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About Christoph Lossin, Ph.D.

Dysfunction of ion channels in the nervous system or in muscle can lead to debilitating disorders. The goal of my research is to examine these disorders at the molecular level in an effort to better understand the underlying pathophysiology and to provide new information for new and improved forms of treatment.
Currently, I am most interested in...
(1) Epilespy
(2) Myotonic disorders
(3) Erythermalgia
(1) EPILEPSY... is a major neurological disorder affecting approximately 2.7 million US citizens. Disturbances in the electrical homeostasis of the brain cause recurrent seizures that can present in a relatively benign fashion such as an intermittent altered state of mind. More often, however, mental and postural control is lost and the patient is drawn into minute-long convulsions. Pharmacological seizure intervention is imperative, not only to prevent the attacks themselves, but also to avoid secondary complications from neurotransmitter toxicity and fall trauma. Especially vulnerable are children, where the brain damage can lead to developmental decline. Social limitations such as lack of independence, peer avoidance, and communal shunting lead to additional reductions in the quality of life.
In approximately one third of all epilepsies, the seizures can only be partially controlled by antiepileptic drugs (AEDs), with side effects calling for therapeutic comprises. Seiuzures completely resistant against all forms of pharmacological intervention exists as well. I am interested in developing new therapeutic approaches, in particular those that may be helpful in the treatment of channelepsies (i.e., epilepsies caused by ion channel defects). My work is mostly electrophysiological, examinging the functional ramifications of different ion channel mutants (e.g., Nav1.1, Nav1.2, Nav1.7, Kir4.1, Kir5.1, etc.). More recently, I introduced in various silico approaches such as meta analyses with locus-specific databases that compile massive data sets on gene variations.

(2) MYOTONIC DISORDERS... especially myotonia congenita (MC; OMIM #160800) are a second interest of mine. Patients afflicted with MC have a greatly reduced skeletal muscle chloride conductance which produces severe but pain-free cramps whenever motor tasks are initiated after short (<1 min) rest. The culprit is the chloride channel ClC-1, which usually acts as the (electrophysiological) pacifier that brings the muscle back to rest once stimulation has ended. Loss of ClC-1 function renders the muscle unable to quickly return to its baseline, producing involuntary muscle contraction at times when it ought to be relaxed. A similar presentation can arise when muscle's main "exciter" is defunct, Nav1.4. Typical for myotonic disorders is that the cramps disappear with repetition, making the patient virtually asymptomatic. This so-called warm-up phenomenon is not explained and it may represent an effective leverage point for pharmacological intervention.
(3) ERYTHERMALGIA... is a rare peripheral nerve disorder with redness, elevated temperature, and pain in the extremities (OMIM #133020). The condition is either secondary to other problems or of genetic origin, in which case it commonly arises from abnormalities in SCN9A, the gene coding for voltage-gated sodium channel Nav1.7. Compared to aforementioned comorbidity type, primary or inheritable erythermalgia is clinically distinct, always bilateral, triggered by exercise or warmth, relieved by cooling but not by aspirin, and never co-presenting with gout or other rheumatological conditions.


Present Principal Investigator/Assistant Ressearcher, University of California, Davis
Present School of Medicine - Department of Neurology, University of California, Davis

Curriculum Vitae

Research Interests

Molecular Neuroscience, Ion channels, Electrophysiology, and Locus-specific databases

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Contact Information

4635 2nd Ave, Room 1004A
Sacramento, CA 95817
Phone/Fax: (916) 703-5511/5512
Email: clossin [at]


Epilepsy (5)

Myotonia (1)

Pharmacology (2)