Keynote Conference - Interevent

Symp#19 Regulators of neural transmission
Chairs Vilma R Martins and Roy Larson
Regulation of neuronal function and dysfunction by protein SUMOylation
Jeremy M. Henley
University of Bristol
The post-translational modification SUMOylation is a major regulator of protein function that plays an important role
in a wide range of cellular processes. SUMOylation involves the covalent attachment of a member of the small
ubiquitin-like modifier (SUMO) family of proteins to lysine residues in specific target proteins via an enzymatic cascade
analogous to, but distinct from, the ubiquitination pathway. The implications for neuronal protein SUMOylation are
far-reaching in both normal cell function and in neurological and neurodegenerative diseases. I will discuss aspects of
our work attempting to identify and functionally characterise SUMO substrates; elucidate the molecular mechanisms
regulating, and consequences of, substrate SUMOylation and deSUMOylation; determine the activity-dependence of
SUMO and SUMO-specific protease trafficking to synapses; and define how SUMOylation regulates synaptic
transmission under basal, stimulated and pathological conditions.
Gain control in the outer retina
Joselevitch, C. 1,2 , Kamermans, M. 1
1 - Retinal Signal Processing, The Netherlands Institute for Neuroscience; The Netherlands.
2 - Department of Experimental Psychology, Universidade de São Paulo, Brazil.
Gain control mechanisms are present at all retinal layers. They are especially important for cells that receive mixedinput
from rods and cones, in order to avoid premature saturation as light levels increase. Here we describe a
mechanism at work in the goldfish retina that modulates the effectiveness of the rod-bipolar cell synapse. Voltageclamp
recordings of mixed-input ON bipolar cells in retinal slices show that a voltage-gated current is activated during
the light-induced depolarization at scotopic levels. The activation of this current effectively diminishes the amplitude
of the bipolar cell rod-driven light response and makes it faster and more transient with increasing light intensity. This
effect can be abolished by the K + channel blocker TEA, which indicates that the voltage-gated current is mediated by K +
ions. Mathematical simulations with NEURON suggest that the K + channels are most likely concentrated at the
dendritic tips of mixed-input ON bipolar cells, close to the site of glutamate release by photoreceptors. Since the
magnitude of activation of such channels depends directly on the amplitude of the light response, they control the
gain of the rod bipolar cell synapse and speed up synaptic transmission as light levels increase and rod responses
themselves inactivate slowly.
Protein synthesis and memory processing
Martin Cammarota
Instituto de Pesquisas Biomédicas, PUCRS, Porto Alegre, Brazil
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