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Review of the Human Brain and EEG Signals
Published in Teodiano Freire Bastos-Filho, Introduction to Non-Invasive EEG-Based Brain–Computer Interfaces for Assistive Technologies, 2020
Alessandro Botti Benevides, Alan Silva da Paz Floriano, Mario Sarcinelli-Filho, Teodiano Freire Bastos-Filho
The EEG mainly records the extracellular currents that arise as a consequence of synaptic activity in dendrites of neurons in the cerebral cortex. The extracellular electric field is mainly generated by the postsynaptic potential (PSP) that may be excitatory postsynaptic potential (EPSP) or inhibitory postsynaptic potential (IPSP). When the AP (100 mV) reaches postsynaptic dendrites, it causes a current flow that enters through the synapse to the postsynaptic dendrites of the next neuron. This current is called extracellular activation current, which is of around 3 nA, and causes the rising potential within the postsynaptic membrane, that is, the EPSP. The current then enters the postsynaptic dendrites toward the soma24 and goes out into the extracellular fluid by the membrane capacitance of the cell, and then returns to the dendrites, making a circular path. This circular current is called excitatory postsynaptic current [4] (Figure 1.14).
The Physics of Neural Activity: A Statistical Mechanics Perspective
Published in Perambur S. Neelakanta, Dolores F. De Groff, Neural Network Modeling, 2018
Perambur S. Neelakanta, Dolores F. De Groff
Essentially, in the neuronal conduction process as discussed in the earlier chapters, a cellular neuron (in a large assembly of similar units) is activated by the flow of chemicals across synaptic junctions from the axon leading from other neurons; and the resulting output response can be viewed as either excitatory or inhibitory postsynaptic potential. If the gathered potentials from all the incoming synapses exceed a threshold value, the neuron fires and this excitatory process sets an action potential to propagate down one of the output axons (which eventually communicates with other neurons, via synaptic tributary branches). After firing, the neuron returns to its quiescent (resting) potential and is sustained in that condition over a refractory period (of about several milliseconds) before it can be excited again. The firing pattern of the neurons is governed by the topology of interconnected neurons and the collective behavior of the neuronal activity.
Neurophysiology of Joints
Published in Verna Wright, Eric L. Radin, Mechanics of Human Joints, 2020
Håkan Johansson, Per Sjölander
Electrical and physiological stimulation has been used to study the effects of joint receptor afferents on α-motoneurons (skeletomotoneurons). Both methods have their advantages. Electrical stimulation makes intracellular potentials easier to discover and allows measurement of latencies (i.e., calculation of the number of synapses in a refle arc). Physiological stimulation can be made more receptor specific and is easier to interpret in terms of naturally occurring events. In early studies with graded electrical stimulation of knee joint afferents, it was reported that α-motoneurons could be activated only by high-threshold afferents (i.e., afferents with stimulation thresholds above two times the nerve threshold), which evoked a flexion reflex pattern in the motoneurons (97,98). Later, Hongo et al. (99) found that excitatory as well as inhibitory potentials in α-motoneurons evoked via low-threshold joint afferents could be disclosed by facilitation via the rubrospinal pathway. More recently, Lundberg et al. (100) observed that even weak electrical stimulation of the posterior articular nerve (below twice the nerve threshold) could evoke postsynaptic potentials in the α-motoneurons (Fig. 6G-K). From these recordings it is clear that, although effects can be discerned at low electrical stimulation intensities, they do not seem to be very potent. However, when lb (Golgi tendon organ) afferent stimulation is used to facilitate inhibitory postsynaptic potential elicited from the posterior articular nerve, the effect can be considerable (Fig. 6A-F). Similarly, high-threshold joint afferents can influence skeletomotoneurons via the la interneurons (101).
Biological function simulation in neuromorphic devices: from synapse and neuron to behavior
Published in Science and Technology of Advanced Materials, 2023
Hui Chen, Huilin Li, Ting Ma, Shuangshuang Han, Qiuping Zhao
Electrical synapse is the gap junction, a special way of cell-to-cell linkage, which makes the action potential direct transmission between cells (Figure 1(c-i)). For this synapse, the synaptic cleft is very small, only several nanometers. In the presynaptic and postsynaptic membrane, there are some connexons that are made up of connexins. Two connexons form a gap junction channel, a non-gate control channel, which allows some small molecules of water-soluble substances and ions to pass through. When the action potential is generated in a neuron, the local current based on ionic current can be directly stimulated and transmitted to another neuron through the gap junction channel. By this way, the action potential is propagated from neuron to neuron. From this, the electrical synapse has lots of outstanding features, such as low resistive, rapid and bidirectional propagation. Different from electrical synapse, chemical synapse depends on the neurotransmitters to accomplish the information transfer from neuron to neuron (Figure 1(c-ii)). In chemical synapse, there are more mitochondria and a large number of vesicles, in which the latter is also called synaptic vesicle with 20–80 nm diameter and high contains concentrations of neurotransmitters such as acetylcholine or amino acid transmitters, catecholamine transmitters and neuropeptide transmitters. When the action potential is transmitted to the presynaptic terminal of a neuron, the presynaptic membrane depolarizes. After the depolarization exceeds the threshold value, Ca2+ channel is activated and Ca2+ enters into the axoplasm of the terminal from the outside of the cell. The increase of Ca2+ can trigger the efflux of synaptic vesicles and cause the quantized release of neurotransmitters. Meanwhile, excess Ca2+ in the axoplasm is transported outside through Na+-Ca2+ reverse transporter in order to its normal concentration in the presynaptic terminal. Once the neurotransmitters are released, they can enter into the synaptic cleft and reach the postsynaptic membrane by diffusion. Ultimately, these neurotransmitters can act on the ionotropic receptor and control the permeability of certain ions. When certain ions enter the postsynaptic terminal, if the terminal occurs depolarization, the signal is called excitatory postsynaptic potential (EPSP). In this process, the excitatory neurotransmitters act on the ionotropic receptors in the postsynaptic terminal to open the specific ion channels (Na+ and K+). The net inward current is generated because Na+ influx of is greater than K+ outflow, in turn, lead to the depolarization of the postsynaptic terminal. On the contrary, inhibitory neurotransmitters are released from the presynaptic terminal to act on the ionotropic receptors, and then open the Cl- channel to generate the outward current that hyperpolarizes the postsynaptic membrane. In this case, it is called inhibitory postsynaptic potential (IPSP). By this way, the information is transmitted to the next neuron by releasing neurotransmitters. The distinguishing between electrical and chemical synapses is listed in Table 1. However, the chemical synapse is the majority of synapses in the human brain.