Neuronal communication

Question 1

Ionotropic glutamate receptors e.g.

Answer 1

AMPAR/Kainate
NMDAR

Question 2

Metabotropic glutamate receptors function by modulating …

Answer 2

NMDAR activity

Question 3

Ionotropic GABA receptor channel

Answer 3

Directly increases Cl- influx

Question 4

Metabotropic GABA receptor channel

Answer 4

Indirectly increases K+ efflux, decreases Ca2+ influx and inhibition of adenylyl cyclase

Question 5

Which neurotransmitter has only ionotropic receptors?

Answer 5

Glycine

Question 6

Inhibitory or excitatory: Glycine

Answer 6

Inhibitory

Question 7

Inhibitory or excitatory: serotonin

Answer 7

Excitatory

Remark: Serotonin is 5-HT, has both ionotropic and metabotropic receptors

Question 8

Inhibitory or excitatory: ATP

Answer 8

Excitatory

Question 9

Inhibitory or excitatory: Ach

Answer 9

Excitatory

Question 10

Migraine characteristics

Answer 10

Unilateral & pulsating, lasting 4-72 hours

Question 11

Migraine etiology

Answer 11

Low levels of serotonin which causes vasodilation of extracranial vessels

Question 12

Cortical spreading depression (CSD) symptoms

Answer 12

Aura - unusual visual, olfactory and other sensory experiences preceding migraine attacks

Question 13

Which receptors contribute to the spreading of cortical spreading depression?

Answer 13

1. Gap junctions
2. NMDAR

Question 14

Calcitonin gene-related peptide (CGPR)

Answer 14

Becomes elevated during migraine attacks. May be involved with vasodilation.

Question 15

NMDA receptor antagonist

Answer 15

Meant to prevent CSD spread. DIRECT EFFECT, IONOTROPIC.
e.g. Magnesium, ketamine

Question 16

Gap junction modulator

Answer 16

Meant to prevent CSD spread
e.g. tonabersat

Question 17

5-HT receptor agonist

Answer 17

5-HT receptors are GPCRs that induce VASOCONSTRICTION. May help with CSD. INDIRECT: METABOTROPIC
e.g. Tryptans, ergotamine, kynurenine

Question 18

CGRP receptor antibody

Answer 18

may help against CSD.
e.g. Erenumab (aimovig)

Question 19

Can analgesics help with CSD?

Answer 19

yes.

Question 20

Synaptogenesis at NMJ requires the formation of

Answer 20

basal lamina or laminin in the synaptic cleft

Question 21

What happens with dysfunctional laminin?

Answer 21

Schwann cell processes invade the NMJ synaptic cleft. In humans, this causes congenital muscle dystrophy.

Question 22

Nerve regeneration at NMJ

Answer 22

Basal lamina ghosts

Question 23

Muscle regeneration at NMJ

Answer 23

Clusters of concetranted AchR

Question 24

Gower’s sign

Answer 24

a patient has to use their hands and arms to “walk” up their body

Question 25

What links the pre and postsynaptic membranes in central neuron junctions?

Answer 25

Adhesion molecules.
neurexin @ pre
neuroligin @ post synaptic

Question 26

Mutation of neurexin-1

Answer 26

Schizophrenia

Question 27

Mutation of neuroligin

Answer 27

Autism, mental retardation, repeated behaviors

Question 28

How does glia help with synaptogenesis?

Answer 28

Secretion of thrombospondin and cholesterol

Question 29

What is astrocytes’ function at synapses?

Answer 29

Lots of K channels
Buffer the excess accumulation of K
Abnormal accumulation of extracellular K results in epileptic neuronal activity

Question 30

Electrical synapses are often…

Answer 30

Dendrodendritic

Question 31

Axoaxonic synapse function

Answer 31

Presynaptic modulation

Question 32

Renshaw cells

Answer 32

Renshaw cells are inhibitory interneurons found in the gray matter of the spinal cord, and are associated in two ways with an alpha motor neuron.

Question 33

Cellular changes in short-term habituation

Answer 33

1. Decrease of presynaptic Ca
2. Decrease of transmitter release

Question 34

Cellular changes in long-term habituation

Answer 34

1. Decrease of sensory AP duration and absence of motor EPSP
2. Decrease of synaptic connection numbers

Question 35

Cellular changes in long-term sensitization

Answer 35

1. increase of synaptic connection numbers
2. Presynaptic facilitation: prolongation of the sensory neuron AP

Question 36

How does presynaptic facilitation work?

Answer 36

5-HTergic local interneuron releases 5-HT into presynaptic neuron, which activates metabotropic pathways.
1. Ca2+ influx increases (MAIN EFFECT)
2. Increase of transmitter release
3. Postsynaptic facilitation of post EPSP

AXOAXONIC SYNAPSE

Question 37

How does presynaptic inhibition work?

Answer 37

GABAergic local interneuron releases GABA into presynaptic neuron. AXOAXONIC SYNAPSE
1. GABAa ionotropic receptor increases Cl- influx, causing hyperpolarization
GABAb metabotropic r. increases K efflux and decreases Ca current
2. Decreased transmitter release
3. Inhibition of postsynaptic EPSP

Question 38

Baclofen

Answer 38

GABA(B)R agonist
Effective in treating spasticity of spinal cord injury and MS.

Question 39

Long-term Potentiation (early)

Answer 39

memory after high frequency stimulation

WHAT HAPPENS POSTSYNAPTIC DURING LTP?
1. NMDAR activation: wave of Ca enters
2. CaMKII activation
Ca and calmodulin cause retrograde (NO, nitric oxide, retrograde neurotransmitter), and tyrosine kinase, and PKC.
3. AMPAR insertion, AMPAR phosphorylation (increased conductance)

Next time the same stimulus is done, there can be more than twice the same postsynaptic EPSP.

Remark:
pre: CA3
post: CA1

Question 40

Later LTP

Answer 40

Synaptogenesis

Question 41

LTP VS sensitization

Answer 41

1. Location: LTP occurs in the CNS (hippocampal).
2. NT: LTP uses glutamate, Sensitization uses serotonin
3. Method of increased postsynaptic EPSP: LTP increases postsynaptic conductance. Sensitization increases presynaptic transmitter release.