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Neurological issues
Published in Andrea Utley, Motor Control, Learning and Development, 2018
Action potentials are the means by which the brain receives, analyzes and conveys information, which is determined by the pathway the signal travels to the brain. The transmission of the action potential is speeded up by a lipid membrane surrounding the axon called the myelin sheath (or principally Schwann cells in the PNS). The axon eventually divides into branches, at the end of which are presynaptic terminals; these allow communication with other neurons through the transmission of the electrical impulses. The passage of information from one neuron to another occurs via synapses, where the axon of one neuron comes into close proximity to, but does not touch or communicate anatomically with, another (postsynaptic) nerve cell. The space that separates two neurons is called the synaptic cleft. The electrical activity in the presynaptic neuron is transmitted across the synaptic cleft to the postsynaptic neuron through further electrical activity or a chemical mediator – a neurotransmitter.
Synopsis of the Nervous System
Published in Walter J. Hendelman, Peter Humphreys, Christopher R. Skinner, The Integrated Nervous System, 2017
Walter J. Hendelman, Peter Humphreys, Christopher R. Skinner
Receptors on the postsynaptic neuron are activated by the neurotransmitter, causing a shift of ions and a net change in the membrane potential of the postsynaptic neuron, leading to either depolarization or hyperpolarization of the membrane. This contributes to an increase in the likelihood of the neuron either to discharge more frequently (depolarization, excitatory) or to discharge less often (hyperpolarization, inhibitory).
The Relaxation System Theoretical Construct
Published in Len Wisneski, The Scientific Basis of Integrative Health, 2017
We now present further compelling medical evidence for the theta healing system. Recall from the prior benzodiazepine discussion that the benzodiazepines increase GABA's ability to inhibit neurotransmission at the postsynaptic binding site by causing the chloride channel to open, thus allowing chloride to enter the second neuron. This effect is typical of the way in which neurons pass on or inhibit a message. However, unlike the benzodiazepines, the cannabinoids work at the site of the presynaptic neurons and their actions involve calcium channels. For over a decade, it has been known that calcium can induce a retrograde inhibition at presynaptic terminals (Llano et al., 1991). The less-conventional retrograde signaling involves a message being returned to the neuron that sent it (i.e., the presynaptic neuron), and the message is: “Stop producing neurotransmitter.” Consequently, the presynaptic cell causes an inhibition of the neurotransmitter at the postsynaptic neuron (Vincent and Marty, 1993). It eventually became clear that a receptor on the presynaptic cell, most likely a cannabinoid receptor, is central to the calcium channel-induced inhibition of the neurotransmitter (Sullivan, 1999; Twitchell et al., 1997). Most interestingly, these experiments were performed on the hippocampus, which is not only central to learning and memory, but is also a critical link to the limbic system, our central processing station for emotion.
Treatment of tardive dyskinesia: a review and update for dermatologists managing delusions of parasitosis
Published in Journal of Dermatological Treatment, 2022
Christian Cheng, Nicholas Brownstone, John Koo
There have been several proposed etiologies regarding the pathogenesis of TD. The most accepted explanation involves the concept of ‘dopamine receptor hypersensitivity state’ (2) (Figure 1, from the reference Citrome 2018). Antipsychotic medications decrease delusions and hallucinations by blocking dopamine receptors and thereby decreasing dopamine-mediated neurotransmission in the brain. Excessive dopamine-mediated neurotransmission appears to cause psychosis, which is manifested by delusions and hallucinations. However, after a prolonged blockage of dopamine receptors by antipsychotic agents, some patients develop hypersensitivity by increasing the number and/or the sensitivity of dopamine receptors in the postsynaptic neuron. This acquired hypersensitivity to dopamine, especially in the motor cortex such as the striatum, is hypothesized as to why TD causes involuntary movements. In addition, there are several other less well substantiated proposed pathogenic pathways of TD including the possibility of oxidative damage to the nerves and the direct neurotoxic effect of antipsychotic agents (3,4).
Immune to addiction: how immunotherapies can be used to combat methamphetamine addiction
Published in Expert Review of Vaccines, 2021
Md Kamal Hossain, Majid Hassanzadeganroudsari, Erica Kypreos, Jack Feehan, Vasso Apostolopoulos
In the setting of the natural reward mechanism, dopamine is secreted from presynaptic neuron into the synaptic cleft (Figure 2). The released dopamine stays in the synaptic cleft for a short duration and transmits a signal by propagating an action potential to the postsynaptic neuron. The dopamine is then returned to the presynaptic neuron by a specific dopamine transporter. With application of METH, dopamine remains in the synaptic cleft for 8 to 12 hours, causing ongoing stimulation of the postsynaptic neuron, and extended feelings of euphoria. The critical action of METH on this mechanism is to block the action of the dopamine transporter, leading to the inability to remove the neurotransmitter and subsequent increased concentration in the synaptic cleft. With this large amount of dopamine, and its sustained action on the reward center, the individual experiences an extreme peak of euphoria, leading to addiction [20,24].
Emerging Drugs for the Treatment of Amyotrophic Lateral Sclerosis: A Focus on Recent Phase 2 Trials
Published in Expert Opinion on Emerging Drugs, 2020
Andrea Barp, Francesca Gerardi, Andrea Lizio, Valeria Ada Sansone, Christian Lunetta
Several evidences underline that altered excitatory neurotransmission has a key role in disease progression, mediated by increased susceptibility to excitotoxicity [66]. Excitotoxicity results from deleterious cellular responses to excitatory stimulation leading ultimately to cell death [64], however exceeding the safe limits of excitatory stimulation can occur either by inappropriately high activity of the presynaptic neuron, by abnormal responsiveness of the postsynaptic neuron to excitatory stimuli (including changes to intrinsic excitability) or both factors combined. Currently the only approved treatment for ALS is Riluzole, which is thought to block persistent sodium currents, thus reducing neuronal excitability [67]. The evidence for altered glutamatergic signaling in ALS comes from electrophysiological studies demonstrating disturbances in upper and lower motor neurons [68,69], from neuropathological studies reporting altered glutamate levels in post mortem ALS tissue [70], and from clinical studies showing increased glutamate levels in the cerebrospinal fluid (CSF) from some ALS patients [71,72]. This may be caused directly, by increased extracellular glutamate, related to increased release [73] or reduced clearance [74], or indirectly by inappropriate response to sub-toxic glutamate, related to altered expression or function of glutamate receptors [75] or altered excitability [76].