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COM: Neuro - Exam 2 > Lecture 15: Chemical Messengers & Excitotoxicity > Flashcards

Lecture 15: Chemical Messengers & Excitotoxicity Flashcards

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1
Q

What are the functions of NO?

A

Long-term potentiation and memory

Cardiovascular and respiratory control

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2
Q

How can NO be very toxic?

A

It leads to the production of free radicals which can kill invading bacteria or other cells

**There is no reuptake mechanism for NO bc it has a half life of 5 sec

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3
Q

Opioid peptide NTs is a class of NTs based on 4 precursor molecules, what are they?

A

Prosencephalon -> met-enkephalin, leu-enkephalin
Pro-opiomelanocortinin (POMC) -> beta-endorphins
Prodynorphin -> leu-enkephalin, dynorphin
Orphanin FQ AKA nociceptin

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4
Q

What is the enzyme that converts NE to epi?

A

Phenylethanolamine N-Methyltransferase (PNMT)

KNOW

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5
Q

How is the action of GABA limited?

A

Reuptake

Catabolism by GABA-transaminase

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6
Q

What are the functions of Histamine in the brain?

A

Waking

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7
Q

What are the 2 subtypes of the non-NMDA receptor for excitatory AAs?

A

AMPA

Kainate

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8
Q

What is the function of endocannibinoids?

A

Modulation of pain

Neuroprotection

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9
Q

Where do you find glycine as a NT>

A

Spinal cord
Brainstem
Forebrain (less than GABA)

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10
Q

AMPA is an exogenous agent that can open only what type of channels?

A

Non-NMDA receptors for excitatory AAs

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11
Q

What is the central location of dopamine?

A

Basal ganglia

VTA

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12
Q

Ach is stored in _________ vesicles and moved not these vesicles by the _________________transporter

A

Clear; vesicular Ach transporter protein (VAchT

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13
Q

What functions are NMDA receptors important for?

A

Long term changes in synaptic strength
Learning
Memory

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14
Q

What is the major excitatory system in the CNS?

A

The excitatory AA system

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15
Q

What are the indirect ion effects of the kappa and delta type opioid peptide NT receptors?

A

Decrease calcium

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16
Q

What is the central location of histamine?

A

Hypothalamus

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17
Q

Explain the mu type receptors for opioid peptide NTs

A

Serpentine receptor important for analgesia (pain relief), respiratory depression, euphoira, sedation, constipation (alters water reabsorption in gut)

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18
Q

What receptor type contains a binding site for benzodiazepines?

A

GABAa ionotropic receptor -> benzodiazepine binds and potentiates the effects which are Cl- influx causing hyperpolarization of the cell

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19
Q

What muscarinic receptor type is found on cerebrovasculature and dopaminergic neurons of the basal ganglia and what type of signaling cascade does it initiate?

A

M5; increased IP3/DAG

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20
Q

During an ischemic event intracellular levels of Ca2+ dramatically increases. One of the consequences of this is the activation of the apoptotic pathway. How does this happen?

A

The disruption of mito and ER function further increases free cytosolic Ca2+. As mito membranes are disrupted they release Cytochrome C and caspase 9. Once caspase 9 is release, it activates caspase 3 which is a proteolytic enzyme that activates the apoptotic pathway

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21
Q

What excitatory AA is the NT in the visual cortex and pyramidal cells?

A

Aspartate

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22
Q

What is glutamate made from?

A

Alpha-ketoglutarate

**Metabolic and NT pools strictly separated

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23
Q

What are the indirect ion effects of mu type opioid peptide NT receptors?

A

Increase K efflux and hyperpolarize the cell

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24
Q

How do NMDA and non-NMDA receptors work together?

A

the excitatory AA binds to the non-NMDA receptor causing Na+ influx which depolarizes the membrane, therefore displacing the Mg2+ from the downstream NMDA receptor and allowing that channel to open

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25
Explain the delta type opioid peptide NT receptors
Serpentine receptors that produce analgesia (pain relief)
26
The NMDA receptor for excitatory AAs has multiple modulators sites with binding site for Mg2+. What isthe role of Mg2+?
It blocks the channel -> at physiological conditions Mg2+ blocks the channel; the cell must depolarize for Mg2+ to leave
27
What type of receptor is utilized by GABAa and what does this cause?
Ionotropic receptor with 5 su This causes the opening of Cl- channels initiating Cl influx and hyperpolarizing the cell
28
What are the general functions of opioid peptide NTs?
Modification of nociceptive inputs (neurophysiology of pain) Modification of mood/affect (limbic system)
29
How is the action of the opioid peptide NTs limited?
Enzymatic, possibly after uptake -> enkephalinase A &B, aminopeptidase
30
What are the general functions of glycine as a NT?
Mediates many spinal inhibitors (reflexes and their modification)
31
During an ischemic event intracellular levels of Ca2+ dramatically increases. One of the consequences of this is the activation of mu calpain (protease). What does this cause?
proteolysis of spectrin leading to more structural damage Proteolysis of eIF4G stopping protein synthesis Also causes further metabolic impairment
32
Non-NMDA receptors for excitatory AAs is similar to the NMDA receptor in the fact that has almost exclusive post-synaptic expression. Non-NMDA receptors allow the influx of what ion?
Sodium (some very small amounts of calcium too)
33
What is the central location of NE?
Pons/brainstem
34
During an ischemic event, there is excessive excitatory NT release leading to widespread NMDA actvation and massive Ca2+ influx. What does the increased intracellular [Ca2+] initiate?
Activation of phospholipase A2 Activation of calcineurin (phosphatase) Activation of mu-calpain (Protease) Activation of the apoptotic pathway
35
The NMDA receptor for excitatory AAs has multiple modulators sites with binding site for PCP. What is the role of PCP?
It binds inside the channel (internal to Mg2+ site) and blocks the channel
36
What are the functions of serotonin in the brain?
Mood | Wakefulness
37
How is GABA made?
Glutamate decarboxylase (GAD) GABA derivative = glutamate **Need to know this enzyme
38
Excitotoxicity is proposed to explain continuing neuronal death after an ischemic event. Why is this?
This is due to oxygen deprivation, causing cells unable to meet metabolic needs to depolarize causing excessive excitatory AA release and the reuptake of these is Na dependent but the Na/K pump is not functional so these excitatory AAs cant be taken up causing massive activation of the NMDA receptor and substantial Ca2+ influx into surrounding cells
39
WHat are the functions of the metabotropic receptors for excitatory AAs?
Learning Memory Motor systems
40
What are the 3 different receptor types that opioid peptide NTs bind to?
Mu, kappa, and delta receptors
41
How are opioid peptide NTs made?
Since peptide, coded and created via DNA/RNA/protein synthetic machinery
42
Where are endocannabinoids located within the CNS?
They have a broad distribution -> hippocampus (memory formation), basal ganglia (affect/motor), spinal cord (modulation of nociceptin), neocortex
43
What is the central location of epi?
Brainstem
44
What is the main inhibitory NT in the Spinal cord?
Glycine
45
What is the NMDA receptor for excitatory AAs activated by?
The exogenous agent N-methyl-D-Aspartate; also glutamate and aspartate
46
Explain GABAb receptors
Serpentine receptors which are heterodimer G proteins (Gq and Gi) -> causes decreased adenylyl cyclase leading to increased K+ efflux, as well as decreased IP3/DAG leading to decreased Ca2+ influx End result = hyperpolarization
47
What types of neurons release excitatory AA NTs that bind to non-NMDA receptors?
Primary afferents and premotor neurons (UMNs)
48
What are the inotropic receptors for serotonin in the brain?
5HT3 (vomiting)
49
Explain ionotropic versus metabotropic NT receptors
Ionotropic = fast; increase conductance to certain ions by binding to ligand gated channels. NT binding induces rapid conformational change allowing ion influx Metabotropic = slow; act to alter membrane properties via a second messanger system such as GCPR
50
``` ***Which of the following is produced almost exclusively in the midline raphe nuclei? A. Dopamine B. Epinephrine C. NE D. Histamine E. Serotonin ```
E. Serotonin **Anytime you hear midline raphe nuclei think serotonin
51
The NMDA receptor for excitatory AA has multiple modulators sites with binding site for what 3 things?
Glycine Mg2+ PCP
52
What are the 2 inhibitory AAs?
GABA (gamma-amino-butyric acid) | Glycine
53
What is the pathway for the synthesis of catecholamines without the enzyme?
Phe -> L-Tyr -> L-Dopa -> Dopamine -> NE -> Epi
54
Explain the glycine recetor
Ionotropic, pentamer Alpha su = glycine binding Beta su = structural A chloride channel -> hyperpolarizes the cell
55
What muscarinic type is the neuronal muscarinic receptor and what type of signaling does it initiate?
M1; increased IP3/DAG via Gq coupled protein receptor -> increase in Ca2+
56
What is the role of excitatory AA NTs in the release of NO?
excitatory AAs bind to NMDA receptors causing influx of Ca2+ -> Ca2+ binds to calcineurin which activates nitric oxide synthase (NOS) -> NOS catalyzes the reaction which creates NO and citrulline from arginine
57
Nicotinic receptors are ____________ and allow for ______ entrance, although some neuronal forms allow for significant ______ influx
Inotropic; Na+; Ca2+
58
During an ischemic event intracellular levels of Ca2+ dramatically increases. One of the consequences of this is the activation of phospholipase A2. What does this cause?
Lots of arachidonate is released from the membrane causing physical damage to the membrane The arachidonate acts on ryanodine receptor on ER causing release of Ca2+ from IC stores including the ER and mitochondria -> this causes the unfolded protein response** (stops making protein) in the ER and impaired function in the mito
59
Name the 2 endcocannabinoids
Anandamide -> arachidonic acid + ethanolamine 2-arachidonylglycerol -> arachidonic acid esterified into the middle positon of glycerol
60
What does aspartate come from and what AA is it commonly found with
From Oxaloacetate and often found with glutamate
61
What enzyme is responsible for the catabolism of Ach and where is it found?
Acetylcholinesterase -> bound to the postsynaptic cell membrane
62
The AMPA non-NMDA receptor has a _________________ site inhibiting the response to the NT and therefore inhibiting the influx of _______
Benzodiazepine; Na+
63
__________ oxidizes “stuff and is used in the metabolism of catecholamines. It has 2 isoforms and is a common target for drugs prescribed for neuropsychiatric disorders
MAO (Monoamine oxidase)
64
What are the ionotropic versus metabotropic receptors for GABA?
Ionotropic receptors = GABAa Metabotropic = GABAb
65
What blocks the glycine receptor?
Strychnine
66
List the opioid peptide NTs
Endorphins Enkephalins Dynorphins Nociceptin
67
Where is GABA located?
Cerebellum Cortex Retina **found higher up in the brain -> this is different from glycine which is found lower
68
Activation of NMDA receptors for excitatory AAs leads to epsp which has a ________ onset with ___________ duration
Slow; prolonged They show longer latency -> time to remove Mg and longer duration -> Ca2+ slower
69
What are the 3 excitatory AAs?
Glutamate Aspartate Taurine
70
What are the functional roles of GABA?
Major inhibitory NT in the higher CNS Critical for producing consciousness/awareness Control of voluntary motion
71
How do neurons and glia get rid of excitatory AA NTs?
A high affinity Na+ dependent secondary active transport -> Glia convert glutamate to glutamine (inactive) and release it into ECF, then neurons take glutamine up and convert it back to glutamate (recycle)
72
List the NT’s that are peptides coded for by genes
``` Tachykinins (includes substance P) Opioids Somatostatin CCK CGRP ```
73
What is the central location of serotonin?
Brainstem (raphe nucleus)
74
What are the 2 types of ionotropic receptors for excitatory AAs?
The NMDA receptor and the non-NMDA receptors
75
What NT is responsible for the control of voluntary motion and initiation of REM sleep?
Ach
76
What are the functions of NE and epi in the brain?
Wakefulness
77
__________ is the predominant mechanism for inactivation of epinephrine released by the adrenal medulla but its also present in the CNS
COMT (Catechol-O-methyltransferase)
78
The NMDA receptor for excitatory AAs has multiple modulators sites, one of which is for glycine. What is its role?
Its a co-agonist! Glycine alone cant open the channel but it must be bound for the channel to open when the excitatory NT binds
79
When the NMDA receptor for excitatory AAs is activated, it allows the influx of what ion?
Ca2+
80
During an ischemic event intracellular levels of Ca2+ dramatically increases. One of the consequences of this is the activation of calcineurin (phosphatase). What does this cause?
Activates NOS increasing NO synthesis -> starts acting on cerebral vasculature (causes vasodilation) causing swelling
81
Explain the kappa type opioid peptide NT receptors
Serpentine receptors that produce analgesia (pain relief), diuresis, mitosis, and dysphoria (different from mu type that cause euphoria)
82
What are the functions of dopamine in the brain?
Motor control Pleasure Consciousness
83
A large number of GABA receptors have been found at extra-synaptic locations throughout the cortex. They appear to be activated by free-floating GABA. These are mostly what type of GABA receptor?
GABAa receptors
84
Opioid peptide NT receptors are all _____________ receptors and inhibit ________________
Serpentine; adenylyl cyclase
85
What is the enzyme that converts L-tyrosine to L-dopa?
Tyrosine hydroxylase **KNOW**
86
What muscarinic receptor type is the presynaptic autoreceptor found on the striatum of the basal ganglia and what type of signaling does it initiate?
M4; decreases cAMP levels via Gi
87
What is the location of the opioid peptide NTs?
Hypothalamus and medulla
88
Explain the CB-1 receptor for endocannabinoids
Axons and presynaptic terminals of EAA and GABA synapses Gi coupled protein receptor Reduced NT release Binds to either anandamide or 2-AG well
89
Explain the CB-2 receptor for endocannabinoids
Found in the brain (microglia, not neurons) Immune system and gut Anti-inflammatory In brain, cause macrophages to remove beta-amyloid

COM: Neuro - Exam 2 (19 decks)

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