Midterm COPY Flashcards
1
Q
What is Necrosis?
A
Premature cell death where cells rupture, spilling their contents into the exracellular space
2
Q
Which type of cell death results in an inflammatory response, which can lead to further distress?
A
Necrosis
3
Q
What is Apoptosis?
A
Programmed cell death, cells are dismantled into membrane-bound vesicles
‘Cell Suicide’
4
Q
What is Acquired Brain Injury (ABI)?
A
Any brain injury that occurs after birth and is not hereditary, congenital, or degenerative
5
Q
What are three possible causes of ABI?
A
- Lack of Oxygen
- Drug toxicity
- Poisoning
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
7
Q
What are three possible causes of TBI?
A
- Concussion (blow to head)
- Blast Injury
- Penetrating Trauma
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
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
10
Q
What is a Contrecoup TBI?
A
When the brain collides with the skull on the opposite side of impact
11
Q
What is a Coup TBI?
A
When the brain collides with the skull on the same side of impact
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
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
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
15
Q
How does Diffuse Axonal Injury (DAI) occur?
A
Twisting and shearing forces cause axons to be torn from cell bodies (axotomy)
16
Q
What is the Energy Crisis faced in TBI?
A
Disrupted blood flow leads to:
Lack of Oxygen (Hypoxia)
Lack of Glucose (Hypoglicemia)
17
Q
What is Excitotoxicity and how does it happen in TBI?
A
Excess Glutamate Release due to rupturing cells (necrosis)
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)
19
Q
ATP is required to make and use _______
_______ is required to make ATP
A
Glucose
Glucose
20
Q
In TBI there is a lack of glucose as a result of decreased _______ flow and _______ production
A
Blood
ATP
21
Q
Hypoglycemia in TBI leads to _______ deficits as neuronal activity _______ after over-excitation
A
Cognitive
Decreases
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
23
Q
What type of cytokines do microglial secrete?
A
Pro-inflammatory Cytokines
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
25
What is Oxidative Stress?
The result of an imbalance of ROS and antiOX
26
What are the effects of TBI in the Frontal Lobe?
Lack of Focus
Irritability
Language difficulty
27
What are the effects of TBI in the Parietal Lobe?
Difficulty with reading
Spatial Misperception
28
What are the effects of TBI in the **Occipital** Lobe?
Blind Spot
Blurred Vision
29
What are the effects of TBI in the **Temporal** Lobe?
Problems with short and long-term memory
30
What the results of TBI in the **Cerebellum**?
Difficulty walking
Slurred speech
31
What are the results of TBI in the **brainstem**?
Changes in breath
Difficulty swallowing
32
What is Immune Privilege?
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
33
How do the innate and adaptive immune systems communicate?
Chemical communication via **Cytokines**
34
What are Cytokines?
Small signalling proteins which act via specific receptors to *coordinate the immune system* and elicit either pro or anti-inflammatory effects
35
What is the Vagus Nerve?
The 10th cranial nerve which contain most of the afferent connection between the CNS and bodily organs
36
What are Paraganglia?
Cells located along the vagus nerve which release Neurotransmitters upon cytokine bonding and send signals to the brain
37
What is a concussion?
A **Mild TBI** which results in a temporary loss of brain function
38
A **concussion** resulting in *alterations of consciousness* most likely affected which brain regions?
Upper Brainstem
Reticular Activating System
39
A **concussion** resulting in *altered neurological function* most likely affected which brain regions?
Corpus Callosum
Anterior Commissure
40
A **concussion** resulting in *headache, dizziness, and fatigue* most likely affected which brain region?
Vascular Injury
41
A **concussion** resulting in *impairments in short-term memory, attention, and concentration* most likely affected which brain regions?
Hippocampus
Frontal Lobe
42
A **concussion** resulting in *changes in mood and emotional function* most likely affected which brain regions?
Amygdala
Basal Forebrain
43
Prior Concussion _______ likelihood of a second concussion and causes greater \_\_\_\_\_\_\_
Increases
Deficits
44
Repeated concussions have _______ effects, even if separated by years
Significant
45
What are some long-term complications which are more likely to occur with multiple concussions?
Loss of long-term memory
Depression
Neurodegenerative Disoders
46
What is Chronic Traumatic Encephalopathy (CTE)?
A progressive degenerative disease found in individuals with a history of multiple concussions
47
What brain changes are seen in a patient with CTE?
Decreased brain weight and enlarged ventricles
Widespread neuronal death
Tau aggregates (tangles of protein) and beta-amyloid plaques
48
What are common symptoms of CTE?
Memory impairments
Erratic behaviors and impulsivity
Depression and suicidal thoughts/behaviour
49
How can we detect CTE?
MRI, EEG
Symptoms inventory, injury evaluation, cognitive tests
50
What arteries do the Brain's blood supply come from?
Common Carotid and Vertebral Arteries
51
What is the **Circle of Willis**
A communication circle at the base of the brain formed by the *common carotid and vertebral arteries*
52
What main arteries of the brain arise from the Circle of Willis?
Anterior Cerebral Artery (ACA)
Middle Cerebral Artery (MCA)
Posterior Cerebral Artery (PCA)
53
What is a stroke?
Interruption of blood flow to the brain
54
What is an Ischemic Stroke?
**Blockage in blood vessels** which leads to *Ischemia* (lack of blood flow to tissue or organ)
80% of strokes
55
What is a **hemorrhagic stroke**?
**Rupture in blood vessel**
20% of strokes but accounts for 40% of all stroke deaths
56
Symptoms and prognosis depend on where stroked occured, _______ and _______ - deficits observed will be specific to affected region
Duration and Severity
57
What is Ataxia?
The result of a **Cerebellar stroke**
Motor impairments and difficulty with walking, balance and coordination
58
Why is blood flow to the brain essential?
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
59
Deposits of _______ in the arteries (Atherosclerosis), which forms plaques, can lead to what? (which can cause a stroke)
Chloresterol
Narrowing of the arteries in the neck or brain
60
A stroke can be caused by certain genetic mutations which can...?
Increase risk of hypercholesterolemia
Damage blood vessel walls
Cause clotting disorders
61
What are some environmental/experiental factors which can cause a stroke?
What are the common link between all of them?
High BP, smoking, obesity, inactivity, trauma, or alcoholism
## Footnote
*Increased inflammation of vessel walls*
62
What is an **Intracerebral Hemorrhagic Stroke** and what does it lead to?
When **blood vessels rupture** and *blood leaks into surrounding brain tissue* which creates *swelling* (edema) and *increased pressure (ICP)*
## Footnote
*Leads to cell death*
63
What are the most common causes of a hemorrhagic stroke and what is the mortality rate?
High blood pressure and aging blood vessels
35% mortality rate
64
What is a **subarachnoid hemorrhage**? What is the most common cause and the mortality rate?
*Bleeding in subarachnoid space*
**Brain Aneurysm** (blood-filled bulge in weakened blood vessel wall)
40-50% mortality rate
65
What is a **Transient Ischemic Stroke**?
A mini-stroke (mild ischemic stroke)
Causes and symptoms are the same as a stroke but only last minutes to hours
66
A TIA leads to a more severe ischemic stroke in \_\_\_\_\_\_\_% of patients
15-30%
67
Why could TIAs potentially be adaptive?
The brain can adapt to things if they occur slowly including lack of oxygen (hypoxia) as a result of lack of blood flow
68
What are the benefits of Ischemic Preconditioning in someone who suffers a global ischemic stroke following a TIA?
Improved neuronal survival
69
What is the treatment for a TIA?
Anti-coagulants (blood thinners) to help prevent blood clotting and larger stroke
70
What is infarction?
Ischemia-induced cell death
71
What is the **core** of a stroke and how is it affected?
*Area directly fed by occluded vessel*
Receives less than 20% of normal blood vessel
Results in *Necrosis* and *Apoptosis*
72
What is the **penumbra** of a stroke and how is it affected?
*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)
73
In a **stroke** how does **Apoptosis** occur?
***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
74
In a **stroke** how does **Necrosis** occur?
**Lack of oxygen** → switch to **anaerobic glucose metabolism** → Acid build-up (**acidosis**) → decreased membrane permeability → Ions and water rush in → **cell swells and ruptures**
75
How does the **Blood Brain Barrier** get damaged in a **stroke**, and how does this effect the immune response?
**Ischemia** → *epithelial cells* weakened (*due to hypoxia and resulting acidosis*) → **reperfusion**, peripheral immune cells leak through → exacerbate immune response and inflammation
76
How do **Micoglia** effect the *inflammatory response* in a **stroke**?
They release pro-inflammatory cytokines
77
What is reperfusion?
When blood flow resumes after a stroke
78
How do *leukocytes* (white blood cells) infilitrate the BBB and what effects do they have on the brain? (Stroke)
Due to the weakened BBB → reperfusion brings leukocytes with it
They release even more inflamamtory molecules, futher compromising stability and impeding recovery
79
How does **Ca2+** effect the brain after a stroke?
**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**
80
What is Collateral Ciruclation?
Blood flow through secondary pathways after the obstruction to the principle pathway occurs
81
In a stroke, survival to the affected region is dependent on?
Degree of vascular obstruction
How quickly obstruction occured
Length of time region is ischemic
**Degree of available collateral circulation**
82
What acute treatment is there for a stroke?
**Tissue Plasminogen Activator** (TPA) - clot buster/dissolver
**Neurothrombectomy** - surgical removal of blood clot
83
What is Neuroplasticity?
The ability of the brain to reorganize and form new connections
84
Following neuronal death and removal of dead tissue after a stroke, nearby, undamaged neurons can _______ to affected area and take over some lost \_\_\_\_\_\_\_
Migrate
Functions
85
What are two forms of Endogenous repair (regrowth) after a stroke?
**Axonal Sprouting** - new connections from surviving neurons
**Angiogenesis** - vascular growth, restores flow of nutrients to affected area
86
What are common motor impairments faced by stroke victims?
Impairment in upper limb use and walking
87
What are common sensory disturbances faced by stroke victims?
Damage to sensory pathways can lead to tingling, numbness, and chronic neuropathic pain
88
What are common cognitive impairment faced by stroke victims?
Memory, learning, and language impairments
Anosognosia
Hemi-Spatial Neglect (right parietal lobe)
89
DNA is packaged into _______ in the cell's nucleus
Chromosomes
90
Humans have _______ pairs of chromosomes
Twenty-Three
91
DNA can be _______ which allows for cell division and \_\_\_\_\_\_\_
Copied
Reproduction
92
What is a Gene?
A **segment of DNA** that *codes* for the **production of specific proteins**
93
Genes are like recipes for \_\_\_\_\_\_\_, they tell the cell how to build them
Proteins
94
What does DNA get wrapped around, what is this called?
DNA gets wrapped around Proteins called **Histones**
**Chromatin** (DNA+Histone)
95
What is an Allele?
A variant (alternative form) of a gene
96
Alleles can be ______ or \_\_\_\_\_\_
Dominant or Recessive
97
Which type of allele only requires one copy to produce a phenotype?
Dominant Allele
98
Which type of allele requires a copy from each parent to produce a phenotype?
Recessive
99
Expression of any trait depends on ______ production
Protein
100
What are the main roles of proteins? (Structural, Enzymatic, and Cell Signalling)
**Structural** - holds cells and tissue together
**Enzymatic** - catalyze reactions and aid in cell metabolism
**Cell Signalling** - Hormone receptors, cytokines, peptide NTs, membrane proteins
101
What is epigenetics?
*Changes in gene expression related to experience*
102
The environment can cause certain genes to be turned on and off by changing accessibility via ______ markers, which ______ or ______ chromatin
Epigenetic
Tighten or Loosen
103
\_\_\_\_\_\_ loosens chromatin, turns on
\_\_\_\_\_\_ tightens chromatin, turns off
Acetylation
Methylation
104
Whats is Huntington's Disease?
A neurodegenerative genetic disorder
105
What type of pattern of inheritance does HD follow?
Autosomal-Dominant (only need one HD allele)
106
When do symptoms typically appear in HD?
Adult onset - 30-40's
107
What is the most commong inherited neurodegenerative disorder? (5-10/100,00)
Huntington's Disease
108
What are some motor symptoms of HD?
Chorea
Occular movements
Clumsiness
Athetosis
Dystonia
109
What is Dystonia?
Persistent and intermittent *muscle contractions* causing abnormal, often repetitive movements or postures
110
What are some Cognitive symptoms of HD?
Restlessness
Agitation/Irritability
Lack of concentration
Short-term memory problems
111
What are some Emotional symptoms in HD?
Depression/Apathy
Anti-social behaviour
Aggression
112
What is the prognosis for HD?
Eventually patient is unable to function independently
Death within 15-20 years of symptom onset
113
What is huntingtin (htt)?
The **protein** which *HD gene codes* for
It is expressed all over in the CNS and peripheral tissue
114
WT htt is expressed and known to be critical during ______ development
Embryonic
115
What codon does HD Gene have a section containing a repeat for?
CAG
116
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?
36-40 repeats = increased risk of HD
\>40 repeats = HD will develop - result in mutant htt
117
What is a mutant htt?
When an HD gene has a section containing over 40 repeats for the codon CAG resulting in a mutant htt protein
118
What does CAG code for?
The AA Glutamine (Gln)
119
What is the result of a multitude of CAG repeats?
*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
HD Pathology is a result of ______ mutant htt function and ______ of WT htt function
Increased
Loss
121
In what area of the brain are neurons most effected in HD?
Basal Ganglia
122
What neurons does HD degeneration observed in the Striatum effect?
**Medium-spiny neurons** (MSNs) of the *caudate nucleus* and *putamen*
MSNs are GABAergic
123
What neurons does HD degeneration in the Cerebral Cortex effect?
**Pyramidal projections neurons**
Neurons with projections to *motor cortex* and *limbic structures*
124
Where are WT htt proteins normally found?
Cytoplasm
125
In HD patients where does mutant htt accumulate?
In the **nucleus** of neurons
Correlated with length of CAG repeats
126
In HD aggregates of protein do not appear to cause cell death, instead what does?
Translocation of aggregates to the nucleus induces pathology
Once localized in the nucleus it appears aggregates form more quickly
127
How do aggregates form in HD?
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
Why is the striatum targeted in HD?
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
What is the main circuit involved in HD?
**Basal Ganglia-Thalamo-Cortical Circuit**
130
How is GABA involved in HD?
Upregulated in early stages of disease followed by marked reduction
Might be initially upregulated to deal with excess Glu
131
In HD, increased unregulated ______ activity + dysfunctional ______ activity in corticostriatal circuit = disruption of integrative processes by \_\_\_\_\_\_
GABA
Glu
MSNs
132
What is Glutamic Acid Decarboxylase (GAD)?
Precursor for GABA, found in BG of HD patients
133
How is Glutamate involved in HD?
Evidence of excitotoxic neuronal death in HD brains
Result from overstimulation of Glu receptors
134
What are Upper motor Neurons?
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
What are Lower Motor Neurons?
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
LMNs can pass through either ______ or ______ nerves
Spinal Nerves - control muscles of limbs and trunk
Cranial Nerves - control muscles of head and neck
137
UMNs release ______ to LMNSs
LMNs release ______ to \_\_\_\_\_\_
Glutamate
ACh to Neuromuscular Junction (NMJ)
138
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
Corticospinal
Limbs and Trunk
Decussate
139
UMNs with axons which project to the brainstem form the ______ tract and control muscles of the ______ and \_\_\_\_\_\_
Some axons ______ and some remain \_\_\_\_\_\_
Corticobulbar tract
Head and Neck
Decussate, Ipsilateral
140
Damage in UMNs results in failure to ______ LMNs
Inhibit
141
Without inhibition LMN keeps telling muscle to \_\_\_\_\_\_, result is ______ contraction that leads to ______ and ______ of muscles (spasticity)
Contract
Sustained
Stiffness and Rigidity
142
What is Hyperreflexia and what motor neuronal damage is it a result of?
Increase in muscle stretch reflex
Upper Motor Neuron damage
143
What is Hyporeflexia and what motor neuronal damage is it a result of?
Decrease in muscle stretch reflexes
Lower Motor Neuron damage
144
With UMN muscle mass is \_\_\_\_\_\_
Preserved
145
Damage to LMNs results in an inability to tell muscle to ______ contracting
Start
146
LMN damage results in no contraction of muscles leading to ______ and \_\_\_\_\_\_
Flaccidity
Atrophy
147
For HD, some genetic components have been identified in \_\_\_\_\_\_\_% of patients
10-15%
148
27 genes for HD have been uncovered so far, usually they cause abnormal ______ production which can lead to protein \_\_\_\_\_\_
Protein
Aggregates
149
What are the mean ages for HD diagnosis?
58-63
150
What does Amyotrpohic Lateral Sclerosis mean?
**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
What does ALS effect?
Upper and Lower motor neurons controlling *voluntary movements* (those controlled by conscious thought)
152
In ALS when motor neurons degenerate they have no way of telling your muscles to \_\_\_\_\_\_
Contract
153
Use it or Lose it - muscles that dot not get used will \_\_\_\_\_\_
Atrophy
154
In ALS muscles are not ______ first - the wires connecting the brain to muscles are ______ and muscles aren't receiving \_\_\_\_\_\_
Dying
Degenerating
Signals
155
What does ALS NOT effect?
Sensation
Heart
Digestion, bladder
Internal organs
Eyes
Cognitive processes
156
Where do symptoms start in ALS?
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
Weakness of respiratory muscles in ALS makes ______ and coughing difficult and poor swallowing control which increases risk of \_\_\_\_\_\_
Breathing
Choking
158
What is the prognosis for ALS?
Death
3 years- 50%
5 years - 80%
8 years - \<8%
159
What treatment is there for ALS?
No cure for ALS
One drug which extends life expectancy 2-3 months - **Riluzole** (blocks sodium channels and decreases Glu)
160
In ALS what does degeneration of UMNs lead to?
Spasms, increased muscle tone, abnormal reflexes
161
In ALS what does degeneration of LMNs lead to?
Muscle atrophy and fasciculations (twitching)
162
How are Astrocytes invovled in ALS?
Astrocytes (which usually protect and nourish motor neurons) **release toxins** which lead to **motor neuronal death** (*Necroptosis* - prgrammed necrosis)
163
What causes Glutamate Excitotoxicity in ALS patients?
Since astrocytes usually help protect neurons from excitotoxicity by reuptaking Glu, decreased levels of these receptors leads to an excess of Glu
164
What is Dementia?
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
Dementia is ______ - symptoms ______ as brain cells die
Progressive
Worsen
166
Memory loss associated with normal aging → ______ neurons
Memory loss associated with dementia → ______ neurons
Dysfunctional
Dying
167
What may resemble mild dementia but is a normal part of aging?
Age-Associated Memory Impairment
168
What is the leading cause of dementia? (60-80% cases)
Alzheimer's
169
Of the top leading causes of death in the US ______ is the only disease which can not be prevented, slowed, or cured
Alzheimer's
170
What is Alzheimer's?
A Neurodegenerative disease following a specific pattern of degeneration
171
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
Sporadic
Familial
172
What is the biggest risk Factor in Alzheimer's?
Age - 50% of cases over 85, only 1% over 65
173
When can Alzheimer's be definitively diagnosed and why?
**After Death**, during autopsy of brain, when patterns of neuronal damage can be clinically assessed in context with exhibited symptoms
174
Where does Degeneration in Alzheimer's begin and where does it spread to?
Begins in the Limbic Structures and spreads to the cortex
175
What are some physical changes in the brain of someone with Alzheimer's?
Brain Atrophies
Gyri get narrower
Sulci get wider
Ventricles enlarge
176
How do beta-amyloid plaques, which form outside cells, affect Alzheimer's?
They can elicit an immune response by glial cells and can deposit near blood vessels, weakening blood vessel walls
177
In Alzheimer's what do Neurofibrillary tangles do?
They lead to dysfunctional axons and cause cells to initiate apoptosis
178
Steps for an Action Potential
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
Refractory Period
Time between when Action Potential starts and membrane potential resets
**Absolute refractory** (-55mv to +30mv) → AP impossible
**Relative refractory** (below -70mv) → AP unlikely
180
Glutamate
Excitatory Neurotransmitter
When it binds to Post-synaptic receptors it causes an influx of positive ions
181
GABA and Glycine
Inhibitory Neurotransmitters
When they bind to post-synpatic receptors they cause an influx of negatively charged ions
182
Saltatory Conduction
Depolarization along axon leaps from node to node
183
Neurotransmitters
Amines - DA, NE, E, 5-HT
Amino Acids - Glu, GABA
Other - ACh
184
Hormones - 5 Principles of Action
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
Hormones vs Neurons
**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
Pituitary
Master Gland
Anterior releases stimulating hormones (ACTH, TSH)
Posterior releases vasopressing and oxytocin
187
HPA Axis
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
Stressor
Stimuli that challenge the body's homeostasis and trigger a response
189
SAM Axis
1. Hypothalamus signals Spinal Cord which activates **Sympathetic Nervous System**
2. SNS projects to **Adrenal Medulla** which releases *Epinephrine and Norepinephrine*
190
Cortisol
Gluccocorticoid hormone which has metabolic and immune effects
191
What causes Excitotoxicity?
TBI → Necrosis - excess Glu due to rupturing cells
Stroke → Neuronal Depolarization
HD & ALS → Decreased Glial reuptake of Glu
Alzheimer's → Atrophy
192
Choroid Plexus
A highly vascular portion of the lining of the ventricles that forms and secretes CSF
193
Dementia
Set of symptoms that are caused by disorders that affect the brain
194
Mild Cognitive Impairment
Memory problems greater than expected for age, but no daily functional impairments observed
195
Prognosis for Alzheimer's?
Fatal within 8-10 years
Cause of death is usually infection
196
Flaccidity
Loss of muscle tony
197
Necroptosis
Programmed Necrosis
198
Infarction
Ischemia-induced cell death
199
Ionotropic Receptor
NT bind directly to receptor and which allows ions into the cell
200
Metabotropic Receptor
NT bind to receptor which causes a G-Protein to activate an ion channel elsewhere in the cell
201
Hippocampal changes from too much stress
Decreased spine density and number of dendrites
Decreased neurogenesis
Impaired negative feedback
202
