ABSTRACT
Channelopathies, neuromuscular junction disorders, and myopathies represent multiple mechanisms by which toxins can affect the peripheral nervous system. These toxins include ciguatoxin, tetrodotoxin, botulinum toxin, metabolic poisons, venomous snake bites, and several medications. These toxins are important to be aware of because they can lead to serious symptoms, disability, or even death, and many can be treated if recognized ear.
Subject(s)
Channelopathies/chemically induced , Muscular Diseases/chemically induced , Neuromuscular Junction Diseases/chemically induced , Neurotoxicity Syndromes/etiology , Toxins, Biological/adverse effects , HumansSubject(s)
Channelopathies/mortality , Death, Sudden, Cardiac/etiology , Channelopathies/chemically induced , Channelopathies/diagnosis , Channelopathies/genetics , Clinical Decision Rules , Europe/epidemiology , Genetic Markers , Genetic Predisposition to Disease , Humans , Prognosis , Risk Assessment , Risk FactorsSubject(s)
Carpal Tunnel Syndrome/diagnostic imaging , Channelopathies/diagnostic imaging , Median Nerve/diagnostic imaging , Antineoplastic Agents/adverse effects , Carpal Tunnel Syndrome/chemically induced , Channelopathies/chemically induced , Electromyography , Humans , Lymphoma, Non-Hodgkin/drug therapy , Male , Middle AgedSubject(s)
Autoimmune Diseases/chemically induced , Isaacs Syndrome/chemically induced , Papillomavirus Vaccines/adverse effects , Adult , Channelopathies/chemically induced , Humans , Immunization, Secondary/adverse effects , Immunosuppressive Agents/therapeutic use , Magnetic Resonance Imaging , Male , Muscle Weakness/chemically induced , Potassium Channels/immunology , Potassium Channels/physiology , Thymus Hyperplasia/chemically induced , Thymus Hyperplasia/pathology , Tomography, X-Ray ComputedABSTRACT
The "Hot Topic Keynotes: Channelopathies" session of the 26th International Neurotoxicology Conference brought together toxicologists studying interactions of environmental toxicants with ion channels, to review the state of the science of channelopathies and to discuss the potential for interactions between environmental exposures and channelopathies. This session presented an overview of chemicals altering ion channel function and background about different channelopathy models. It then explored the available evidence that individuals with channelopathies may or may not be more sensitive to effects of chemicals.
Subject(s)
Channelopathies/chemically induced , Channelopathies/metabolism , Environmental Exposure/adverse effects , Animals , Congresses as Topic/trends , Drug-Related Side Effects and Adverse Reactions/chemically induced , Drug-Related Side Effects and Adverse Reactions/metabolism , Humans , Ion Channel Gating/physiologyABSTRACT
Organ toxicity caused by poisons or drug therapy is diverse and may not be commonly encountered clinically. In general, commonly encountered conditions caused by drug/toxin pharmacology can be classified into 7 categories by shared mechanisms of organ injury. This review of drug/toxin-induced injury discusses drug or toxin-induced pathology that the clinician may encounter and therapeutic approaches to these syndromes.
Subject(s)
Anesthesia , Poisoning/therapy , Acidosis/chemically induced , Acidosis/complications , Acidosis/therapy , Adult , Aged , Arrhythmias, Cardiac/chemically induced , Arrhythmias, Cardiac/complications , Bites and Stings/complications , Bites and Stings/therapy , Carbon Monoxide Poisoning/complications , Carbon Monoxide Poisoning/therapy , Channelopathies/chemically induced , Channelopathies/therapy , Child , Child, Preschool , Drug-Related Side Effects and Adverse Reactions , Electrocardiography , Female , Humans , Hypothermia/chemically induced , Hypothermia/therapy , Long QT Syndrome/chemically induced , Long QT Syndrome/therapy , Male , Methemoglobinemia/chemically induced , Methemoglobinemia/complications , Methemoglobinemia/therapy , Middle Aged , Substance-Related Disorders/complications , TerrorismABSTRACT
Ion channelopathy plays an important role in human epilepsy with a genetic cause and has been hypothesized to occur in epilepsy after acquired insults to the CNS as well. Acquired alterations of ion channel function occur after induction of status epilepticus (SE) in animal models of epilepsy, but it is unclear how they correlate with the onset of spontaneous seizures. We examined the properties of hyperpolarization-activated cation (HCN) channels in CA1 hippocampal pyramidal neurons in conjunction with video-EEG (VEEG) recordings to monitor the development of spontaneous seizures in the rat pilocarpine model of epilepsy. Our results showed that dendritic HCN channels were significantly downregulated at an acute time point 1 week postpilocarpine, with loss of channel expression and hyperpolarization of voltage-dependent activation. This downregulation progressively increased when epilepsy was established in the chronic period. Surprisingly, VEEG recordings during the acute period showed that a substantial fraction of animals were already experiencing recurrent seizures. Suppression of these seizures with phenobarbital reversed the change in the voltage dependence of I(h), the current produced by HCN channels, but did not affect the loss of HCN channel expression. These results suggest two mechanisms of HCN channel downregulation after SE, one dependent on and one independent of recurrent seizures. This early and progressive downregulation of dendritic HCN channel function increases neuronal excitability and may be associated with both the process of epileptogenesis and maintenance of the epileptic state.