike pattern resulting from each stimulus presentation varies from trial to trial, but the averaged response from several trials often converges to a clear pattern. Consequently, the models in this category generate a probabilistic relationship between the input stimulus to spike occurrences. Importantly, the recorded neurons are often located several processing steps after the sensory neurons, so that these models summarize the effects of the sequence of processing steps in a compact form The non-homogeneous Poisson process model (Siebert) Siebert modeled the neuron spike firing pattern using a non-homogeneous Poisson process model, following experiments involving the auditory system. studied neuronal refractoriness using a stochastic model that predicts spikes as a product of two terms, a function f(s(t)) that depends on the time-dependent stimulus s(t) and one a recovery function w(t-\hat{t}) that depends on the time since the last spike : \rho(t) = f(s(t))w(t-\hat{t}) The model is also called an inhomogeneous Markov interval (IMI) process. Similar models have been used for many years in auditory neuroscience. Since the model keeps memory of the last spike time it is non-Poisson and falls in the class of time-dependent renewal models. In the case that output spikes feed back, via a linear filtering process, we arrive at a model that is known in the neurosciences as Generalized Linear Model (GLM). produces the probability of the neuron firing a spike as a function of either an external or pharmacological stimulus. • y(t) is the input of the model and is interpreted as the neurotransmitter concentration on the cell surrounding (in most cases glutamate). For an external stimulus it can be estimated through the receptor layer model: : y(t) \simeq g_\text{gain} \cdot \langle s^2(t)\rangle, with \langle s^2(t)\rangle being a short temporal average of stimulus power (given in Watt or other energy per time unit). • R0 corresponds to the intrinsic spontaneous firing rate of the neuron. • R1 is the recovery rate of the neuron from the refractory state. Other predictions by this model include: 1) The averaged evoked response potential (ERP) due to the population of many neurons in unfiltered measurements resembles the firing rate. 2) The voltage variance of activity due to multiple neuron activity resembles the firing rate (also known as Multi-Unit-Activity power or MUA). 3) The inter-spike-interval probability distribution takes the form a gamma-distribution like function. == Pharmacological input stimulus neuron models ==
{{anchor|PharmacologicalModels}} Pharmacological input stimulus neuron models
The models in this category produce predictions for experiments involving pharmacological stimulation. Synaptic transmission (Koch & Segev) According to the model by Koch and Segev, conductance (around 1S) and is the equilibrium potential of the given ion or transmitter (AMDA, NMDA, Cl, or K), while describes the fraction of open receptors. For NMDA, there is a significant effect of magnesium block that depends sigmoidally on the concentration of intracellular magnesium by . For GABAB, is the concentration of the G-protein, and describes the dissociation of G in binding to the potassium gates. The dynamics of this more complicated model have been well-studied experimentally and produce important results in terms of very quick synaptic potentiation and depression, that is fast, short-term learning. The stochastic model by Nossenson and Messer translates neurotransmitter concentration at the input stage to the probability of releasing neurotransmitter at the output stage. For a more detailed description of this model, see the Two state Markov model section above. == HTM neuron model ==
HTM neuron model
The HTM neuron model was developed by Jeff Hawkins and researchers at Numenta and is based on a theory called Hierarchical Temporal Memory, originally described in the book On Intelligence. It is based on neuroscience and the physiology and interaction of pyramidal neurons in the neocortex of the human brain. (A), the biological neuron (B), and the HTM neuron (C) == Applications ==
Applications
Spiking Neuron Models are used in a variety of applications that need encoding into or decoding from neuronal spike trains in the context of neuroprosthesis and brain-computer interfaces such as retinal prosthesis: or artificial limb control and sensation. Applications are not part of this article; for more information on this topic please refer to the main article. == Relation between artificial and biological neuron models ==
Relation between artificial and biological neuron models
The most basic model of a neuron consists of an input with some synaptic weight vector and an activation function or transfer function inside the neuron determining output. This is the basic structure used for artificial neurons, which in a neural network often looks like : y_i = \varphi\left( \sum_j w_{ij} x_j \right) where is the output of the th neuron, is the th input neuron signal, is the synaptic weight (or strength of connection) between the neurons and , and is the activation function. While this model has seen success in machine-learning applications, it is a poor model for real (biological) neurons, because it lacks time-dependence in input and output. When an input is switched on at a time t and kept constant thereafter, biological neurons emit a spike train. Importantly, this spike train is not regular but exhibits a temporal structure characterized by adaptation, bursting, or initial bursting followed by regular spiking. Generalized integrate-and-fire models such as the Adaptive Exponential Integrate-and-Fire model, the spike response model, or the (linear) adaptive integrate-and-fire model can capture these neuronal firing patterns. Moreover, neuronal input in the brain is time-dependent. Time-dependent input is transformed by complex linear and nonlinear filters into a spike train in the output. Again, the spike response model or the adaptive integrate-and-fire model enables to prediction of the spike train in the output for arbitrary time-dependent input, whereas an artificial neuron or a simple leaky integrate-and-fire does not. If we take the Hodkgin-Huxley model as a starting point, generalized integrate-and-fire models can be derived systematically in a step-by-step simplification procedure. This has been shown explicitly for the exponential integrate-and-fire model and the spike response model. In the case of modeling a biological neuron, physical analogs are used in place of abstractions such as "weight" and "transfer function". A neuron is filled and surrounded with water-containing ions, which carry electric charge. The neuron is bound by an insulating cell membrane and can maintain a concentration of charged ions on either side that determines a capacitance . The firing of a neuron involves the movement of ions into the cell, that occurs when neurotransmitters cause ion channels on the cell membrane to open. We describe this by a physical time-dependent current . With this comes a change in voltage, or the electrical potential energy difference between the cell and its surroundings, which is observed to sometimes result in a voltage spike called an action potential which travels the length of the cell and triggers the release of further neurotransmitters. The voltage, then, is the quantity of interest and is given by . If the input current is constant, most neurons emit after some time of adaptation or initial bursting a regular spike train. The frequency of regular firing in response to a constant current is described by the frequency-current relation, which corresponds to the transfer function \varphi of artificial neural networks. Similarly, for all spiking neuron models, the transfer function \varphi can be calculated numerically (or analytically). == Cable theory and compartmental models ==
Cable theory and compartmental models
All of the above deterministic models are point-neuron models because they do not consider the spatial structure of a neuron. However, the dendrite contributes to transforming input into output. For static inputs, it is sometimes possible to reduce the number of compartments (increase the computational speed) and yet retain the salient electrical characteristics. ==Conjectures regarding the role of the neuron in the wider context of the brain principle of operation ==
Conjectures regarding the role of the neuron in the wider context of the brain principle of operation
The neurotransmitter-based energy detection scheme The neurotransmitter-based energy detection scheme suggests that the neural tissue chemically executes a Radar-like detection procedure. As shown in Fig. 6, the key idea of the conjecture is to account for neurotransmitter concentration, neurotransmitter generation, and neurotransmitter removal rates as the important quantities in executing the detection task, while referring to the measured electrical potentials as a side effect that only in certain conditions coincide with the functional purpose of each step. The detection scheme is similar to a radar-like "energy detection" because it includes signal squaring, temporal summation, and a threshold switch mechanism, just like the energy detector, but it also includes a unit that emphasizes stimulus edges and a variable memory length (variable memory). According to this conjecture, the physiological equivalent of the energy test statistics is neurotransmitter concentration, and the firing rate corresponds to neurotransmitter current. The advantage of this interpretation is that it leads to a unit-consistent explanation which allows for bridge between electrophysiological measurements, biochemical measurements, and psychophysical results. The evidence reviewed in suggests the following association between functionality to histological classification: • Stimulus squaring is likely to be performed by receptor cells. • Stimulus edge emphasizing and signal transduction is performed by neurons. • Temporal accumulation of neurotransmitters is performed by glial cells. Short-term neurotransmitter accumulation is likely to occur also in some types of neurons. • Logical switching is executed by glial cells, and it results from exceeding a threshold level of neurotransmitter concentration. This threshold crossing is also accompanied by a change in neurotransmitter leak rate. • Physical all-or-non movement switching is due to muscle cells and results from exceeding a certain neurotransmitter concentration threshold on muscle surroundings. Note that although the electrophysiological signals in Fig.6 are often similar to the functional signal (signal power/neurotransmitter concentration / muscle force), there are some stages in which the electrical observation differs from the functional purpose of the corresponding step. In particular, Nossenson et al. suggested that glia threshold crossing has a completely different functional operation compared to the radiated electrophysiological signal and that the latter might only be a side effect of glia break. ==General comments regarding the modern perspective of scientific and engineering models==
General comments regarding the modern perspective of scientific and engineering models
• The models above are still idealizations. Corrections must be made for the increased membrane surface area given by numerous dendritic spines, temperatures significantly hotter than room-temperature experimental data, and nonuniformity in the cell's internal structure. == External links ==
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