Dopamine release regulation by astrocytes during cerebral ischemia

Intermittent theta‐burst stimulation rescues dopamine‐dependent corticostriatal synaptic plasticity and motor behavior in experimental parkinsonism: Possible role of glial activity

“…Microglia is implicated in the production of neurotrophins, interleukines, and proinflammatory and antiinflammatory citokines that, if dysregulated, may contribute to abnormal plasticity. Also the finding of astrocytic changes in shape and functions in association with DA levels is supported by studies demonstrating that these cells in critical conditions release DA and express enzymes and the complete machinery to metabolize it . Moreover, relevant to PD, astrocytes can manage striatal DA levels, working as a reservoir for circulating levodopa …”

“…Also the finding of astrocytic changes in shape and functions in association with DA levels is supported by studies demonstrating that these cells in critical conditions release DA and express enzymes and the complete machinery to metabolize it. [38][39][40] Moreover, relevant to PD, astrocytes can manage striatal DA levels, working as a reservoir for circulating levodopa. 41 On this view, a different time course in sham-versus 6-OHDA-lesioned rats might reflect different mechanisms (synaptic vs nonsynaptic) by which DA levels change in response to TMS.…”

Alpha-Synuclein: From Early Synaptic Dysfunction to Neurodegeneration

“…Also, astrocytes have been reported to take up aggregated alpha syn. The most fascinating aspect of astrocyte involvement in neuronal degeneration, relevant to PD, is that astrocytes change in shape and function to provide support to DA neurons under intense stressful conditions ( 120 – 122 ). Astrocytes are also able to take up circulating DA precursor l -DOPA to release DA ( 123 ), as they express enzymes and the complete machinery for its metabolism, suggesting a close relationship to DA systems.…”

Kinase-dependent Regulation of Monoamine Neurotransmitter Transporters

“…Historically, vesicular and nonvesicular, transporter-mediated neurotransmitter release have been considered distinguishable on the basis of Ca 2+ dependence, with vesicular release being Ca 2+ dependent and transporter reversal being Ca 2+ independent. Such distinctions, however, have been drawn in relation to efflux that arises from changes in the ion gradients (e.g., Na + /Cl 2 ) needed to drive concentrative uptake, as for example when the Na + /K + ATPase is poisoned with ouabain, when extracellular Na + is lowered experimentally, or during ischemia (Kim et al, 1995;Elverfors et al, 1997;Oliva et al, 2013). As previously noted, DAT, NET, and SERT support another form of efflux that occurs upon AMPH stimulation and here significant evidence supports an important role for Ca 2+ as well as CaMKII.…”