Physiology of Astroglia

Abstract

Astrocytes are principal cells responsible for maintaining the brain homeostasis. Additionally, these glial cells are also involved in homocellular (astrocyte-astrocyte) and heterocellular (astrocyte-other cell types) signalling and metabolism. These astroglial functions require an expression of the assortment of molecules, be that transporters or pumps, to maintain ion concentration gradients across the plasmalemma and the membrane of the endoplasmic reticulum. Astrocytes sense and balance their neurochemical environment via variety of transmitter receptors and transporters. As they are electrically non-excitable, astrocytes display intracellular calcium and sodium fluctuations, which are not only used for operative signalling but can also affect metabolism. In this chapter we discuss the molecules that achieve ionic gradients and underlie astrocyte signalling. Keywords Astrocytes; Brain homoeostasis; Neurotransmitter receptors; Ion channels; SLC transporters; Ca 2+ signaling; Na + signalling 3.1 Definition of Astroglia Astroglia (also known as astrocytes) are a class of neural cells of ectodermal, neuroepithelial origin that sustain homeostasis and provide for defence of the central nervous system (CNS) (Fig. 3.1; [410]). The term astrocyte (αστρoν κψτoσ; astron, star and kytos, a hollow A.

Preventing neurodegeneration by adrenergic astroglial excitation

“…Astrocytes are morphologically and functionally heterogeneous cells primarily responsible for homeostasis of the CNS. These functions were recently reviewed [51], and include regulation of synaptic formation, control of connectivity of synapses, integration and synchronization of neuronal networks and the maintenance of BBB integrity [52][53][54][55][56][57][58][59][60][61][62][63][64][65][66][67][68][69][70]. Importantly, astrocytes are also the fundamental defensive elements of the nervous tissue; insults to the brain or spinal cord trigger reactive astrogliosis, which spatially contains damaged area, while also facilitating postdamage regeneration of neural tissue [54,62,64]; in certain context astrogliosis can be maladaptive and neurotoxic [71].…”

Single synapse indicators of impaired glutamate clearance derived from fast iGluu imaging of cortical afferents in the striatum of normal and Huntington (Q175) mice

“…Nevertheless, the present iGlu u -based postulate of non-saturating Glu uptake for ITand PT-type corticostriatal synapses will need further verification under a wider range of conditions. It was already shown that the state of astrocytes could affect the structural plasticity of PAPs (Theodosis et al, 2008;Reichenbach et al, 2010;Bernardinelli et al, 2014;Heller and Rusakov, 2015;Verkhratsky and Nedergaard, 2018). Activity-and diseasedependent PAP retraction could produce a large variety of spill-out and spill-in effects which may not only change the access of the available transmitter(s) to respective neuronal and glial receptors, but also influence the efficacy of the astrocytic transport machinery itself (Armbruster et al, 2016).…”

Deletion of calcineurin from astrocytes reproduces proteome signature of Alzheimer’s disease and epilepsy and predisposes to seizures

“…The observations that glial cells change very early during neuropathology (Rodríguez et al, 2014;Verkhratsky et al, 2016) led to hypothesize that an insufficient homeostatic support to other cells in the CNS may be among the primary events which predispose neurons to dysfunction (Verkhratsky et al, 2016(Verkhratsky et al, , 2019. In this context, we have proposed that deregulation of astroglial Ca 2+ signalling, downstream of CaN, may contribute to this homeostatic failure (Lim et al, 2014(Lim et al, , 2016b.…”