The progressive
loss of rod and conephotoreceptors in human subjects with
retinitis pigmentosa causes a gradual decline in vision and can result
in blindness. Current treatment strategies for the disease rely on the
integrity of inner retinal neurons, such as amacrine cells, that are
postsynaptic to photoreceptors. Previous work has demonstrated that
a specialized subclass of retinal amacrine cell that synthesizes and
releases the key neurotransmitter dopamine remains morphologically
intact during the disease; however, the pathophysiological function of
these neurons remains poorly understood. Here we examined spontaneous
and light-evoked spike activity of genetically labeled dopamine
neurons from the retinas of retinal degeneration 1 (rd1) mice. Our
results indicated that rd1 dopamine neurons remained functionally
intact with preserved spontaneous spiking activity and light-evoked
responses. The light responses were mediated exclusively by melanopsin phototransduction, not by surviving cones. Our data also
suggested that dopamine neurons were altered during photoreceptor
loss, as evidenced by less spontaneous bursting activity and increased
light-evoked responses with age. Further evidence showed that these
alterations were attributed to enhanced GABA/melanopsin signaling
to dopamine neurons during disease progression. Taken together, our
studies provide valuable information regarding the preservation and
functional modification of the retinal dopamine neuronal system in
rd1; this information should be considered when designing treatment
strategies for retinitis pigmentosa.
Researchers in the laboratory of Assistant Professor Dao-Qi Zhang, of the Eye Research Institute, published an article in the Journal of Neurophysiology.
Created by Brad Roth (roth@oakland.edu) on Thursday, April 11, 2013 Modified by Brad Roth (roth@oakland.edu) on Tuesday, April 30, 2013 Article Start Date: Thursday, April 11, 2013