is this theory right?
Pathway 1: the fast increase of intercellular [K+] produced by the spiking activity of the postsynaptic neuron.
Pathway 2: the slow production of a mediator (Glutamat) triggered by the synaptic activity.
This may help;
1. J Biol Phys. 2012 Jun; 38(3): 465–496.
Published online 2012 May 27. doi: 10.1007/s10867-012-9267-7
PMCID: PMC3388198
A mathematical model of the tripartite synapse: astrocyte-induced synaptic plasticity
Shivendra G. Tewari1,2 and Kaushik Kumar Majumdarcorresponding author
Bassam, your ideas seem really good.
1: As you surely know, astrocytes are "hepatocytes and nephrocytes" of the CNS because they buffer everything that can be and should be buffered. Considering elevated extracellular K+, they buffer it as well in order to prevent uncontrolled neuronal hyper-excitability. Your question can be precised and reformulated as follow: does increasing of the intracellular K+ in astrocytes induce release of the Glu, or GABA, or Gly, or anything else (e.g. ATP) that can influence inter-neuronal synapses in the way synaptic (co)transmitters do?
2: Astrocytes are quite rich in mitochondria, although they are highly resistant to the oxygen lack So, they can (re)uptake and release not only glutamine, but Glu (and GABA) as well. Now, we know it for Glu but, before the year 2000, it was thought they release only glutamine towards neurons. In principle, nothing prevents astrocytes to release it both fastly and slowly. Simply, everything should be checked before jumping to the conclusion because, sometimes, "speedy" conclusions become illusions. It's all a question of the functional optimization between astrocytes and neurons including synapses.
Hi Bassam,
The answer to your question varies based on what specific brain regions you refer to as well as whose experimental data you believe. That said, I think the most up to date primer on astrocyte signaling is this review from Bazargani and Attwell: Nature Neuroscience 19, 182–189 (2016) doi:10.1038/nn.4201.
Additionally, with respect to the theory you mention, acute buffering of K+ is known to influence neuronal signaling directly (see, e.g., PLoS Comput Biol. 2015 Mar; 11(3): e1004137.) Additionally, some work from Maiken Nedergaard's lab (Sci Signal. 2012 Apr 3; 5(218): ra26.) suggests that there is an interaction between GPCR-mediated Ca2+ influx and slower K+ buffering in astrocytes. The upshot of this story is that this enhanced K+ buffering serves to enhance signal to noise in neuronal firing behavior.
References are linked in the order I laid them out above.
Best,
Joey
http://www.nature.com/neuro/journal/v19/n2/full/nn.4201.html
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4380507/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3515082/
Thanks all for these answers and rich information you have just given me.a actually my motivation from the question was to get knowledge from experts like you ... I published a publication last year, real time astrocytes in spiking neural network. It was modeling of astrocytes in artificial neural networks... I chose one functional model ...it was for postnov... And the original interaction pathways were taken from deitmer J.
That model was based on the two pathways of activation astrocytes ...one from glutamate neurotransmitter from synapse to astrocytic receptor mGluR ...Slow one ...
Triggered IP3 to trigger Calcium ... intracellular calcium of course from ER...the second pathway was from depolarization from postsynaptic neuron current .. buffering potassium ... And the mediator receptor is NMDA.. fast... Trigger also calcium of astrocytes...in turn ... Once calcium reached a threshold... It triggers the astrocytic gliotransmitters ... glutamate release to both synaptic cleft and postsynaptic neuron to affect its IPSP or EPSP ...or the frequency of action potential...
I prepare new paper now ... I just wanted to know if I can disregard the patway of mediator from postsynaptic neuron current... Because I will model just feedforward only ..without the feedback from postsynaptic neuron to astrocytes again ..
Local increase includes
1, K+ release from axons as a results of APs.
2, synaptic transmission, which is a major source.
by modeling i mean to generalize this biological model to artificial network model... the pathways are right? or something is missing? like i should add the feedback from post-synaptic neuron to astrocyte.
i mean it will be a big mistake in biological point of view....
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