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Pharmacology of Local Anesthetics
Published in Pamela E. Macintyre, Stephan A. Schug, Acute Pain Management, 2021
Pamela E. Macintyre, Stephan A. Schug
Local anesthetics block voltage-gated sodium channels in cell membranes (Becker & Reed, 2012). They prevent the influx of sodium ions into cells and thereby the generation of action potentials and the conduction of nerve impulses (see Figure 5.1). Local anesthetics may also modify a number of other neuronal membrane channels or even receptors, contributing to their effect (Lirk et al, 2018). Interaction with calcium, potassium, and hyperpolarization-gated ion channels and ligand-gated channels (for example NMDA receptors) have been identified. Therefore, local anesthetics interfere with neuronal function in multiple other ways, primarily by cell membrane effects. Last, but not least, effects on G-protein coupled receptors may explain some of the antiinflammatory effects of local anesthetics.
Marine Biotoxins: Symptoms and Monitoring Programs
Published in Hafiz Ansar Rasul Suleria, Megh R. Goyal, Health Benefits of Secondary Phytocompounds from Plant and Marine Sources, 2021
Huma Bader Ul Ain, Farhan Saeed, Hafiza Sidra Yaseen, Tabussam Tufail, Hafiz Ansar Rasul Suleria
The main source of neurotoxic shellfish poisoning or brevetoxin is Karenia brevis (a dinoflagellate). Its mechanism of action is at the site 5 of voltage-gated sodium channels. The toxicity appears from fifteen minutes to three hours after the use of neurotoxic shellfish. Neurotoxic shellfish poisoning can likewise be contracted by means of inhalation [17, 41, 62].
Low-Dose Naltrexone
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
Adaptive pain is a result of tissue damage either from trauma or surgery and is propagated through the processes of transduction, conduction, transmission, perception, and modulation. Transduction involves the release of cytokines and chemokines from nociceptors in the somatic and visceral structures activated by mechanical, thermal, or chemical stimuli. Conduction involves the generation of action potentials by the depolarization of voltage-gated sodium channels. Transmission through afferent nerve fibers causes the release of glutamate and substance P acting as excitatory neurotransmitters, ultimately propagating the pain signal to the thalamus, where the signal is relayed to higher cortical structures. Perception is the result of the pain signals that reach the higher cortical structures becoming a conscious experience. Modulation is the result of many different neurotransmitters and receptor interactions that either strengthen or attenuate the pain signal. Excitatory neurotransmitters involved in pain include glutamate and substance P. Inhibitory neurotransmitters involved in pain include enkephalins, β-endorphins, GABA, norepinephrine, and serotonin. Additionally, NMDA receptors seem to influence opioid receptor responsiveness to exogenous and endogenous opioids.
Association of sodium voltage-gated channel genes polymorphisms with epilepsy risk and prognosis in the Saudi population
Published in Annals of Medicine, 2022
Mansour A. Alghamdi, Laith N. AL-Eitan, Ashwag Asiri, Doaa M. Rababa’h, Sultan A. Alqahtani, Mohammed S. Aldarami, Manar A. Alsaeedi, Raghad S. Almuidh, Abdulbari A. Alzahrani, Ahmad H. Sakah, Eman Mohamad El Nashar, Mansour Y. Otaif, Nawal F. Abdel Ghaffar
Epilepsy is a complex neurological condition that impacts the brain and cause seizure [24]. Genetic predisposition to epilepsy has been a fundamental part of the disorder aetiology [25]. Voltage-gated sodium channels are critical for genetics epilepsy, and these channels play a key role in mediating the electrical excitability. Thus, it is lucid that any genetic mutations in these gene coding channels can interfere the epilepsy development or progression. When the channels are activated by membrane depolarization, it will cause conformational change that increases the sodium ion influx in addition to cell depolarization and later the channels will be deactivated ending in resting of membrane potential [11]. This study investigated several genetic variants of SCN genes (SCN1A, SCN2A, SCN3A, SCN1B, SCN2B, SCN3B and SCN8A) and their association with epilepsy risk; these genes have been studied in this regard and conflicted results were reported [7]. rs3812718 is a common intronic variant that located in splice donor site, and it modifies alternative splicing of exon 5. We suggest that TT genotype of rs3812718 in SCN1A may be a protective factor against epilepsy and may decrease the risk of the disease in Saudi population. In contrast to our finding, rs3812718 was reported as a risk factor for GEFS + in Chinese population [26,27]. In one meta-analysis they revealed that the rs3812718 TT genotype was involved in high risk of developing drug resistance in epilepsy children [28].
Emerging drugs for the treatment of postsurgical pain
Published in Expert Opinion on Emerging Drugs, 2021
Esra Kutlu Yalcin, Jorge Araujo-Duran, Alparslan Turan
Also, there are nine voltage-gated sodium channel (VGSC) subtypes (Nav) characterized by their biophysical properties, tissue localization, and function. Nav1.3, Nav1.7, Nav1.8, and Nav1.9 have been associated with nociceptive transmission. They also have roles in the hyperexcitability characteristics of inflammatory and neuropathic pain [41]. Nav 1.7 has become an important drug target after preclinical and human genetic studies, as it was shown to have an essential role in pain transduction and conduction. A previous study has found that loss of function type mutations in the SCN9A gene encoding human Nav1.7 were associated with congenital insensitivity to pain whereas, the gain of function mutations in SCN9A were associated with extreme pain disorders [41]. These findings led to the fact that Nav 1.7 might be a good target with high selectivity for postoperative pain management.
Advances in the design and discovery of novel small molecule drugs for the treatment of Dravet Syndrome
Published in Expert Opinion on Drug Discovery, 2021
Barbara Miziak, Stanisław Czuczwar
DS represents very severe symptoms of refractory epilepsy due to serious therapeutic challenges. The disease generally starts in infancy in between 4 and 8 months in the form of prolonged generalized (sometimes unilateral) clonic seizures. High fever may be frequently a precipitating factor. Subsequent seizure activity follows the first attack within 2 weeks – 2 months and the disease enters the next phase (worsening stage) in 1–4 year old children characterized by different seizure types associated with impairment of consciousness and autonomic symptoms. Mental retardation and behavioral disorders tend to emerge from the 2nd year of life. After a slight improvement in seizure activity, the patients enter the third phase, so-called stabilization stage. In this stage, seizure activity is mainly manifested during sleep and cognitive impairment is still observed. Also, even severe intellectual impairment may persist in some patients. A genetic background concerns a variety of gene mutations, the dominant one is related to voltage-gated sodium-channel gene α 1 subunit. Noteworthy, DS is associated with a high risk of SUDEP.