Select mechanisms for astrocyte-induced plasticity.
a Hebbian plasticity. Recruitment of NMDA receptors is mediated by astrocyte-derived Hevin and the cell adhesion molecules Neuroligin-1 (NL1) and Neurexin-1 (Nrxn1) during the ocular dominance plasticity critical period. Astrocyte chondroitin sulfate proteoglycans (CSPGs) and SPARC stabilize AMPA postsynaptic receptors. Astrocyte gap junction proteins Connexins 30 and 43 regulate metabolite transport through monocarboxylate transporters (MCT1/2) between astrocytes and neurons in an activity-dependent manner to facilitate plasticity.
b Homeostatic plasticity. Astrocyte-derived SPARC limits aggregation of AMPA receptors to facilitate synaptic scaling in response to chronic silencing. Additionally, receptors and transporters located in the astrocytic membrane monitor neuronal Ca2+ transients and release of neurotransmitters, resulting in gliotransmitter release.
c Structural-homeostatic plasticity. Astrocyte-secreted Chrdl1 restricts neuronal plasticity by directly switching postsynaptic neurotransmitter receptor identity. Astrocyte-derived Neuroligin (NL) binds dendritic Neurexin (Nrxn) to mediate the closure of critical periods by stabilizing dendrite microtubule populations. Synapse elimination is driven by neuronal activity, and is regulated by astroglial MERTK and MEGF10.
d Repeated excitatory postsynaptic potentials evoke more robust synaptic activity in potentiated circuits over time. Conversely, synapses targeted by long term depression display lower levels of excitability following stimulation.
e Homeostatic mechanisms decrease the difference between synaptic input and output by bidirectionally adjusting the probability of transmitting an action potential postsynaptically