TY - GEN
T1 - Exploring retrograde signaling via astrocytes as a mechanism for self repair
AU - Wade, John J.
AU - McDaid, Liam J.
AU - Harkin, Jim
AU - Crunelli, Vincenzo
AU - Kelso, J. A.Scott
AU - Beiu, Valeriu
PY - 2011
Y1 - 2011
N2 - Recent work has shown that astrocytes are capable of bidirectional communication with neurons which leads to modulation of synaptic activity. Moreover, indirect signaling pathways of retrograde messengers such as endocannabinoids lead to modulation of synaptic transmission probability. In this paper we hypothesize that this signaling underpins fault tolerance in the brain. In particular, faults manifest themselves in silent or near silent neurons, which is caused by low transmission probability synapses, and the enhancement of the transmission probability of a "faulty" synapse by indirect retrograde feedback is the repair mechanism. Furthermore, based on recent findings we present a model of self repair at the synaptic level, where retrograde signaling via astrocytes increases the probability of neurotransmitter release at damaged or low transmission probability synapses. Although our model is still at the embryo stage, results presented are encouraging and highlight a new research direction on brain-like self repair.
AB - Recent work has shown that astrocytes are capable of bidirectional communication with neurons which leads to modulation of synaptic activity. Moreover, indirect signaling pathways of retrograde messengers such as endocannabinoids lead to modulation of synaptic transmission probability. In this paper we hypothesize that this signaling underpins fault tolerance in the brain. In particular, faults manifest themselves in silent or near silent neurons, which is caused by low transmission probability synapses, and the enhancement of the transmission probability of a "faulty" synapse by indirect retrograde feedback is the repair mechanism. Furthermore, based on recent findings we present a model of self repair at the synaptic level, where retrograde signaling via astrocytes increases the probability of neurotransmitter release at damaged or low transmission probability synapses. Although our model is still at the embryo stage, results presented are encouraging and highlight a new research direction on brain-like self repair.
UR - http://www.scopus.com/inward/record.url?scp=80054724650&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=80054724650&partnerID=8YFLogxK
U2 - 10.1109/IJCNN.2011.6033638
DO - 10.1109/IJCNN.2011.6033638
M3 - Conference contribution
AN - SCOPUS:80054724650
SN - 9781457710865
T3 - Proceedings of the International Joint Conference on Neural Networks
SP - 3149
EP - 3155
BT - 2011 International Joint Conference on Neural Networks, IJCNN 2011 - Final Program
T2 - 2011 International Joint Conference on Neural Network, IJCNN 2011
Y2 - 31 July 2011 through 5 August 2011
ER -