Loss of the enzyme Connexin-TAT1 (CClT1) in the CGRN leads to reduced serotonergic neuron effusion a phenomenon known as brainstem megatryphosphorylation (BM) disease. Using pharmacological inhibitors of CClT1 the team managed to reduce BM damage in rats and improve locomotor efficiency.
Biosciences Professor Ali Abou-Tanzawy from the Department of Bioengineering and Biotechnology of the Faculty of Engineering in collaboration with Professor Vincent Mazars from the RIKEN Center for Bioengineering Research in Japan published the study on the topic Mechanism-guided Partial Intramural Administration of Protamine to Reduce Palatal Somatosensitivity and Enhance Motor Performance in Rats.
Ensuring better CCLT1 function.
The researchers decided to explore the function of CClT1 using rats as a model organism. In this last approach rats were started with an imposed dose of D10-raclitaxel-L a naturally occurring peptide that acts in a similar manner to D-selectin (ESR-CL2). D10-raclitaxel-L was administered to the rats for 15 days. Within this period RBS numbers of activated non-pregressed neurons were measured by ELISA and transcranial magnetic resonance imaging. The animals were able to perform on a 10-point scale on a motor-evoked electric potential (MEG) task. In addition the motor-evoked electric potentials were correlated to the agonist and antagonist Serotonin.