astrocytes and diseases

Jackson

the main difference between glia and neurotransmitters is that glia cannot elicit an [blank blank]

action potential

fibrous astrocytes are found in [blank] matter tracts and orient parallel to neuronal axons

white

[blank] astrocytes are larger than protoplasmic astrocytes and also have higher levels of glia fibrillary acid protein (GFAP)

fibrous

protoplasmic astrocytes are found in gray matter, have fine processes, and a very [blank] membrane potential

negative

[blank] astrocytes have prominent glutamate uptake

protoplasmic

astrocytes form perivascular [blank] around CNS capillaries and arterioles

end-feet

over [x]% of capillary surface is covered by astrocytes and help form the blood-brain barrier

80

astrocytes are major sites of [blank] uptake via GLUT1

glucose

astrocyte secreted factors help control endothelial function and [blank blank] maintenance

tight junction

Astrocyte processes contact pre-and post-synaptic elements forming a structure called the [blank] synapse

tripartite

neurotransmitters from the [blank] terminal activate astrocytes and are involved with administering neurotransmitters or removing them

presynaptic

astrocytes help propagate the [blank] wave when transplanted into mice

Ca2+

most astrocytes have a [blank] current-voltage relationship and are highly coupled (do not fire APs)

linear

high [blank] permeability of glial cells which is mediated by Kir4.1 channels.

potassium

during signaling astrocytes exhibit large inward current for potassium and [blank]

glutamate

Astrocytes are highly coupled by [blank] junctions but are blocked by carbenoxolone (CBX)

gap

Astrocytes in cortex are highly [blanked], facilitating the transfer of signaling molecules/metabolites/dyes

coupled

examples of gliotransmitters include glutamate, ATP, D-Serine, Lactate, [blank], and K+

Endocannabinoids

astrocytes are involved in [blank] synthesis and glucose uptake

glycogen

astrocytes are also involved in [blank] and synaptic pruning,

synaptogenesis

radial glia serve as structural scaffold support and are a source of [blank] cells

progenitor

[blanks] form structural but not functional synapses

thrombospondins

[blank] facilitates presynaptic activity/increases release probability

cholesterol

astrocytes induce functional synapses from silent synapses via insertion of [blank] receptors

AMPA

in astrocyte conditioned media, [blank] and hevin influence synaptogenesis

sparc

Potassium transfer by current flow through astrocyte syncytium via gap junction is known as [blank x3]

K+ spatial buffering

potassium uptake is how astrocytes modulate [blank] of neurons

excitability

astrocytes regulate glutamate availability via the glial transporters: EAAT1 ([blank]) and EAAT2 (GLT1)

GLAST

EAAT2/GLT-1 is the predominant Glu transporter in the brain and problems can lead to [blank/blank] within hours

hypoxia/ischemia

Glutamate is converted to glutamine by [blank blank] (GS), which keeps intracellular glutamate concentration low

glutamine synthetase

Glutamine exported to neurons. Converted back to glutamate via [blank]. Glutamate also precursor for GABA

glutaminase

glutamate may also be sent through the [blank] cycle for metabolism

TCA

Glucose converts to lactate in the presence of oxygen, which is known as [blank] glycolysis or fermentation

aerobic

glycogen is converted to [blank] which is a major fuel source for the brain and is exported via MCTs

lactate

Astrocytes control aspects of cerebral [blank blank] through neurovascular coupling

blood flow

Photolysis of caged Ca2+ in astrocytic endfeet is sufficient to trigger arteriole [blank]

dilation

Astrocyte-mediated vasodilation requires [blank] activity

COX-1

in response to inflammation, astrocytes increase Ca2+ signaling, upregulate [blank] and lose activity of GS

GFAP/Vimentin

Neurotoxic astrocytes secrete inflammatory [blank], mediate cell death of neurons and oligodendrocytes

cytokines

neurotoxic astrocytes are marked by C3 while [blank] astrocytes are marked by s100a10

neuroprotective

Astrocytes become reactive after injury/[blank]

epilepsy

epilepsy astrocytes decrease [blank], decrease glutamate removal, and decrease glutamate-glutamine cycling

K+ buffering

[blank] neurotransmission is impaired near reactive astrocytes and causes eIPSC failure

Inhibitory

Altered glutamate-glutamine cycle results in loss of vesicular [blank]

GABA

Alexander’s disease results from mutation of [blank] and accumulation into Rosenthal fibers (movement disorders)

GFAP

Reactive astrocytes surround [blank] brain tumors

melanoma

Astrocyte secreted factors drive melanoma migration and growth, also activate [blank] signaling pathways in MBM

oncogenic