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Theoretical Paradigms in Cognitive Science and in Theoretical Neurophilosophy
Published in Harald Maurer, Cognitive Science, 2021
This neuronal information processing is thus based on the functioning of biological neurons and synapses and the neurophysiological processes in the (neo-)cortex (Squire et al. 2008, Bear et al. 2016, Kandel et al. 2013). The model simulates the neurobiological information in the brain that the "membrane potential" of a biological neuron generates along its axon – an "action potential"138 – from the state of the "resting potential." This means that a neuron generates a neuroelectric impulse (the postsynaptic neuron "fires"). This requires that the temporal and spatial summation of the action potentials of the presynaptic neurons, which are transmitted along their presynaptic axons to the dendrites of the postsynaptic neurons via the neurochemical synapses, exceed a certain "threshold potential". On the basis of the synaptic intensity of neurotransmitter transmissions in the synapse gap, a weighting ("synaptic plasticity" (Bear et al. 2016, Rösler 2011)) of the incoming excitatory or inhibitory impulses ("synaptic integration" [Squire et al. 2008, Kandel et al. 2013]) takes place (see Fig. 3.3).
Miscellaneous
Published in Bobby Krishnachetty, Abdul Syed, Harriet Scott, Applied Anatomy for the FRCA, 2020
Bobby Krishnachetty, Abdul Syed, Harriet Scott
The electrical energy delivered by a nerve stimulator should be sufficient to cause increase in membrane potential so as to exceed the threshold potential leading to depolarisation and propagation of an action potential.
Cell Components and Function
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
In the resting state, the positively charged sensor is attracted by the negative charge on the inside of the membrane. Depolarization to the threshold potential swings the sensor towards the outside of the membrane, and the activation gate opens. After opening, the channel is inactivated before it can open again.
Efficient simulations of stretch growth axon based on improved HH model
Published in Neurological Research, 2023
Xiao Li, Xianxin Dong, Xikai Tu, Hailong Huang
When the axon reaches a length of 0.5 cm and a diameter of 2 µm, mechanical force can be used to activate the action potential. The action potential is formed at the force point and reaches the threshold potential after 3.5 ms, as illustrated in Figure 6. The action potential’s amplitude reaches a maximum in the fifth millisecond and then begins to fade. The action potential propagates from the center to both sides for 10 ms before dissipating. After prolonged stretch growth, the axon achieves a length of 1 cm and a diameter of around 2.6 µm. The action potential approaches the threshold potential after 2.4 ms, as illustrated in Figure 7. The amplitude of the action potential then reaches a maximum and then vanishes after 12 ms. When axon stretch growth reaches 1.8 cm, the diameter of the axon is approximately 5.71 µm. As illustrated in Figure 8, the time required for the axon to initiate excitation decreases. Within roughly 1.2 ms, the action potential exceeds the threshold potential. Excitation transmission to the sides accelerates, and action potential conduction terminates after 15.5 ms. When the axon reaches 2.5 cm in length, the diameter is approximately 12.56 µm. The action potential approaches the threshold potential within around 0.8 ms, as illustrated in Figure 9. The action potential waveform gets smaller, and the time interval between threshold and peak potential becomes shorter, around 1.5 ms. When the axon reaches 3.2 cm in length, the diameter is approximately 16.31 µm. As illustrated in Figure 10, the action potential reaches the threshold potential in around 0.6 ms and then vanishes after 16.8 ms. In general, the longer the axon stretch length, the greater the membrane capacitance, and the easier it is to induce an action potential.
Biological therapies targeting arrhythmias: are cells and genes the answer?
Published in Expert Opinion on Biological Therapy, 2018
Debbie Falconer, Nikolaos Papageorgiou, Emmanuel Androulakis, Yasmin Alfallouji, Wei Yao Lim, Rui Providencia, Dimitris Tousoulis
Triggered activity and re-entry are the major arrhythmogenic mechanisms in AF. Triggered activity refers to impulse initiation caused by afterdepolarizations. Afterdepolarizations are depolarizations triggered by one or more preceding action potentials and can be early, or delayed. Not all afterdepolarizations reach threshold potential, but if they do, they may trigger another afterdepolarization and, thus, self-perpetuate, leading to arrythmogenesis [9–14].
Preclinical insights into therapeutic targeting of KCC2 for disorders of neuronal hyperexcitability
Published in Expert Opinion on Therapeutic Targets, 2020
Phan Q. Duy, Miao He, Zhigang He, Kristopher T. Kahle
In settings of low KCC2 activity, intraneuronal Cl− concentrations are expected to increase due to diminished extrusion capacity, leading to a depolarizing response marked by Cl− efflux following GABAergic input. In other words, these changes can render GABA a paradoxically excitatory rather than an inhibitory neurotransmitter. Although membrane depolarization is usually thought to be excitatory (by bringing membrane potential toward threshold potential), depolarizing GABA can also exert inhibitory actions under specific circumstances due to other mechanisms such as shunting inhibition (see [29,36] for detailed explanation). KCC2 hypofunction has been observed in some physiological settings, such as those during early neural development when KCC2 activity is minimal in young neurons [37,38]. During early postnatal life, KCC2 upregulation in postnatal neurons reduces intracellular chloride concentrations, leading to a reversal of GABAergic responses from depolarization to hyperpolarization [39–41]. Depolarizing GABA in early neural development has been shown to regulate multiple aspects of brain morphogenesis and maturation, including neural stem cell proliferation, migration, and differentiation [42–45]. These functional effects of depolarizing GABA on neural development are thought to be mediated by activation of voltage-gated calcium channels, leading to recruitment of calcium-dependent second-messenger pathways [46,47]. Consequently, by influencing GABA polarity and the attendant signaling cascades, the spatiotemporal dynamics of KCC2 activity constitutes a mechanism that allows developing neuronal cells to execute the appropriate cellular program at the right time in response to developmental cues. The transition from low to high KCC2 activity across neuronal development is regulated at the posttranslational level by reciprocal phosphorylation and dephosphorylation events at critical amino acid residues [48,49] (Figure 2).