[TNJC] Neuro Journal Club next week (20/5, 2pm, Tuesday)

[Ben Dongsung Huh]

On next Tuesday TNJC Joana will be presenting the following paper:

"Deficient GABAergic Gliotransmission May Cause Broader Sensory Tuning in Schizophrenia"  Osamu Hoshino.

http://www.mitpressjournals.org/doi/abs/10.1162/NECO_a_00519#.U3Y6jaaygak

The plan is to continue with the topic that Gergo introduced last week: glia cells. We thought it would be a good idea to team up so that we could cover a particular subject in more depth. 

Last week we learned about one of the possible mechanisms by which astroglial cells regulate synaptic efficacy. Researchers found that the protein connexin30 modulates glutamate transport by inducing a morphological change in astroglial cells, which makes them invade the synaptic cleft with their processes. 
Next week I will talk about another important glial modulatory effect: GABAergic gliotransmission, focussing on the role that such mechanism could play, when dysfunctional, in schizophrenia.

Abstract

We examined how the depression of intracortical inhibition due to a
reduction in ambient GABA concentration impairs perceptual infor-
mation processing in schizophrenia. A neural network model with a
gliotransmission-mediated ambient GABA regulatory mechanism was
simulated. In the network, interneuron-to-glial-cell and principal-cell-to-
glial-cell synaptic contacts were made. The former hyperpolarized glial
cells and let their transporters import (remove) GABA from the extracel-
lular space, thereby lowering ambient GABA concentration, reducing ex-
trasynaptic GABAa receptor-mediated tonic inhibitory current, and thus
exciting principal cells. In contrast, the latter depolarized the glial cells
and let the transporters export GABA into the extracellular space, thereby
elevating the ambient GABA concentration and thus inhibiting the prin-
cipal cells. A reduction in ambient GABA concentration was assumed for
a schizophrenia network. Multiple dynamic cell assemblies were orga-
nized as sensory feature columns. Each cell assembly responded to one
specific feature stimulus. The tuning performance of the network to an
applied feature stimulus was evaluated in relation to the level of ambi-
ent GABA. Transporter-deficient glial cells caused a deficit in GABAergic
gliotransmission and reduced ambient GABA concentration, which
markedly deteriorated the tuning performance of the network, broad-
ening the sensory tuning. Interestingly, the GABAergic gliotransmission
mechanism could regulate local ambient GABA levels: it augmented am-
bient GABA around stimulus-irrelevant principal cells, while reducing
ambient GABA around stimulus-relevant principal cells, thereby ensur-
ing their selective responsiveness to the applied stimulus. We suggest
that a deficit in GABAergic gliotransmission may cause a reduction in
ambient GABA concentration, leading to a broadening of sensory tun-
ing in schizophrenia. The GABAergic gliotransmission mechanism pro-
posed here may have an important role in the regulation of local ambient
GABA levels, thereby improving the sensory tuning performance of the
cortex.

See you then!

TNJC website:   www.gatsby.ucl.ac.uk/tnjc/

Future presenter list:

Kyo	27/5/2014
Tri-center Meeting	3/6/2014
Federico	10/6/2014
Mehdi	17/6/2014

Ben Dongsung Huh
Gatsby Computational Neuroscience Unit