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NEUR 1203 > Midterm COPY > Flashcards

Midterm COPY Flashcards

1
Q

What is Necrosis?

A

Premature cell death where cells rupture, spilling their contents into the exracellular space

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2
Q

Which type of cell death results in an inflammatory response, which can lead to further distress?

A

Necrosis

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3
Q

What is Apoptosis?

A

Programmed cell death, cells are dismantled into membrane-bound vesicles

‘Cell Suicide’

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4
Q

What is Acquired Brain Injury (ABI)?

A

Any brain injury that occurs after birth and is not hereditary, congenital, or degenerative

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5
Q

What are three possible causes of ABI?

A
  • Lack of Oxygen
  • Drug toxicity
  • Poisoning
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6
Q

What is Tramautic Brain Injury (TBI)?

A

A sub-category of ABI which includes only damage to brain caused by an external mechanical force

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7
Q

What are three possible causes of TBI?

A
  • Concussion (blow to head)
  • Blast Injury
  • Penetrating Trauma
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8
Q

What is a major cause of death and disability across the world and the number one cause of death in children in youth?

A

Traumatic Brain Injury

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9
Q

How does a TBI occur?

A

When a blow to the head is sufficiently forceful the CSF is unable to protect the brain resulting in a collision of the brain with the skull

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10
Q

What is a Contrecoup TBI?

A

When the brain collides with the skull on the opposite side of impact

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11
Q

What is a Coup TBI?

A

When the brain collides with the skull on the same side of impact

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12
Q

TBI severity depends mostly on degree of _______ force.

How does this occur and what can result from it?

A

Rotational Force

Skull rotates and brain is too slow to catch up

Can result in sheared corpus callosum or torn bridging veins

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13
Q

What happens at the site of contact with skull in a TBI? (The Primary Phase)

A

Swelling (Edema) and Bleeding (Hematoma) which can lead to Inceased Intracranial Pressure (ICP)

Necrotic Death - result of direct impact leading to rupturing of cells

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14
Q

What is Generalized Damage in TBI?

A

Diffuse injury throughout the brain as a result of white and grey matter having different densities and shifting during impact

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15
Q

How does Diffuse Axonal Injury (DAI) occur?

A

Twisting and shearing forces cause axons to be torn from cell bodies (axotomy)

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16
Q

What is the Energy Crisis faced in TBI?

A

Disrupted blood flow leads to:

Lack of Oxygen (Hypoxia)

Lack of Glucose (Hypoglicemia)

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17
Q

What is Excitotoxicity and how does it happen in TBI?

A

Excess Glutamate Release due to rupturing cells (necrosis)

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18
Q

How does Excitotoxicty effect neurons?

A

Glu continously binds to and activates post-synaptic receptors which causes neurons to depolarize and fire leading to influx of Ca2+ and K+

Ca2+ (Calcium) ends up sequestered in mitochondira which disrupts production of ATP and increased production of Reactive Oxygen Species (ROS)

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19
Q

ATP is required to make and use _______

_______ is required to make ATP

A

Glucose

Glucose

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20
Q

In TBI there is a lack of glucose as a result of decreased _______ flow and _______ production

A

Blood

ATP

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21
Q

Hypoglycemia in TBI leads to _______ deficits as neuronal activity _______ after over-excitation

A

Cognitive

Decreases

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22
Q

Lack of Oxygen (Hypoxia) in TBI as a result of decreased blood flow causes a switch to _______ glucose metabolism which can lead to overproduction of _______ _______ (acidosis) which damages BBB

A

Anaerobic

Lactic Acid

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23
Q

What type of cytokines do microglial secrete?

A

Pro-inflammatory Cytokines

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24
Q

What is ROS and what causes it?

A

Reactive Oxygen Species which can lead to DNA damage, protein admage and lipid abnormalities

ROS levels increase during times of environmental stress

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25
Q

What is Oxidative Stress?

A

The result of an imbalance of ROS and antiOX

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26
Q

What are the effects of TBI in the Frontal Lobe?

A

Lack of Focus

Irritability

Language difficulty

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27
Q

What are the effects of TBI in the Parietal Lobe?

A

Difficulty with reading

Spatial Misperception

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28
Q

What are the effects of TBI in the Occipital Lobe?

A

Blind Spot

Blurred Vision

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29
Q

What are the effects of TBI in the Temporal Lobe?

A

Problems with short and long-term memory

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30
Q

What the results of TBI in the Cerebellum?

A

Difficulty walking

Slurred speech

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31
Q

What are the results of TBI in the brainstem?

A

Changes in breath

Difficulty swallowing

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32
Q

What is Immune Privilege?

A

Sites of the body are able to tolerate introduction of foreign substance without eliciting inflammatory response

Brain is not immune privileged due to interaction with peripheral immune system

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33
Q

How do the innate and adaptive immune systems communicate?

A

Chemical communication via Cytokines

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34
Q

What are Cytokines?

A

Small signalling proteins which act via specific receptors to coordinate the immune system and elicit either pro or anti-inflammatory effects

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35
Q

What is the Vagus Nerve?

A

The 10th cranial nerve which contain most of the afferent connection between the CNS and bodily organs

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36
Q

What are Paraganglia?

A

Cells located along the vagus nerve which release Neurotransmitters upon cytokine bonding and send signals to the brain

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37
Q

What is a concussion?

A

A Mild TBI which results in a temporary loss of brain function

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38
Q

A concussion resulting in alterations of consciousness most likely affected which brain regions?

A

Upper Brainstem

Reticular Activating System

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39
Q

A concussion resulting in altered neurological function most likely affected which brain regions?

A

Corpus Callosum

Anterior Commissure

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40
Q

A concussion resulting in headache, dizziness, and fatigue most likely affected which brain region?

A

Vascular Injury

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41
Q

A concussion resulting in impairments in short-term memory, attention, and concentration most likely affected which brain regions?

A

Hippocampus

Frontal Lobe

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42
Q

A concussion resulting in changes in mood and emotional function most likely affected which brain regions?

A

Amygdala

Basal Forebrain

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43
Q

Prior Concussion _______ likelihood of a second concussion and causes greater _______

A

Increases

Deficits

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44
Q

Repeated concussions have _______ effects, even if separated by years

A

Significant

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45
Q

What are some long-term complications which are more likely to occur with multiple concussions?

A

Loss of long-term memory

Depression

Neurodegenerative Disoders

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46
Q

What is Chronic Traumatic Encephalopathy (CTE)?

A

A progressive degenerative disease found in individuals with a history of multiple concussions

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47
Q

What brain changes are seen in a patient with CTE?

A

Decreased brain weight and enlarged ventricles

Widespread neuronal death

Tau aggregates (tangles of protein) and beta-amyloid plaques

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48
Q

What are common symptoms of CTE?

A

Memory impairments

Erratic behaviors and impulsivity

Depression and suicidal thoughts/behaviour

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49
Q

How can we detect CTE?

A

MRI, EEG

Symptoms inventory, injury evaluation, cognitive tests

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50
Q

What arteries do the Brain’s blood supply come from?

A

Common Carotid and Vertebral Arteries

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51
Q

What is the Circle of Willis

A

A communication circle at the base of the brain formed by the common carotid and vertebral arteries

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52
Q

What main arteries of the brain arise from the Circle of Willis?

A

Anterior Cerebral Artery (ACA)

Middle Cerebral Artery (MCA)

Posterior Cerebral Artery (PCA)

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53
Q

What is a stroke?

A

Interruption of blood flow to the brain

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54
Q

What is an Ischemic Stroke?

A

Blockage in blood vessels which leads to Ischemia (lack of blood flow to tissue or organ)

80% of strokes

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55
Q

What is a hemorrhagic stroke?

A

Rupture in blood vessel

20% of strokes but accounts for 40% of all stroke deaths

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56
Q

Symptoms and prognosis depend on where stroked occured, _______ and _______ - deficits observed will be specific to affected region

A

Duration and Severity

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57
Q

What is Ataxia?

A

The result of a Cerebellar stroke

Motor impairments and difficulty with walking, balance and coordination

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58
Q

Why is blood flow to the brain essential?

A

The brain relies on blood supply to get its glucose and oxygen (energy supply)

Four minutes without perfusion can result in permanent cellular damage and functional deficits

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59
Q

Deposits of _______ in the arteries (Atherosclerosis), which forms plaques, can lead to what? (which can cause a stroke)

A

Chloresterol

Narrowing of the arteries in the neck or brain

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60
Q

A stroke can be caused by certain genetic mutations which can…?

A

Increase risk of hypercholesterolemia

Damage blood vessel walls

Cause clotting disorders

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61
Q

What are some environmental/experiental factors which can cause a stroke?

What are the common link between all of them?

A

High BP, smoking, obesity, inactivity, trauma, or alcoholism

Increased inflammation of vessel walls

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62
Q

What is an Intracerebral Hemorrhagic Stroke and what does it lead to?

A

When blood vessels rupture and blood leaks into surrounding brain tissue which creates swelling (edema) and increased pressure (ICP)

Leads to cell death

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63
Q

What are the most common causes of a hemorrhagic stroke and what is the mortality rate?

A

High blood pressure and aging blood vessels

35% mortality rate

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64
Q

What is a subarachnoid hemorrhage? What is the most common cause and the mortality rate?

A

Bleeding in subarachnoid space

Brain Aneurysm (blood-filled bulge in weakened blood vessel wall)

40-50% mortality rate

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65
Q

What is a Transient Ischemic Stroke?

A

A mini-stroke (mild ischemic stroke)

Causes and symptoms are the same as a stroke but only last minutes to hours

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66
Q

A TIA leads to a more severe ischemic stroke in _______% of patients

A

15-30%

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67
Q

Why could TIAs potentially be adaptive?

A

The brain can adapt to things if they occur slowly including lack of oxygen (hypoxia) as a result of lack of blood flow

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68
Q

What are the benefits of Ischemic Preconditioning in someone who suffers a global ischemic stroke following a TIA?

A

Improved neuronal survival

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69
Q

What is the treatment for a TIA?

A

Anti-coagulants (blood thinners) to help prevent blood clotting and larger stroke

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70
Q

What is infarction?

A

Ischemia-induced cell death

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71
Q

What is the core of a stroke and how is it affected?

A

Area directly fed by occluded vessel

Receives less than 20% of normal blood vessel

Results in Necrosis and Apoptosis

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72
Q

What is the penumbra of a stroke and how is it affected?

A

Outskirts of lesion, receive blood flow from other vessels

Receives between 20-40% of normal blood flow

Results in Apoptosis due to Ripple Effect (toxic signalling cascades spilling over from core)

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73
Q

In a stroke how does Apoptosis occur?

A

Lack of glucose → no fuel for Na/K pumps → resting potential of neurons can’t be maintained → cells depolarize → flooding of Glu → cells initiate self-destruct

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74
Q

In a stroke how does Necrosis occur?

A

Lack of oxygen → switch to anaerobic glucose metabolism → Acid build-up (acidosis) → decreased membrane permeability → Ions and water rush in → cell swells and ruptures

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75
Q

How does the Blood Brain Barrier get damaged in a stroke, and how does this effect the immune response?

A

Ischemia → epithelial cells weakened (due to hypoxia and resulting acidosis) → reperfusion, peripheral immune cells leak through → exacerbate immune response and inflammation

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76
Q

How do Micoglia effect the inflammatory response in a stroke?

A

They release pro-inflammatory cytokines

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77
Q

What is reperfusion?

A

When blood flow resumes after a stroke

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78
Q

How do leukocytes (white blood cells) infilitrate the BBB and what effects do they have on the brain? (Stroke)

A

Due to the weakened BBB → reperfusion brings leukocytes with it

They release even more inflamamtory molecules, futher compromising stability and impeding recovery

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79
Q

How does Ca2+ effect the brain after a stroke?

A

Excess Ca2+ (Calcium), as a result of neuronal depolarization, results in production of ROS - in turn Mitochondria can’t deal with this stress and release signals to induce apoptosis

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80
Q

What is Collateral Ciruclation?

A

Blood flow through secondary pathways after the obstruction to the principle pathway occurs

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81
Q

In a stroke, survival to the affected region is dependent on?

A

Degree of vascular obstruction

How quickly obstruction occured

Length of time region is ischemic

Degree of available collateral circulation

82
Q

What acute treatment is there for a stroke?

A

Tissue Plasminogen Activator (TPA) - clot buster/dissolver

Neurothrombectomy - surgical removal of blood clot

83
Q

What is Neuroplasticity?

A

The ability of the brain to reorganize and form new connections

84
Q

Following neuronal death and removal of dead tissue after a stroke, nearby, undamaged neurons can _______ to affected area and take over some lost _______

A

Migrate

Functions

85
Q

What are two forms of Endogenous repair (regrowth) after a stroke?

A

Axonal Sprouting - new connections from surviving neurons

Angiogenesis - vascular growth, restores flow of nutrients to affected area

86
Q

What are common motor impairments faced by stroke victims?

A

Impairment in upper limb use and walking

87
Q

What are common sensory disturbances faced by stroke victims?

A

Damage to sensory pathways can lead to tingling, numbness, and chronic neuropathic pain

88
Q

What are common cognitive impairment faced by stroke victims?

A

Memory, learning, and language impairments

Anosognosia

Hemi-Spatial Neglect (right parietal lobe)

89
Q

DNA is packaged into _______ in the cell’s nucleus

A

Chromosomes

90
Q

Humans have _______ pairs of chromosomes

A

Twenty-Three

91
Q

DNA can be _______ which allows for cell division and _______

A

Copied

Reproduction

92
Q

What is a Gene?

A

A segment of DNA that codes for the production of specific proteins

93
Q

Genes are like recipes for _______, they tell the cell how to build them

A

Proteins

94
Q

What does DNA get wrapped around, what is this called?

A

DNA gets wrapped around Proteins called Histones

Chromatin (DNA+Histone)

95
Q

What is an Allele?

A

A variant (alternative form) of a gene

96
Q

Alleles can be ______ or ______

A

Dominant or Recessive

97
Q

Which type of allele only requires one copy to produce a phenotype?

A

Dominant Allele

98
Q

Which type of allele requires a copy from each parent to produce a phenotype?

A

Recessive

99
Q

Expression of any trait depends on ______ production

A

Protein

100
Q

What are the main roles of proteins? (Structural, Enzymatic, and Cell Signalling)

A

Structural - holds cells and tissue together

Enzymatic - catalyze reactions and aid in cell metabolism

Cell Signalling - Hormone receptors, cytokines, peptide NTs, membrane proteins

101
Q

What is epigenetics?

A

Changes in gene expression related to experience

102
Q

The environment can cause certain genes to be turned on and off by changing accessibility via ______ markers, which ______ or ______ chromatin

A

Epigenetic

Tighten or Loosen

103
Q

______ loosens chromatin, turns on

______ tightens chromatin, turns off

A

Acetylation

Methylation

104
Q

Whats is Huntington’s Disease?

A

A neurodegenerative genetic disorder

105
Q

What type of pattern of inheritance does HD follow?

A

Autosomal-Dominant (only need one HD allele)

106
Q

When do symptoms typically appear in HD?

A

Adult onset - 30-40’s

107
Q

What is the most commong inherited neurodegenerative disorder? (5-10/100,00)

A

Huntington’s Disease

108
Q

What are some motor symptoms of HD?

A

Chorea

Occular movements

Clumsiness

Athetosis

Dystonia

109
Q

What is Dystonia?

A

Persistent and intermittent muscle contractions causing abnormal, often repetitive movements or postures

110
Q

What are some Cognitive symptoms of HD?

A

Restlessness

Agitation/Irritability

Lack of concentration

Short-term memory problems

111
Q

What are some Emotional symptoms in HD?

A

Depression/Apathy

Anti-social behaviour

Aggression

112
Q

What is the prognosis for HD?

A

Eventually patient is unable to function independently

Death within 15-20 years of symptom onset

113
Q

What is huntingtin (htt)?

A

The protein which HD gene codes for

It is expressed all over in the CNS and peripheral tissue

114
Q

WT htt is expressed and known to be critical during ______ development

A

Embryonic

115
Q

What codon does HD Gene have a section containing a repeat for?

A

CAG

116
Q

How many repeats of CAG result in an increased risk of HD, and how many repeats guarantee HD will develop during a normal life span?

A

36-40 repeats = increased risk of HD

>40 repeats = HD will develop - result in mutant htt

117
Q

What is a mutant htt?

A

When an HD gene has a section containing over 40 repeats for the codon CAG resulting in a mutant htt protein

118
Q

What does CAG code for?

A

The AA Glutamine (Gln)

119
Q

What is the result of a multitude of CAG repeats?

A

Many Gln residues linked together (polyglutamine residues) which cause conformational changes in the htt protein reulting in misfolding and toxic protein aggregates in cells

120
Q

HD Pathology is a result of ______ mutant htt function and ______ of WT htt function

A

Increased

Loss

121
Q

In what area of the brain are neurons most effected in HD?

A

Basal Ganglia

122
Q

What neurons does HD degeneration observed in the Striatum effect?

A

Medium-spiny neurons (MSNs) of the caudate nucleus and putamen

MSNs are GABAergic

123
Q

What neurons does HD degeneration in the Cerebral Cortex effect?

A

Pyramidal projections neurons

Neurons with projections to motor cortex and limbic structures

124
Q

Where are WT htt proteins normally found?

A

Cytoplasm

125
Q

In HD patients where does mutant htt accumulate?

A

In the nucleus of neurons

Correlated with length of CAG repeats

126
Q

In HD aggregates of protein do not appear to cause cell death, instead what does?

A

Translocation of aggregates to the nucleus induces pathology

Once localized in the nucleus it appears aggregates form more quickly

127
Q

How do aggregates form in HD?

A

When mhtt is produced the cell knows this is an irregular protein and releases factors to cut these proteins up and dispose of them - unfortunately some of these fragments end up sticking together and creating protein aggregates

128
Q

Why is the striatum targeted in HD?

A

Due to increased susceptibility to excitotoxicity arising from cortical glutamatergic projections - lots of Glu projected to this region, so if the cells are compromised we are at higher risk of excitotoxic events

129
Q

What is the main circuit involved in HD?

A

Basal Ganglia-Thalamo-Cortical Circuit

130
Q

How is GABA involved in HD?

A

Upregulated in early stages of disease followed by marked reduction

Might be initially upregulated to deal with excess Glu

131
Q

In HD, increased unregulated ______ activity + dysfunctional ______ activity in corticostriatal circuit = disruption of integrative processes by ______

A

GABA

Glu

MSNs

132
Q

What is Glutamic Acid Decarboxylase (GAD)?

A

Precursor for GABA, found in BG of HD patients

133
Q

How is Glutamate involved in HD?

A

Evidence of excitotoxic neuronal death in HD brains

Result from overstimulation of Glu receptors

134
Q

What are Upper motor Neurons?

A

Motor Neurons which originate in the motor cortex or brainstem and have axons which extend to LMNs

Tell LMNs to carry start or stop signals to muscles

May act directly or through interneurons

135
Q

What are Lower Motor Neurons?

A

Motor Neurons which originate in the brainstem or spinal cord

Axons leave the CNS and synapse onto muscles at the Neuromuscular Junction

Receive signls from UMNs and tell muscles to contract

136
Q

LMNs can pass through either ______ or ______ nerves

A

Spinal Nerves - control muscles of limbs and trunk

Cranial Nerves - control muscles of head and neck

137
Q

UMNs release ______ to LMNSs

LMNs release ______ to ______

A

Glutamate

ACh to Neuromuscular Junction (NMJ)

138
Q

UMN’s with axons which synapse at LMNs in the spinal cord form the ______ tract and control muscles of the ______ and ______

Most axons ______ at the medulla

A

Corticospinal

Limbs and Trunk

Decussate

139
Q

UMNs with axons which project to the brainstem form the ______ tract and control muscles of the ______ and ______

Some axons ______ and some remain ______

A

Corticobulbar tract

Head and Neck

Decussate, Ipsilateral

140
Q

Damage in UMNs results in failure to ______ LMNs

A

Inhibit

141
Q

Without inhibition LMN keeps telling muscle to ______, result is ______ contraction that leads to ______ and ______ of muscles (spasticity)

A

Contract

Sustained

Stiffness and Rigidity

142
Q

What is Hyperreflexia and what motor neuronal damage is it a result of?

A

Increase in muscle stretch reflex

Upper Motor Neuron damage

143
Q

What is Hyporeflexia and what motor neuronal damage is it a result of?

A

Decrease in muscle stretch reflexes

Lower Motor Neuron damage

144
Q

With UMN muscle mass is ______

A

Preserved

145
Q

Damage to LMNs results in an inability to tell muscle to ______ contracting

A

Start

146
Q

LMN damage results in no contraction of muscles leading to ______ and ______

A

Flaccidity

Atrophy

147
Q

For HD, some genetic components have been identified in _______% of patients

A

10-15%

148
Q

27 genes for HD have been uncovered so far, usually they cause abnormal ______ production which can lead to protein ______

A

Protein

Aggregates

149
Q

What are the mean ages for HD diagnosis?

A

58-63

150
Q

What does Amyotrpohic Lateral Sclerosis mean?

A

A-Myo-Trophic - No Muscle Nourishment

Lateral - Area in spine where brain tells muscle what to do

Sclerosis - Hardening: as disease progresses lateral areas harden and signals stop

151
Q

What does ALS effect?

A

Upper and Lower motor neurons controlling voluntary movements (those controlled by conscious thought)

152
Q

In ALS when motor neurons degenerate they have no way of telling your muscles to ______

A

Contract

153
Q

Use it or Lose it - muscles that dot not get used will ______

A

Atrophy

154
Q

In ALS muscles are not ______ first - the wires connecting the brain to muscles are ______ and muscles aren’t receiving ______

A

Dying

Degenerating

Signals

155
Q

What does ALS NOT effect?

A

Sensation

Heart

Digestion, bladder

Internal organs

Eyes

Cognitive processes

156
Q

Where do symptoms start in ALS?

A

Weakness in the arms and legs

Loss of arm function usually occurs first with sporadic forms of ALS, while loss of leg function ususally occurs first with familial forms of ALS

157
Q

Weakness of respiratory muscles in ALS makes ______ and coughing difficult and poor swallowing control which increases risk of ______

A

Breathing

Choking

158
Q

What is the prognosis for ALS?

A

Death

3 years- 50%

5 years - 80%

8 years - <8%

159
Q

What treatment is there for ALS?

A

No cure for ALS

One drug which extends life expectancy 2-3 months - Riluzole (blocks sodium channels and decreases Glu)

160
Q

In ALS what does degeneration of UMNs lead to?

A

Spasms, increased muscle tone, abnormal reflexes

161
Q

In ALS what does degeneration of LMNs lead to?

A

Muscle atrophy and fasciculations (twitching)

162
Q

How are Astrocytes invovled in ALS?

A

Astrocytes (which usually protect and nourish motor neurons) release toxins which lead to motor neuronal death (Necroptosis - prgrammed necrosis)

163
Q

What causes Glutamate Excitotoxicity in ALS patients?

A

Since astrocytes usually help protect neurons from excitotoxicity by reuptaking Glu, decreased levels of these receptors leads to an excess of Glu

164
Q

What is Dementia?

A

A set of symptoms which are caused by disorders of the brain - including: memory loss, problems thinking, problem-solving and with language as well as changes in mood and behavior

165
Q

Dementia is ______ - symptoms ______ as brain cells die

A

Progressive

Worsen

166
Q

Memory loss associated with normal aging → ______ neurons

Memory loss associated with dementia → ______ neurons

A

Dysfunctional

Dying

167
Q

What may resemble mild dementia but is a normal part of aging?

A

Age-Associated Memory Impairment

168
Q

What is the leading cause of dementia? (60-80% cases)

A

Alzheimer’s

169
Q

Of the top leading causes of death in the US ______ is the only disease which can not be prevented, slowed, or cured

A

Alzheimer’s

170
Q

What is Alzheimer’s?

A

A Neurodegenerative disease following a specific pattern of degeneration

171
Q

90-95% of cases of Alzheimer’s are ______ (late onset) and causes are not understood, while only 5-10% of cases are ______ (early onset) involving a dominant gene that speeds up progression of disease

A

Sporadic

Familial

172
Q

What is the biggest risk Factor in Alzheimer’s?

A

Age - 50% of cases over 85, only 1% over 65

173
Q

When can Alzheimer’s be definitively diagnosed and why?

A

After Death, during autopsy of brain, when patterns of neuronal damage can be clinically assessed in context with exhibited symptoms

174
Q

Where does Degeneration in Alzheimer’s begin and where does it spread to?

A

Begins in the Limbic Structures and spreads to the cortex

175
Q

What are some physical changes in the brain of someone with Alzheimer’s?

A

Brain Atrophies

Gyri get narrower

Sulci get wider

Ventricles enlarge

176
Q

How do beta-amyloid plaques, which form outside cells, affect Alzheimer’s?

A

They can elicit an immune response by glial cells and can deposit near blood vessels, weakening blood vessel walls

177
Q

In Alzheimer’s what do Neurofibrillary tangles do?

A

They lead to dysfunctional axons and cause cells to initiate apoptosis

178
Q

Steps for an Action Potential

A
  1. Depolarization → Threshold of -55mv reached → Na+ ions rush into cell → membrane potential rises to +30mv
  2. Repolarization → At +30mv, Na+ channels close and K+ channels open → K+ rushes OUT → Cell becomes more negative
  3. Hyperpolarization → too much K+ leaves and mebrane potential drops below -70mv → Na/K+ pumps reset concentrations
179
Q

Refractory Period

A

Time between when Action Potential starts and membrane potential resets

Absolute refractory (-55mv to +30mv) → AP impossible

Relative refractory (below -70mv) → AP unlikely

180
Q

Glutamate

A

Excitatory Neurotransmitter

When it binds to Post-synaptic receptors it causes an influx of positive ions

181
Q

GABA and Glycine

A

Inhibitory Neurotransmitters

When they bind to post-synpatic receptors they cause an influx of negatively charged ions

182
Q

Saltatory Conduction

A

Depolarization along axon leaps from node to node

183
Q

Neurotransmitters

A

Amines - DA, NE, E, 5-HT

Amino Acids - Glu, GABA

Other - ACh

184
Q

Hormones - 5 Principles of Action

A
  1. Act in gradual fashion
  2. Change probability or intensity of behavior
  3. Have reciprocal relationship with behavior
  4. May have multiple effects
  5. Often show pulsatile pattern of release
185
Q

Hormones vs Neurons

A

Neurons → Hormones

Local → Distant

Fast → Slow

Voluntary → Involuntary

Precise → Imprecise

Both: Produced and stored in neurons or glands and released upon stimulation, bind to receptors to stimulate target cells

186
Q

Pituitary

A

Master Gland

Anterior releases stimulating hormones (ACTH, TSH)

Posterior releases vasopressing and oxytocin

187
Q

HPA Axis

A
  1. Stress stimulates Hypothalamus which releases CRH
  2. CRH stimulates Anterior Pituitary which releases ACTH
  3. ACTH stimulates Adrenal Cortex which releases Cortisol
  4. Cortisol induces metabolic changes
  5. Negative feedback tells hypothalamus to shut off stress response
188
Q

Stressor

A

Stimuli that challenge the body’s homeostasis and trigger a response

189
Q

SAM Axis

A
  1. Hypothalamus signals Spinal Cord which activates Sympathetic Nervous System
  2. SNS projects to Adrenal Medulla which releases Epinephrine and Norepinephrine
190
Q

Cortisol

A

Gluccocorticoid hormone which has metabolic and immune effects

191
Q

What causes Excitotoxicity?

A

TBI → Necrosis - excess Glu due to rupturing cells

Stroke → Neuronal Depolarization

HD & ALS → Decreased Glial reuptake of Glu

Alzheimer’s → Atrophy

192
Q

Choroid Plexus

A

A highly vascular portion of the lining of the ventricles that forms and secretes CSF

193
Q

Dementia

A

Set of symptoms that are caused by disorders that affect the brain

194
Q

Mild Cognitive Impairment

A

Memory problems greater than expected for age, but no daily functional impairments observed

195
Q

Prognosis for Alzheimer’s?

A

Fatal within 8-10 years

Cause of death is usually infection

196
Q

Flaccidity

A

Loss of muscle tony

197
Q

Necroptosis

A

Programmed Necrosis

198
Q

Infarction

A

Ischemia-induced cell death

199
Q

Ionotropic Receptor

A

NT bind directly to receptor and which allows ions into the cell

200
Q

Metabotropic Receptor

A

NT bind to receptor which causes a G-Protein to activate an ion channel elsewhere in the cell

201
Q

Hippocampal changes from too much stress

A

Decreased spine density and number of dendrites

Decreased neurogenesis

Impaired negative feedback

202
Q
A

NEUR 1203 (9 decks)

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