In addition to being essential supporters of neuronal function, astrocytes are now recognized as active elements in the brain. Astrocytes sense and integrate synaptic activity and, depending on intracellular Ca(2+) levels, release gliotransmitters (e.g. glutamate, d-serine and ATP) that have feedback actions on neurons. Recent experimental results have raised the possibility that quantitative variations in gliotransmission might contribute to disorders of the nervous system. Here, we discuss targeted molecular genetic approaches that have demonstrated that alterations in protein expression in astrocytes can lead to serious changes in neuronal function. We also introduce the concept of 'astrocyte activation spectrum' in which enhanced and reduced gliotransmission might contribute to epilepsy and schizophrenia, respectively. The results of future experimental tests of the astrocyte activation spectrum, which relates gliotransmission to neurological and psychiatric disorders, might point to a new therapeutic target in the brain.
"TNF-alpha is one of only a handful of recognized gliotransmitters. TNF-alpha released by glia, has been demonstrated to control synaptic strength. NSAIDS inhibit COX enzymes and thereby decrease the production of cytokines & microglial activation, platelet aggregation, iNOS and beta secretase. "
"+ signals was positively correlated to spike frequency , and the duration of Ca 2+ signals was correlated with spike number . So , Ca 2+ levels in a neuron indicated its response strength in vivo ( Petersen et al . , 2005 ; Yaksi and Friedrich , 2006 ; Moreaux and Laurent , 2007 ) . The activity of the astrocytes also altered their Ca 2+ signals ( Halassa et al . , 2007 ) . The synchrony of Ca 2+ signals among cell pairs was analyzed by correlation coefficients to represent their activity synchrony ( Hirase et al . , 2004 ; Takata and Hirase , 2008 ; Golshani et al . , 2009 ) ."
[Show abstract][Hide abstract] ABSTRACT: Associative learning and memory are essential to logical thinking and cognition. How the neurons are recruited as associative memory cells to encode multiple input signals for their associated storage and distinguishable retrieval remains unclear. We studied this issue in the barrel cortex by in vivo two-photon calcium imaging, electrophysiology, and neural tracing in our mouse model that the simultaneous whisker and olfaction stimulations led to odorant-induced whisker motion. After this cross-modal reflex arose, the barrel and piriform cortices connected. More than 40% of barrel cortical neurons became to encode odor signal alongside whisker signal. Some of these neurons expressed distinct activity patterns in response to acquired odor signal and innate whisker signal, and others encoded similar pattern in response to these signals. In the meantime, certain barrel cortical astrocytes encoded odorant and whisker signals. After associative learning, the neurons and astrocytes in the sensory cortices are able to store the newly learnt signal (cross-modal memory) besides the innate signal (native-modal memory). Such associative memory cells distinguish the differences of these signals by programming different codes and signify the historical associations of these signals by similar codes in information retrievals.
"While astrocytes are not electrically excitable like neurons, one mode of prominent activity of astrocytes is the release of calcium from internal stores following activation of a variety of G-protein coupled receptors. Many groups have hypothesized that calcium signaling in astrocytes underlies the release of many signaling molecules, termed 'gliotransmitters', which can directly impact neural circuit excitability . While dynamic calcium transients have been readily observed in the somas and proximal thick processes of astrocytes maintained in culture and/or in brain slices prepared from very young animals, synthetic calcium-indicating dyes have been difficult to deliver in either adult or sclerotic tissue. "
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