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Chemical Messengers And Excitotoxicity Flashcards

1
Q

What are the presynaptic channels?

A

Presynaptic voltage gated gated calcium channels

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2
Q

What do presynaptic voltage gated calcium channels do?

A

Allows calcium to come in and bind at docking proteins

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3
Q

What are inotropic receptors?

A

Ligand gated ion channel

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4
Q

What are metabotropic receptors?

A

Activated G protein

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5
Q

What are IPSPs?

What is this assoc. w/?

A

Small, localized hyperpolarizations

Chloride entry

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6
Q

What are EPSPs?

What is this assoc. w/?

A

Small, localized depolarization

Assoc.w/ Na or Ca entry

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7
Q

What is temporal summation?

Where does it occur?

A

Multiple IPSPs or EPSPs elicited from DIFFERENT synapses

Post synaptic cells

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8
Q

What is spatial summation?

A

Multiple IPSPs and EPSPs elicited from REPETITIVE activation at the SAME synapse

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9
Q

What happens when a cell reaches threshold?

A

An action potential occurs

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10
Q

What kind of receptor is a

Nicotinic cholinergic R.?

A

Ligand gated ion channel (ionotropic)

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11
Q

How many subunits does a nicotinic cholinergic r. Have?

A

5 subunits

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12
Q

What does a ligand binding a nicotinic cholinergic r. Do?

A

Ligand binds —> conf. Change in pore —> allows ions to enter

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13
Q

What causes the selectively of nicotinic cholinergic rs?

A

Charge of AAs that make up the pore

Size of the pore

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14
Q

What are metabotropic receptors also known as?

A

Serpentine

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15
Q

What codes for metabotropic receptors?

A

1 gene

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16
Q

What produces the variations in metabotropic receptors?

A

Post translational modifications

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17
Q

Have many membrane spanning domains do metabotropic receptors ahve?

A

7

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18
Q

How do metabotropic exert post synaptic effects?

A

Via 1 or more secondary messengers

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19
Q

What are the 2 major types of G proteins associated w/ intracellular domain of metabotropic Rs?

A

Gs

Gi

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20
Q

What do Gs proteins do?

A

Activate adenylate cyclase

Increase production of cAMP from ATP
CAMP interacts with PKA
PKA phosphorylates downstream targets and changes activities

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21
Q

What effects can Gs have?

A

Have effects on protein synthesis at level of gene due to existence of CREB

(cyclic amp response element binding protein)

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22
Q

What does Gi do?

A

Inhibit adenylate cyclase

Decrease cAMP and PKA activation

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23
Q

What does Gq do?

A

Activate phospholipase C

Creates IP3 and DAG

IP3 activates Ca release

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24
Q

What will Ca do?

A

Calcium influences cellular functions

Calcium can work with DAG and activate protein kinase C —> further phosphorylates other proteins

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25
Q

What is the Jak-Stat pathway?

A

Receptors with tyrosine kinase that activates its dimer when a ligand binds

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26
Q

What will activation of Jack stat pathway cause?

A

Active dimer activates associated kinase and autophosphorylates the receptor

then phosphorylates STAT protein

STAT dimerizes and goes to nucleus

Activates synthesis of various proteins

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27
Q

What does retrograde transport cause for rabies?

A

The 1-3 mo. Long incubation period fo rabies

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28
Q

What are the requirements for NTRs?

A

Neuron making NTR had proper machinery

NTR is released in a chemically or pharmacologically identifiable form

Exogenous application of NTR reproduces post-syn. Effects

Blocking receptor for chemical will block effects of activating pre-synaptic neuron

Mechanism for termination exists

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29
Q

What is the cholinergic system?

Where is it prevalent at?

A

Any synapse that uses ACh

Peripheral nervous system

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30
Q

What uses the cholinergic system?

A

Alpha motor neurons at NMJ

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31
Q

What is cholinergic input critical for?

What could damage cause?

A

To being conscious

Comatose state or development of Alzheimer’s diseae

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32
Q

Where do we see ACh as a NTR in the PNS?

A 
NMJ
Autonomic preganglionic synapses
Parasym. Post-g fibers
Symp post-g fibers to sweat glands/muscles
Amacrine cells in retina
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33
Q

Where do we see ACh as a NTR in the CNS?

A

Striatum

Brainstem arousal

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34
Q

How is acetylcholine made?

A

Acetate CoA + choline

Via choline acetyltransferase

Gives: acetylcholine

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35
Q

What move ach into vesicles for a controlled release?

A

Vesicular ACh transporter protein (VAChT)

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36
Q

How do you break down ACh?

A

Acetylcholinesterase hydrolyzes ACh back to acetate and choline

Choline recycled by presynaptic cell
Acetate diffuses away

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37
Q

What are the receptors of the cholinergic system?

A

Muscarine

Nicotinic

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38
Q

What activates the muscarine receptors for smooth muscle cells and glands?
What blocks it?

A

Muscarine

Atropine

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39
Q

What are the 5 types of muscarine receptors linked with?

A

G proteins

M1 - Gq
M2 - Gi
M3 - Gq
M4 - Gi
M5 - Gq
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40
Q

Where are M1 Rs?

What do they do?

A

Post -g neurons of ans, broadly distributed

Increase IP3, DAG, Ca

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41
Q

Where are M2 Rs?

What do they do?

A

Decrease cAMP —> increase K conductance —> hyperpolarization

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42
Q

Where are M3 Rs?

What do they do?

A

Smooth muscle of bronchi and vasculature

Will increase IP3 and DAG

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43
Q

Where are M4 Rs?

What do they do?

A

Presynaptic autoreceptors

Control ACh release in Striatum of basal ganglia for motor control

Decrease adenylate cyclase —> decrease cAMP

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44
Q

Where are M5 Rs?

What do they do?

A

Cerebral vasculature
On basal ganglia dopaminergic neurons

For motor controls

Increase IP3 and DAG

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45
Q

What are the 2 subdivisions of nicotinic receptors?

A

NMJ

Neuronal

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46
Q

How many subunits make up a nicotinic receptor?

A

5 subunits each from a different genes

Can be homo or heteromeric

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47
Q

What is the make up of fetal NMJ AChRs?

A

2 alpha
Beta
Gamma
Sigma

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48
Q

What i the make up of adult NMJ AChRs?

A

2 alpha
Beta
Gamma
Epsilon

The changed subunit allows for more sodium entry and thus a larger conductance

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49
Q

What do high ca conductance or neuronal NMJ AChRs. Contribute to?

Are these metabotropic or ionotropic?

A

Ionotropic

Learning and memory

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50
Q

What are all the NTRs in the monoamine system from?

A

Created by modifying AAs

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51
Q

What are the catecholamines of the monoamine system?

A

Epi
NE
Dopamine

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52
Q

What are the 5 NTRs making up the Monoamine system?

A 
Epi
NE
Dopamine
Serotonin
Histamine
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53
Q

What is epi, NE, and dopamine all derived from?

A

Tyrosine

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54
Q

How do you synthesize catecholamines?

A

‣ Tyrosine + tyrosine hydroxylate**—> L-DOPA
= rate limiting step

‣ L-DOPA + L-DOPA decarboxylase —> Dopamine

‣ Dopamine + enzymes(assoc. w/ intracellular vesicular membrane) —> NE

• NE actually synthesized within vesicles

‣ NE leaves vesicle + Phylethanolamine-N-Methyl-transferase (PNMT)*** —> Epi

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55
Q

What 4 major pathways use Dopamine?

A
  1. Substantia nigra dopaminergic pathway
  2. Mesolimbic dopaminergic pathway
  3. Mesocortical dopaminergic pathway
  4. Tuberinfundibular pathway
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56
Q

What is the role of dopamine?

What is damage assoc. with?

A

Role in producing pleasure and addiciton

Parkinson’s disease

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57
Q

What is the Mesolimbic dopaminergic pathway?

What could alteration of this pathway cause?

A

From ventral tegmental area to nucleus accumbens

Core of pleasure/reward pathways in brains

Addiction

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58
Q

Where is NE found within the CNS?

A

Locus ceruleus in upper brainstem (Pons)

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59
Q

What is the role of NE?

A

Waking us up (!!!!!) and awareness

Produces inhibition of msucle activity that occurs during REM sleep

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60
Q

Where is Epi mostly used?

A

Used as hormone released by adrenal medulla

Not really used in the CNS

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61
Q

How are catecholamines stored?

A

Via vesicular monoamine transporters (VMATs) catecholamines are moved into vesicle where they will be stored

(And where NE will be created)

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62
Q

Where is VMAT 2?

A

Neuronal form found in any neuron that releases monoamines

VMAT 1 found in adrenal medulla

63
Q

What do NE and E bind to ?

A

Alph and beta adrenergic Rs which are mediated by 2nd messenger system

64
Q

What is the second messenger system associated with alpha 1, 2 ,and betas?

A

Alpha 1 - Gq
Alpha 2 - Gi
Beta 1,2,3,- Gs

QISSS

65
Q

What is the receptor for dopamine?

A

Dopaminergic receptors with differerent subtypes D1-5

66
Q

Where do we find high concentrations of receptors D1 and D2?

What are they involved in?

A

In regions of brain innervated by substantia nigra

Involved in normal control of motion and emotion

67
Q

How are catecholamines removed?

A

Dopamine, NE and E are all removed via

High affinity uptake protein then enzymatic destruction by MAO or COMT

68
Q

What is serotonin derived froM?

A

Tryptophan

69
Q

Where is serotonin found in brainstem?

A

Raphe nuclei

70
Q

What is serotonin for?

A

Critical in mood

71
Q

How is serotonin synthesized?

A

‣ Typtophan + tryptophan hydroxylase —> Rate limiting step

amt. of Trypt. Available and activity level of enzyme determines amt. of serotonin)

‣ ___ + 5-HT Decarboxylase —> serotonin

72
Q

Where are seronergic neurons in the CNS?

A

Midline raphe nuclei use serotonin as NTR in CNS

73
Q

Serotonin from midline raphe nuclei control what?

What could disruption cause?

A

Attention and mood

Depression

74
Q

What are serotonergic receptors associated with?

A

All associated with G proteins

EXCEPT 5-HT-3

75
Q

what is the only ionotropic serotonergic receptor?

What is it assoc. w?

A

5-HT 3

Opens sodium channel

Assoc. w/ chemotactic trigger zone in medulla

76
Q

What is the role of 5-HT6?

A

High affinity for several anti-depressants

77
Q

What is the role of 5-HT2c?

A

Controlling normal body weight and preventing seizures

78
Q

How is serotonin removed?

A

Taken up and metabolized by MAO

79
Q

What is histamine derived from?

A

Histidine

80
Q

What i the role of Histamine

A

Waking you up (!!!!)

81
Q

What wakes you up?

What keep you awake?

A

Norepinephrine

Histamine

82
Q

Where is histamine made and released in the CNS?

A

By neurons of tuberomammillary body/nucleus in the posterior thalamus

83
Q

What are the purines that serve as NTRs?

A

ATP
AMP
Adenosine

84
Q

What do purine NTRs bind to?

A

Purinergic receptors

85
Q

What purine is linked to sensation of sleepiness/fatigue?

A

Adenosine

86
Q

Where is caffeine an antagonist at?

A

Adenosine receptors

87
Q

How are purine NTRs removed?

A

Via adenosine Deaminase

Converted to inosine and removed via circulation

88
Q

Where does adenosine bind?

A

P1 receptor

89
Q

What is the function of adenosine?

A

Sleep induction

Feedback inhibition for atp release

90
Q

What are the 5 groups of peptides that bind opioid receptors?

A 
Endorphins
Enkephalins
Dynorphins
Endomorphins
Nociception
91
Q

What are opioids associated with?

All except which one?

A

Pain relief

Except for nociceptin

92
Q

Where are opioid NTRs located?

A

Striatum
Hypothalamus

Periaqueductal gray
Nucleus parabrachialis
Raphe nuclei (serotonin also here!)

93
Q

What is the pre-cursor to dynorphins?

Where are they found?

A

Prodynophrins

hypothalamus
Thalamus
Brainstem
Retina

94
Q

What will nociceptin produce?

A

Produces pain

95
Q

What are the 3 receptors of opioid NTRs?

A

Mu
Kappa
Delta

96
Q

What does the Mu opioid receptor produce when activated?

A

Analgesia
Respiratory depression
Euphoria

97
Q

What does the Kappa opioid receptor produce when activated?

A

Analgesia

Dysphoria

98
Q

What does the Delta opioid receptor produce when activated?

A

Analgesia

99
Q

All of the opioid receptors are paired with what and cause what?

A

Gi

Cause inhibition of adenylyl cyclase

Mu- increases k out = hyperpolarization

Kappa and Delta = decrease Ca in

100
Q

What are the 2 ligands that bind cannibinoid receptors?

A

Anandamide

2-arachidonoylglycerol

101
Q

What is the endocannibinoid system assoc. with?

A

Pain relief actions

Control of hunger and energy balance
May produce neuroprotection

102
Q

What blocks the uptake of endocannabinoids?

A

Acetaminophen

103
Q

How is anandamide and 2-AG metabolized?

A

Cyclooxygenase

Lipooxygenase

104
Q

What does the CB-1 receptor bind?

A

Anandamide and 2AG

105
Q

What does CB2 preferentially bind ?

A

2-AG

106
Q

What is the production of NO tied to?

A

Activation of excitatory AA receptor - NMDA

107
Q

What are inhibitory AAs?

A

Glycine

GABA

108
Q

How do inhibitory AAs enact their actions?

A

Open Cl channel and produce hyperpolarization of membrane

109
Q

What is the major inhibitory AA of the brain?

A

GABA

110
Q

Where does benzodiazepene work to produce sensation?

A

GABA Receptors

111
Q

What are the major EAAs in the brain?

A

Glutamate

Aspartate

112
Q

What is the role of EAAs?

A

Sensory processing
Memory formation
Learning
Motor control

113
Q

What do EAA Receptors allow for?

A

Allow ca to enter cell

114
Q

What is excess activation of the EAA system associated with?

A

Neuronal damage via excitotoxicity

115
Q

What is GABA made from?

A

Glutamate + GAD

116
Q

Where is gaba localized? Glycine?

A

GABA - cerebellum and cortex, and retina

Glycine: Spinal cord mostly

117
Q

What has the most extra-synaptic receptors? Why?

A

GABA

Bc it is the most inhibitory and will hyperpolarized neurons non specifically for sedation

118
Q

For the EAA system, what is the role of glycine and glutamine?

A

Glutamine forces Mg off the receptor allowing for docking to occur and glycine is needed for the channel to work:)

119
Q

What is the majority of atp created by neurons used for?

A

To drive Na/K ATPase pump to help maintain RMP

120
Q

What happens is oxygen or glucose to the brain is blocked?

What could cause blockage potentially?

A

No ATP = no maintenance of RMP = depolarization of brain = AP for a short period of time with NTR release

Stroke, drowning, cardiac arrest

121
Q

What will the depolarization of the brain inadvertently cause?

A

Will produce APs

Release NTRs (EAAs)

Xs activation - xc Ca entering = Ca binds enzymes and changes activity

122
Q

What can huge amounts of calcium entering a post synpatic cell cause?

A

Will bind enzymes and change activity

Lead to production of NO

Release arachidonic acid damaging membrane

Hydrolyzed proteins

Activate apoptotic enzymes

123
Q

What are the receptors for EAAs?

Metabotropic or ionotropic?

A

NMDA
non-NMDA

Both ionotropic

124
Q

What do NMDA receptors do?

What binding sites do they have?

A

Open channel for Ca to enter (and Na)

Glycine
Zinc
PCP
MG

125
Q

What binding side of NMDA receptors is needed to have an Epsp occur?

A

Glycine

126
Q

What does the PCP binding site of NMDA receptors do?

A

Blocks calcium current from inside the channel

127
Q

What does the Mg binding site of NMDA receptors do?

A

Inside the channel and blocks it

128
Q

What needs to be removed from a NMDA receptor in order for an epsp it occur?

A

Mg

129
Q

What are two non-NMDA receptors for EAAs?

A

AMPA r.

Kainate R.

130
Q

How are EAAs removed?

A

By astrocytes and neurons

Can use Na dependent 2ndary active transport
High affinity system
Loss of Na gradient

131
Q

What is Rasmussuen’s encephalopathy?

What receptor is it assoc. w?

A

Severe intractable seizures that develop in a child and can cause brain damage that destroys one hemisphere of the brain

NMDA r.

132
Q

How is production of NO tied to activation of the EAA receptor NMDA?

A

NMDA will allow calcium in

Lead to calcineurin activation which will cleave a phosphate group from NOS activating it

NOS + arginine = NO

133
Q

What are the actions of nitric oxide?

A

Induce guanylyl cyclase and form cGMP

CGMP will relax smooth muscle, change presynaptic neuron for long term potentiation or depression

134
Q

What are the roles of NO?

A

Major controller of cerebral vasculature bc it dilates vasculature

135
Q

How is NO removed from the synpase?

A

No uptake mechanisms bc it is too lipid soluble

Hemoglobin could potentially bind but not likely

136
Q

What is the only rate limiting factor of NO?

A

It’s half life (5 seconds)

137
Q

What kinds of brain damage is excitotoxicity linked to?

A

Domoic acid poisoning from contaminated muscles

Hypoxia or anoxia

Cerebral ischemia/stroke

Mechanical trauma to the CNS

Hypoglycemia

138
Q

What is the sequence of events for excitotoxicity?

A
  1. Ischemic insult
  2. Increased intracellular calcium
  3. Activation of enzymes by calcium
  4. Deranged cellular metabolism
  5. Induction of apoptotic pathways
139
Q

What happens as a result of ischemic insult?

A

Rapid reduction in ATP levels leading to cell depolarizaiton, release of NTRs, activation of Non-NMDA and NMDA receptors, further increase of EAA concentration in synapse

140
Q

What happens once NMDA receptors are activated by the ischemic insult?

A

Allow xs calcium into cell and voltage gated calcium channels to open

141
Q

After the ischemic insult activates NMDA and that increases intracellular calcium,
What effects does calcium have?

A

Activates

Phospholipase A2
Calcineurin —> NO
Mu-Calpain(protease)

Maybe enzymes for an apoptotic cycle

142
Q

What happens as a result of enzyme activation from calcium?

Concerning phospholipase

A

Phospholipase will act on cell membranes

Release arachidonic acid

Act on intracellular organelles to cause more Ca release
organelles will malfunction (ER will unfold and activate kinases)

143
Q

What happens as a result of enzyme activation from calcium?

Concerning mu-calpain

A

Mu-calpain

Damages structural and functional proteins within the cell and inhibits protein synthesis

144
Q

What happens as a result of enzyme activation from calcium?

Concerning calcineurin

A

Activates NOS

Produces xc NO

145
Q

How are apoptotic pathways induced during excitotoxicity?

A

High Ca will disrupt the mitochondrial membrane

Releases cyto c and caspase 9

Activates caspase 3 —> major proteolytic enzyme associated w/ apoptosis

146
Q

What happens when one tries to restablish blood flow following an ischemic insult?

A

Reperfusion injury

147
Q

What happens in a reperfusion injury?

A

Blood gives oxygen to tissues
Neurons take it up and mito. Uses it to make atp
But leftover is made into peroxide radicals

Peroxide radicals damage lipids, membranes, organelles

Blood also delivers blood borne chemicals

148
Q

During a reperfusion injury what are the blood borne chemicals being reintroduced into the brain?

A

Epinephrine - further depolarizes cell and activates PKA

White blood cells- further calcium influx

Growth factors - no funct. Organelles to respond to this

149
Q

What happens as a result of calcium activating calcineurin which makes excess NO?

A

NO will cause vasodilation and smooth muscle relaxation

Allows for influx of fluid into damaged areas and causes EDEMA

Increased ICP - blood flow compromised - tonsillar and uncal herniations can develop

150
Q

What are some treatments for excitotoxicity?

A

Block EAA neurotransmission

Prevent influx of WBC

Uptake Ca

Free radical scavenger

151
Q

What are the 2 important things concerning excitotoxicity?

A

Time (cascade initiated too quickly)

Scope of treatments (not wide enough)

(Also drugs that would be delivered via blood cannot happen bc of ischemic event)
(Cells are damaged and cannot respond to drug)

152
Q

Denervation hypersensitivity occurs when the alpha–motoneuron innervating skeletal muscle is transected. The muscle cell begins to respond to any acetylcholine, whether it is at the neuromuscular junction or not.

What is the mechanism for this response?

A

When there is no synaptic activity, Nicotinic cholinergic R. At motor end plate is released

migrates away and may come into contact with Ach from non neural sources

becomes activated and produces AP/contraction in sk. M. In absense of intention

appear as twitches or fasciculations of muscle rather than organized contractions

153
Q

What contributes to the variations in processes seen after an ischemic event?

A

Genetic difference of non-NMDA and NMDA receptors that change amt. of cations entering the cell

Depressants in s system can lead to better neurological outcomes

154
Q

How do systemic hypothermia and induced comas improve neurological outcomes/survival of people who have different brain injuries?

A

Metabolism by neurons is decreased

Reduced o2 demand
Decreased APs = decreased NTR
Decreased enzyme activity (caspases)

Can use Valium (benzodiazepene) to activate GABA and produce inhibitory effects in brain or act on non-NMDA AMPA receptors to reduce flow thru them and allow for less Na and Ca in cell (hyperpolarizing)

.. (19 decks)

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