Introduction:
Rapid opening and closing of the connexons (connexin hemi channels) allows the transport
of small molecules between adjacent cells. In the inner ear, this leads to the formation
and preservation of the endocochlear potential and thus to the physical basis of hearing.
Disorders of homeostasis lead to hearing loss. In preliminary studies, we were able
to show that patients with heterozygous connexin mutations despite initial perfect
inner ear function lose their hearing of time. Pathologies associated with changes
in the physical environment such as coclear inflammation, which is associated with
a change in temperature, could be responsible for this. However, there is no screening
procedure to evaluate the patient-specific risk potential.
Method:
The activity of the connexin 26 hemichannels was measured as function of temperature.
This was done using a liposome vesicle flux assay directly on the protein in vitro.
Xenopus-oocytes injected with human variants of connexin 26 were used as a reference
system.
Results:
The temperature-dependent opening of the connexin hemichannels could be demonstrated
directly at the protein and was verified with the established frog oocyte model.
Summary: The present results could provide the basis for the development of a valid
microarray for a patient-specific screening, with which the sensitivity of temperature
changes of hemichannels can be determined.
