Astrocytic Vesicle Mobility in Health and Disease

Abstract

Astrocytes are no longer considered subservient to neurons, and are, instead, now understood to play an active role in brain signaling. The intercellular communication of astrocytes with neurons and other non-neuronal cells involves the exchange of molecules by exocytotic and endocytotic processes through the trafficking of intracellular vesicles. Recent studies of single vesicle mobility in astrocytes have prompted new views of how astrocytes contribute to information processing in nervous tissue. Here, we review the trafficking of several types of membrane-bound vesicles that are specifically involved in the processes of (i) intercellular communication by gliotransmitters (glutamate, adenosine 5′-triphosphate, atrial natriuretic peptide), (ii) plasma membrane exchange of transporters and receptors (EAAT2, MHC-II), and (iii) the involvement of vesicle mobility carrying aquaporins (AQP4) in water homeostasis. The properties of vesicle traffic in astrocytes are discussed in respect to networking with neighboring cells in physiologic and pathologic conditions, such as amyotrophic lateral sclerosis, multiple sclerosis, and states in which astrocytes contribute to neuroinflammatory conditions.

Excitable Astrocytes: Ca2+- and cAMP-Regulated Exocytosis

“…in astrocytes can trigger exocytotic release of glutamate [21,29,30,63,64], ATP [35,36], secretogranin II [34], ANP [33], and D-serine [32]. On the contrary, increases in cAMP in astrocytes in connection with exocytotic gliosignal release are much less studied; however cAMP [123] can trigger exocytotic release of secretogranine II from peptidergic vesicles [34] and ATP from late endolysosomes. Moreover, enhanced Ca 2?…”

“…from the ER to the plasma membrane), asynchronous coupling between astroglial rapid Ca 2? signals and vesicle fusion [24,113], the slow delivery of vesicles to the plasma membrane fusion sites [123] and/or slow molecular mechanisms governing the merger of the vesicle and the plasma membrane, which needs to be further studied in the future.…”

Corticosterone treatment results in enhanced release of peptidergic vesicles in astrocytes via cytoskeletal rearrangements

“…Interestingly, ANP as well as its binding sites have been localized in neurons and astrocytes from different brain regions ((McKenzie et al, 1992((McKenzie et al, , 1990((McKenzie et al, , 2001. In pathophysiological conditions like amyotrophic lateral sclerosis, multiple sclerosis and in conditions in which astrocytes contribute to neuroinflammation, the dynamics of vesicular traffic and release are significantly altered (Potokar et al, 2013). Therefore ANP released from astrocytes could modulate activity of neurons, astrocytes as well as cerebral blood flow in physiological as well as pathophysiological conditions.…”

The uptake, retention and clearance of drug-loaded dendrimer nanoparticles in astrocytes – electrophysiological quantification

“…[30][31][32][33][34][35] Astrocytes outnumber neurons in the neocortex, the largest structure of the human brain with a mass exceeding 80% of the brain, where they perform a variety of important functions. [35][36][37][38] In principle, as with any other disease, neurological diseases result from a homeostatic failure. However, it is the neuroglia that provides full homeostatic and neuroprotective support.…”