Astrocytes, the Tripartite Synapse, Glia

Question 1

endfoot

Answer 1

specialized compartment of the astrocyte that contacts the blood supply

Question 2

domain architecture

Answer 2

formed because astrocyte fine processes do not overlap with neighboring astrocytes

Question 3

glial fibrillary acidic protein (GFAP)

Answer 3

a predominant structural protein expressed by astrocytes, gives the astrocyte its star like shape (does not exist in the fine astrocyte processes)

Question 4

which part of the astrocyte interacts with synapses?

Answer 4

the fine processes which makes extensive contacts with multiple dendrites

Question 5

how do astrocytes support and influence the synapse?

Answer 5

1) ionic homeostasis, e.g. K+ clearance
2) neurotransmitter clearance and recycling
3) modulate synaptic transmission

Question 6

how do astrocytes communicate with each other?

Answer 6

through Ca2+ waves (involves activation of PLC which produces IP3 and releases intracellular Ca2+ stores)

Question 7

how do astrocytes communicate across gaps, “gap jumping” ?

Answer 7

releases a diffusible messenger (ATP), this continues propagation of Ca2+ wave

Question 8

IP3 dependent Ca2+ waves

Answer 8

Ca2+ waves in the soma, not reduced by removing extracellular Ca2+ (relies on intracellular Ca2+ levels)

Question 9

IP3 independent Ca2+ waves

Answer 9

small waves and microdomain Ca2+ events, reduced by removing extracellular Ca2+ (these waves are spontaneous and transient)

Question 10

strong synaptic activity can increase free intracellular Ca2+ in the astrocyte because:

Answer 10

increased glutamate spillage can activate astrocyte mGluR which activates IP3 pathway

Question 11

gliotransmitters

Answer 11

released by astrocytes in response to neurotransmitters (e.g. ATP, glutamate, d-serine) and can affect neural excitability and/or synaptic transmission

Question 12

BAPTA

Answer 12

buffers Ca2+ (calcium-chelating agent), blocks astrocyte signalling and prevents effects in neurons

Question 13

knock out astrocyte IP3 receptors

Answer 13

stops release of Ca2+ from intracellular stores, blocks astrocyte signalling and prevents effects in neurons

Question 14

toxins (tetanus toxin)

Answer 14

cleaves proteins in the SNARE complex necessary for vesicle release, blocks astrocyte signalling and prevents effects in neurons

Question 15

technique to stimulate astrocytes and measure effects in neurons?

Answer 15

uncaging or photolysis of intracellular Ca2+ or IP3 in astrocytes (generates a Ca2+ wave that spreads from astrocyte to astrocyte, propagation through astrocyte fine processes)

Question 16

what happens when astrocyte internal Ca2+ spreads to the neuron?

Answer 16

synaptic strength increases (increases sEPSC amplitude)

Question 17

what happens when astrocyte Ca2+ does not reach the neuron?

Answer 17

synaptic strength does not change

Question 18

PPADS

Answer 18

purinergic receptor antagonist blocks the plasticity but not astrocyte signals (does not block astrocyte activation)

Question 19

MCPG

Answer 19

non-selective glutamate antagonist, blocks astrocyte activation, suggests that mGluRs are on astrocyte and P2X channels are on the neuron

Question 20

astrocyte glutamate acts on:

Answer 20

presynaptic NMDA receptors and mGluRs to increase the releease probability of presynaptic glutamate, this effect on synaptic transmission can be transient or long-lasting

Question 21

D-serine

Answer 21

endogenous co-agonist of the NMDA receptors

Question 22

primary site of D-serine synthesis in the brain

Answer 22

astrocytes

Question 23

astrocyte release of D-serine

Answer 23

helps neurons activate NMDA receptors, necessary for NMDA receptor mediated plasticity, such as LTP

Question 24

myelin segment

Answer 24

increases the input resistance (less current leak) and decreases the capacitance (voltage changes faster) of the axon to enhance action potential propagation