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Neuro Exam 2 - JLJ > Chemical Messengers and Excitotoxicity > Flashcards

Chemical Messengers and Excitotoxicity Flashcards

1
Q

What are the 3 things that are vital to our normal function?

A

EAA neurotransmitter system, calcium, and oxygen

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2
Q

When does over-stimulation of the EAA system occur?

A

After ischemia in the brain; responsible for damage to neurons whether or not they were exposed to the ischemia

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3
Q

What are some things that over-stimulation of the EAA system is implicated in?

A

Strokes, global hypoxia/anoxia, traumatic injury to the brain, hypoglycemia, and epilepsy

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4
Q

What is step 1 in excitotoxicity?

A

Depolarization of the membrane

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5
Q

Describe step 1 in excitotoxicity?

A

Starts with a localized event (stroke)

1) Immediate loss of blood flow
2) Within 4 minutes, O2 levels drop to 0 near mitochondria and ATP production ceases
3) Na/K ATPase activity drops quickly
4) Causes depolarization of neuronal cell membrane

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6
Q

What is step 2 in excitotoxicity?

A

Action potentials

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7
Q

Describe step 2 in excitotoxicity?

A

As neurons depolarize, they reach threshold and the voltage-gated sodium channels open, leading to action potentials

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8
Q

What is step 3 in excitotoxicity?

A

Releasing the EAA

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9
Q

Describe step 3 in excitotoxicity?

A

Once action potentials reach presynaptic terminal, release of the neurotransmitter into the cleft occurs; because so many synapses in the cortex use EAA, this results in a lot of EAA being released into many different parts of the brain

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10
Q

What is the uptake of EAA dependent on?

A

Secondary active transport of Na

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11
Q

What is step 4 in excitotoxicity?

A

Increasing calcium levels in the post-synaptic cell

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12
Q

Describe step 4 in excitotoxicity?

A

Many synapses express both non-NMDA and NMDA receptors; activation of the non-NMDA produces the depolarization that will force the Mg out of the Ca channel, allowing Ca to enter the post-synaptic cell

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13
Q

What are the consequences of high intracellular calcium? What does this cause?

A

1) Increase in phospholipase A activity
2) Activation of u(mu)-calpain
3) Activation of calcineurin
4) Activation of the apoptotic pathway

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14
Q

Describe what happens when there is an increase in phospholipase A activity

A

Acts on membrane to release arachidonic acid and causes physical damage to the membrane; arachidonic acid release leads to Ca release from ER and mito, unfolded protein response (ER stops making proteins), eIF2a-kinase activation, and mitochondrial dysfunction

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15
Q

Describe what happens when u(mu)-calpain is activated

A

Proteolysis of structural proteins including spectrin, proteolysis of other enzymes and proteins including eIF4G; leads to metabolic and structural impairment of neurons

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16
Q

Describe what happens when calcineurin is activated

A

Leads to excess production of nitric oxide (NO) via activation of nitric oxide synthase (NOS)

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17
Q

Describe what happens when the apoptotic pathway is activated

A

Results as a consequence of the previous steps, particularly the release of Ca from intracellular stores; mitochondria release enzymes including caspase 9; caspase 9 release leads to activation of caspase 3, which is pro-apoptotic

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18
Q

Repurfusion (bringing back oxygen) sounds like a good idea after this has taken place, however the mitochondria have released many of their enzymes, impairing their ability to use oxygen to make ATP. So, what happens to the oxygen that is brought in?

A

Results in production of free radicals; some mitochondria may be able to synthesize ATP but a different set of proteins are now active compared to the healthy state

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19
Q

The ATP that is able to be produced in this unhealthy state, what happens to it?

A

Kinases take ATP -> ADP + PO4

Leads to phosphorylation which further modifies enzyme action; phosphorylation of eIF2a kinase leads to a further decrease in protein synthesis and further activates caspase 3, which further increases apoptotic signaling

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20
Q

What is an ionotropic receptor?

A

Receptor is associated with an ion channel that opens in response to the binding of the neurotransmitter

Also called ligand-gated ion channel

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21
Q

What is a metabotropic (serpentine) receptor?

A

Binding of neurotransmitter to the receptor activates a 2nd messenger system

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22
Q

What are the 2nd messenger systems and what do they do?

A

Gs: stimulates adenylate cyclase

Gi: inhibits adenylate cyclase

Gq: production of DAG and IP3 (think calcium release from intracellular stores)

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23
Q

What are EPSPs and IPSPs?

A

EPSP: excitatory post-synaptic potential; depolarizes cell membrane

IPSP: inhibitory post-synaptic potential; hyperpolarizes cell membrane

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24
Q

What neurotransmitters are part of the monoamines group?

A

Epinephrine, norepinephrine, dopamine, serotonin, histamine

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25
Q

Where do you find norepinephrine? Epinephrine?

A

Norepi: locus ceruleus, pontine/medullary areas, wakefulness/alertness

Epi: medulla

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26
Q

Where are epinephrine, dopamine, and norepinephrine derived from?

A

Tyrosine

27
Q

What moves norepi and epi into the vesicles? What inhibits this process?

A

Moved into vesicles by VMAT1 and VMAT2; inhibited by reserpine, which leads to synaptic failure

28
Q

What receptors do epi and norepi bind to?

A

alpha and beta adrenergic

29
Q

Where do you find dopamine?

A

Basal ganglia, hypothalamus, limbic system, and cortex

30
Q

What breaks down dopamine and serotonin?

A

MAO and COMT

31
Q

Where do you find serotonin?

A

Hypothalamic and limbic systems, cerebellum, brainstem, and raphe nuclei

32
Q

Where is serotonin derived from?

A

Tryptophan

33
Q

Where is histamine found?

A

Tuberomammillary nucleus of hypothalamus

34
Q

Where is histamine derived from?

A

Histidine

35
Q

What breaks down histamine?

A

Diamine oxidase and COMT

36
Q

Where is acetylcholine found?

A

Striatum of basal ganglia, midbrain, and pons

37
Q

What is acetylcholine synthesized from?

A

Choline and acetate

38
Q

What receptors do acetylcholine bind to?

A

Muscarinic and nicotinic

39
Q

What are the inhibitory amino acids?

A

GABA and glycine

40
Q

What is GABA critical in?

A

Consciousness, motor control, and vision (retina)

41
Q

What is GABA synthesized from?

A

Glutamate

42
Q

What removes GABA and glycine from the synapse?

A

GAT proteins

43
Q

Where is glycine found?

A

Spinal cord and medulla

44
Q

Where are the purines (ATP, ADP, adensoine) found?

A

Virtually everywhere, but special mention to cortex, cerebellum, hippocampus, and basal ganglia

45
Q

What are considered opioids?

A

Endorphins, enkephalins, dynorphins, and nociceptin

46
Q

What is the function of the opioids?

A

Modification of nociceptive inputs and mood

47
Q

What are endorphins derived from?

A

Proopiomelanocortinin (POMC)

48
Q

What are enkephalins derived from?

A

Pro-enkephalin

49
Q

What are dynorphins derived from?

A

Pro-dynorphin

50
Q

What is nociceptin derived from?

A

Orphanin FQ

51
Q

What breaks down opioids?

A

Enkephalinase and aminopeptidiase

52
Q

What are the endocannabinoids?

A

Anandamide and 2-arachidonylglycerol (2AG)

53
Q

Where are the endocannabinoids found?

A

Basal ganglia, spinal cord, cortex, hippocampus, and hypothalamus

54
Q

What is anandamide derived from?

A

N-arachidonoyl phosphatidyl ethanol

55
Q

What is 2-arachidonylglycerol derived from?

A

Arachidonoyl-containing phosphatidyl inositol bis-phosphate

56
Q

What are the excitatory amino acids?

A

Glutamate and aspartate

57
Q

What receptors do EAA bind to?

A

NMDA and non-NMDA receptors

58
Q

What are the modulatroy sites on the NMDA receptors?

A

Glycine, PCP, and Mg2+ binding sites

59
Q

What are the non-NMDA receptor types?

A

AMPA and kainate

60
Q

What do NMDA and non-NMDA receptors function in?

A

NMDA: short and long-term memory

non-NMDA: primary sensory afferents and UMNs

61
Q

What are the neural functions of nitric oxide?

A

Long-term potentiation of memory in hippocampus and cerebellum; also cariovascular and respiratory control in pons and medulla

62
Q

What are the non-neural functions of nitric oxide?

A

Immunological and cardiovascular functions

63
Q

What are the cons of nitric oxide?

A

Very unstable, leads to production of free radicals, and it is toxic to neurons in high concentrations

Neuro Exam 2 - JLJ (16 decks)

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