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Molecular sensory physiology group – Universität Innsbruck

Molecular sensory physiology group (Head: A. Koschak) 


  • Contribution of L-type calcium channels in sensory physiology of vision
  • Role of L-type calcium channels in visual disorders
  • The retina as window to the brain

 

Koschak Group 

 

 

 
Researchers:
- Matthias Ganglberger
- Elisa Roth
- Alexandra Koschak
  
Technicians:
- Mareike Uthoff
- Bettina Tschugg (derzeit in Karrenz)
  
Collaborators:
- Petronel Tuluc
- Jörg Striessnig
 


ALUMNI

- Lucia Zanetti
- Hartwig Seitter 
- Thomas Heigl

 

 

This research group is interested in L-type calcium channels in molecular sensory physiology and pharmacology:

 

Photoreceptors are morphologically and physiological highly specialised light sensing cells of the retina. In darkness their membrane potential is depolarized up to -36 mV due to the activity of cGMP activated cation channels. Sustained release of glutamate from photoreceptor ribbon synapses is Ca2+ dependent and L-type calcium channels (LTCCs) serve as the predominant source for Ca2+ entry. Cav1.4 LTCCs channels – which are encoded by the CACNA1F gene - are located in close vicinity to the typical horseshoe shaped ribbon synapses and play an important role for signal retinal transmission.

 

We currently focuses on the following topics:

  1. Role of L-type calcium channels in visual disorders
  2. L-type calcium channels in retinal bipolar cells
  3. Pharmaco-therapeutic potential of Cav1.4 L-type Ca2+ channels

 

  1. Role of L-type calcium channels in visual disorders

A number of channel dysfunctions 2 have been described that are caused by mutations in the CACNA1F gene, which encodes for the Cav1.4 LTCC alpha1 subunits. A majority of mutations was, however, identified among patients originally diagnosed with congenital night blindness type 2 (CSNB2; OMIM: 30071). Many Cav1.4 mutations are predicted to cause severe structural changes that they are unlikely to form functional channels, often due to premature truncation forming a large group of ‘loss-of-function’ mutations. ‘Gain-of-function’ mutations would promote pronounced Ca2+ entry through the channel. We still wish to better understand how the different functional channel phenotypes can all result in defective retinal synaptic transmission underlying CSNB2 symptoms.

 

  1. L-type calcium channels in retinal bipolar cells

This is a joint project by Alexandra Koschak and Hartwig Seitter, Molecular Sensory Physiology group at the Pharmacology and Toxicology at the University of Innsbruck. The aim of this project is to gain a better insight into the specific function of L-type calcium channel subunit Cav1.4 on selected retinal cells’ physiology and synaptic output. To this end, rod bipolar cells are targeted for genetic manipulation to allow for investigation of the morphological and physiological impact of cell-specific perturbations.

 

  1. Pharmaco-therapeutic potential of Cav1.4 L-type Ca2+ channels

This project evaluates the pharmaco-therapeutic potential of different retinal L-type calcium channels and develops a concept for viral based therapies for Cav1.4-mediated retinal diseases. Adeno-associated virus (AAV)-mediated gene transfer is currently the golden standard for stable and long-term expression of transgenes in the retina. We further study Cav1.4 channel mutants in virally transduced retinal neurons to our understanding of Cav1.4 channel dysfunction.

 

 

 

If you are interested in more general information about:

‘The Organisation of the Retina and the Visual System’ – click here

 
‘Pathologies of Calcium Channels’– click here
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