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Bio 1A > Midterm 3 - Physiology > Flashcards

Midterm 3 - Physiology Flashcards

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1
Q

another name for adrenaline

A

epinephrine

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2
Q

how is adrenaline produced? and what effects does it have?

A

sensory organs –> signaling in brain activates “fight or flight mode”

  • -> pituitary gland releases chemical signals to the adrenal gland
  • -> adrenal gland releases adrenaline
  • -> adrenaline binds to pacemaker cells in the heart, increasing heart rate
  • -> adrenaline binds to muscle cells –> contract
  • -> adrenaline binds to cells surrounding the blood and can cause constriction or dilation to control blood supply
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3
Q

cell signaling involves ligands and receptors. What are ligands? receptor proteins? signal transduction?

A

Ligand - signaling molecule
receptor proteins - bind to ligands
signal transduction - pathway which signal is converted to cellular responses

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4
Q

a generic signal transduction pathway is consisted of 3 steps:

A
  1. reception
  2. transduction
  3. response
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5
Q

4 types of cell signaling in animal cells:

A
  1. endocrine (long, blood circulation needed)
  2. paracrine (nearby, local mediator)
  3. synaptic (nervous system, synapse)
  4. contact-dependent (physical contact required)
  5. autocrine (self-signaling)
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6
Q

GTP-binding proteins (G-proteins) activation and deactivation

A

Signal switches GDP in G-proteins for ATP, thus switching on the G-proteins
Signal out, ATP hydrolyzed, G-proteins switched off

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7
Q

GPCR signaling through G-proteins

G-protein-coupled receptor

A
  1. inactive G-proteins and GPCR
  2. ligand and G-proteins bind to GPCR –> activated GPCR –> GTP/GDP exchange on G-proteins
  3. tranduction of G-protein to enzyme (ligand falls off) –> cellular response
  4. hydrolysis of ATP to ADP, inactivation
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8
Q

basic unit of gustatory system (taste)

A

pipallae (sing. papilla)

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9
Q

signal transduction during bitter taste

A
  1. bitter tastant –> taste GPCR –> G proteins
  2. G proteins interact with phospholipase C –> IP3
  3. IP3 receptor –> Ca2+ conc increases in cells
  4. releases ATP as neurontransmitters –> brain
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10
Q

protein phosphorylation - protein activation and deactivation

A

signal in –> protein phosphorylated by protein kinase
signal –> phosphate removed by protein phosphotase
(add Pi on serine/threonine/tyrosine)

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11
Q

receptor tyrosine kinase (RTK) signaling

A
  1. inactive RTK proteins
  2. signal binds to RTK proteins, dimerization occurs
  3. tyrosine on RTK proteins get phosphorylated
  4. relay proteins take phosphate off tyrosines –> cell response by activated relay proteins
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12
Q

what is genomic equivalence?

A

all cells in the body derive from a single cell and have the same genetic material

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13
Q

what is development?

A

events in changing from a single to a more complex form

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14
Q

4 subprocesses in development

A
  1. cell division
  2. differentiation
  3. morphogenesis
  4. patterning
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15
Q

what is cell differentiation

A

potential fates become more limited until a cell is committed to its fate

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16
Q

cell fate differentiation

A

cells become more specialized in structure and function

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17
Q

molecular basis of cell fate determination

A
  1. differential inheritance of cytoplasmic determinants (asymmetric cell division)
  2. cell-cell communication
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18
Q

what are stem cells?

A
  1. capable of continued division

2. give rise to differentiated cells

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19
Q

degrees of determination:

A
  1. totipotent - give rise to any tissue in a organism (embryo and extra-embyronic)
  2. pluripotent - give rise to all cells in the adult
  3. multipotent - give rise to limited number of cells
  4. unipotent - give rise to only a single cell type
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20
Q

embryonic stem cells and adult stem cells have different degrees of determination

A

embryonic stem cells - pluripotent

adult stem cells - multipotent or unipotent

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21
Q

what are the feeder cells for embryonic stem cells

A

fibroblasts

secreting signaling molecules/growth factors important for stem cell growth, differentiation, and survival

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22
Q

C. elegans vulva forming cell fate determination experiment approach

A
  1. isolate mutants with no vulva
  2. map and sequence of mutated genes
  3. identified growth factor and receptor
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23
Q

epidermal growth factor (EGF) and its receptor (EGFR) in vulva cell fate

A
  1. anchor cell secretes EGF
  2. activates EGF receptor
  3. high EGF promotes primary fate (P6 cells)
  4. lower EGF promotes secondary fate (P5 or P7 cells)
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24
Q

both EGF and NGF receptors are what kind of receptors?

A

receptor tyrosine kinases (RTK)

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25
Q

what causes type I diabetes

A

loss of insulin producing beta cells

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26
Q

what kind of receptor is insulin receptor? and its general pathway?

A

RTK

also insulin receptor activated –> insulin response protein activated –> glucose converted into glycogen

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27
Q

what does fertilization happen?

A
  1. sperm penetrates the protective layer around the egg
  2. receptors on the egg surface bind to molecules on the sperm surface
  3. changes at the egg surface prevent polyspermy, the entry of multiple sperm nuclei into the egg
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28
Q

what is the acrosomal reaction?

A

the acrosomal reaction is triggered when the sperm meets the egg

  1. when the sperm comes in contact with the egg, the acrosome at the tip of the sperm fuses, releasing hydrolytic enzymes
  2. the enzymes digest the protective coat of the egg
  3. sperm-binding receptors bind to the sperm, driving the reaction that allows the sperm to fuse with the membrane
  4. signaling cascade increases the Ca2+ concentration in cell
  5. fertilization envelop forms, all receptors leave the surface of the egg
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29
Q

how is egg activated by signaling cascade? and why is calcium wave important?

A
  1. sperm binding stimulates PLC (phospholipase C)
  2. PLC cleaves phospholipid –> DAG, IP3 (diacyl glycerol, inositol trisphosphate)
  3. IP3 binds to IP3 receptor (on endoplasmic reticulum)
  4. ER increases Ca2+ concentration in cell
  5. fusion of nuclei, cell division resumes, fertilization envelope
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30
Q

which step comes after cleavage?

A

cleavage, a period of rapid cell division without growth

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31
Q

in cytoplasm, one large cell is cleaved into smaller cells called?

A

blastomeres

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32
Q

what is blastula? what is blastocoel?

A

blastula is a monolayer ball of cells with a fluid-filled cavity called a blastocoel

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33
Q

what is the step that comes after cleavage?

A

morphogenesis -
generation of ordered form and structure
from blastula to 3 germ layers (gastrulation)

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34
Q

what are the 3 embryonic germ layers

A
  1. ectoderm
  2. mesoderm
  3. endoderm
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35
Q

cell fate of ectoderm

A
  1. epidermis (skin)

2. nervous and sensory system

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36
Q

cell fate of mesoderm

A
  1. skeletal and muscular systems

2. circulatory and lymphatic systems

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37
Q

cell fate of endoderm

A
  1. organs

including the digestive track and associated organs

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38
Q

what is patterning?

A

establishing the coordinate system of the body

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39
Q

coordinate system of the body

A
  1. dorsal/ventral
    (dorsal fate of cells –> nervous system)
  2. anterior/posterior (heads and tails)
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40
Q

patterning by chemical inducers - dorsal/ventral axis

A

ectoderm (nervous system + skin/epidermis)
dorsal lip of blastopore –> neural tube (paracrine)
1. dorsal lip secretes BMP (a signaling molecule)
2. BMP binds to a RTK –> protein phosphorylation
3. phosphorylated proteins translocate into the nucleus, acting as a transcription factor
4. expression of genes which determines cell fate

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41
Q

what are homeotic mutations?

A

the appearance of entire body part in the wrong location

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42
Q

homeotic mutations are in which gene clusters?

A

homeobox (Hox) gene clusters

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43
Q

what does Hox gene clusters regulate transcription?

A

Homeotic genes encode for DNA-binding proteins that regulate transcription, acting as transcription factors

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44
Q

How are Hox genes related to anterior-posterior patterning?

A

physical positions of Hox genes are related to different parts along the anterior-posterior axis

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45
Q

How do the star-nosed moles find food?

A

By touch (texture sensors)

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46
Q

levels of organization

A

cell –> tissue –> organ –> organ system

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47
Q

what is tissue? and what 4 types of tissues are there?

A

Tissues are collections of cells that perform similar functions and held together by extracellular material (cell-cell junctions)
connective, epithelial, muscle, nervous

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48
Q

What 2 kinds of cells make up nervous tissue?

A

neurons and glia cells

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49
Q

What are the 4 functions of nervous tissue?

A
  1. sensory input
  2. control of muscles and glands
  3. homeostasis
  4. mental activity
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50
Q

What are the 3 types of muscle tissues?

A
  1. skeletal (striated) - voluntary control, moves skeleton
  2. smooth - form walls of organ and surround blood vessels
  3. cardiac: found in the heart (like striated muscles)
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51
Q

is bone a connective tissue? is blood a connective tissue? what is adipose? and is it connective tissue?

A

YES AND YES

fat and yes

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52
Q

what is epithelial tissue?

A

covers the outside of the body and lines the organ and cavities within the body

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53
Q

what is special about epithelial cells?

A

they are polarized!
apical surface facing lumen (outside of organs, exposed to air or fluid)
basal surface

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54
Q

what are organs?

A

2 or more primary tissues organized to perform a function

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55
Q

what are the 5 vital organs?

A

the brain, the heart, the liver, the lungs, and the kidney

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56
Q

layers of organs

A
  1. epithelial layer
  2. connective tissues
  3. smooth muscle
  4. connective tissues
  5. epithelial layer
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57
Q

what are organ systems?

A

collections of organs that perform related functions essential to survival

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58
Q

what are the 11 organ systems?

A

nervous, muscular, endocrine, circulatory, excretory, digestive, respiratory, immune, skeletal, integumentary, reproductive

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59
Q

2 systems that regulate body functions? and their characteristics and differences?

A
  1. endocrine system (transmits chemical signals called hormones to receptive cells throughout the body vid BLOOD; many targets, depending on the presence of receptors; hormones are relatively slow acting, but can have long lasting effects)
  2. nervous system (transmits information between specific locations; target depends on signal’s pathway; nervous signal transmission is very FAST)
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60
Q

difference between negative feedback and positive feedback

A

negative feedback: maintaining homeostasis

positive feedback: promote rapid changes

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61
Q

animals:

temperature regulators vs. temperature conformers

A

homeotherms

poikiltherms

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62
Q

animals:

generate heat by metabolism vs. gain heat from external sources

A

endothermic (active at greater range of external T)

ectothermic (tolerate greater variations in internal T)

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63
Q

5 adaptations help animals thermoregulate

A
  1. insulation (hair, blubber)
  2. evaporative heat loss (sweating, panting)
  3. behavioral responses
  4. circulatory adaptations
  5. adjusting metabolic heat production (hibernation)
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64
Q

1 insect example of behavioral thermoregulation adaptation

A

shivering –> increase body temperature

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65
Q

1 animal example of circulatory thermoregulation adaptation

A

countercurrent exchange (in fins and legs)

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66
Q

how is temperature regulated in humans?

A

hypothalamus
1. body temperature increases: cooling mechanism activated –> sweating, blood vessels dilation
2. body temperature decreases: heating mechanism activated –> shivering, blood vessels constriction
NEGATIVE FEEDBACKS

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67
Q

how is temperature set point set inside hypothalamus?

A

the binding of prostaglandin E (PGE) to hypothalamus
hypothalamus fires action potential
temperature set point increases

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68
Q

what are essential nutrients? (definition and which?)

A

nutrients that are required for normal physiological function but cannot be synthesized by the body
vitamins, minerals, fatty acids, amino acids

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69
Q

stages in food processing

A
  1. ingestion
  2. digestion (mechanical, chemical)
  3. absorption
  4. elimination
70
Q

alimentary canal (gastrointestinal tract/ GI tract)

A

tongue/oral cavity –> esophagus –> esophagus –> stomach –> small intestine –> large intestine –> rectum –> anus

71
Q

accessory glands of digestive system

A

salivary glands
liver
gall-bladder
pancreas

72
Q

where is the lumen inside alimentary canal?

A

interior of the tube

73
Q

what kind of cells are glands composed of?
which system do glands belong to?
what do glands do and where do they secrete?

A

specialized epithelial cells
endocrine system
into the blood stream or into the lumen

74
Q

digestion of carbohydrates

A

salivary glands –> mouth –> small polysaccharides
pancreas –> small intestine –> dissachrides
small intestinal enzymes –> monosaccharides

75
Q

protein digestion

A

stomach (pepsin) –> small polypeptides
pancreas (small intestine) –> small peptides
small intestine –> amino acids

76
Q

nucleic acid digestion

A 
small intestine (pancreas) --> nucleotides
small intestine --> nitrogenous bases, sugars, phosphates
77
Q

fat digestion

A

pancreas (small intestine) –> glycerol, fatty acids

78
Q

cells in the stomach

how are pepsin made? (what kind of feedback loop?)

A 
gastric pit on the interior surface of stomach (goes in deep)
epithelial cells
mucous cells (secretes mucous, protection from acid)
chief cells (secretes pepsinogen)
parietal cell (secretes HCl)
  1. parietal cells secretes HCl, chief cells secrete pepsinogen
  2. Hcl helps convert pepsinogen –> pepsin
  3. pepsin cleaves pepsinogen to make more pepsinogen

positive feedback loop

79
Q

cell types and

how are nutrients absorbed in the small intestine

A
  1. smooth muscles move food along the canal
  2. epithelial cells make up the lining
  3. microvilli at apical surface (lumenal surface) - increases surface area and help with absorption
80
Q

how to treat disease associated with poor gut microbiome?

A

take probiotic pills that come from people with healthy gut micrbiome

81
Q

how do gut microbes cause stomach ulcer?

A

H. pylori infection –> protease secretion –> epithelial cells damaged (especially those secreting mucous) –> gastric ulcers

82
Q

heart are comprised of how many chambers? what are they?

A 
4 chambers
2 atria (sing. atrium) and 2 ventricles
83
Q

what are the functions of the 2 right chambers

A

RA receives and holds deoxygenated blood

RV pumps blood through the pulmonary circuit

84
Q

what are the functions of the 2 left chambers

A

LA receives and holds oxygenated blood

LV pumps blood through the systemic circuit

85
Q

blood circulation in human body

A

RA –> RV –> pulmonary arteries –> capillaries in lungs –> pulmonary veins –> RA –> RV –> aorta –> systemic capillaries –> inferior/superior vena cava –> RA

86
Q

what is vasculature? and what is it composed of?

A

system of veins, arteries, and capillary beds

87
Q

difference between arteries and veins?

A

arteries carry blood away from the heart

veins carry blood toward the heart

88
Q

what is special about pulmonary arteries/veins?

A

pulmonary arteries: carry deoxygenated blood

pulmonary veins: carry oxygenated blood

89
Q

what is diastole?

what is systole?

A

diastole: the heart muscle relaxes
systole: the heart muscle contracts

90
Q

the cardiac cycle: heart as a pump

A
  1. atrial and ventricular diastole (0.4s) –> blood comes in
  2. atrial systole and ventricular diastole (0.1s) –> blood pumped into ventricles
  3. ventricular systole and atrial diastole (0.3s) –> blood pumped out from the ventricles
91
Q

EKG: heart as an electrical circuit

electrocardiogram

A
  1. signals from pacemaker cells (sinoatrial or SA node) spread through the atria – first bump
  2. signals are delayed at AV node (atrioventricular node) – small pause
    [[3. bundle branches pass signals to heart apex (the bottom tip of the heart) – small dip]]
  3. signals spread throughout ventricles through Purkinje fibers – giant peak
92
Q

regulation of cardiovascular system – adrenaline’s influence

A

adrenaline binds to adrenergic receptors (GPCRs) on pacemaker cells –> faster oscillation –> increases heartbeat
walls of arteries have cells that contain adrenergic receptors –> arteries relax –> vasodilation –> more blood pumped to skeletal muscles

93
Q

what cells carry oxygen in blood?

A

erythrocytes (red blood cells)

94
Q

how long do erythrocytes live? and how are they generated?

A

~120 days

multipotent stem cells in bone marrow regenerate

95
Q

how can red blood cells carry oxygen?

A

erythrocytes have hemoglobin
hemoglobin is made of 4 subunits, each with 1 heme
each heme has 1 iron molecules, O2 binding site

96
Q

what are the components of the respiratory system?

A

trachea - bronchus (bronchi) - bronchiole - alveoli

97
Q

what causes respiratory distress syndrome (RDS)?

A

lack of lung surfactant
surfactant lowers the surface tension –> the lack thereof leads to high surface tension of the fluid inside alveoli –> collapse of alveoli

98
Q

major function of kidney

A

maintain the ionic composition of the body (Na+, K+, Ca2+, Pi, H+)

99
Q

how does blood go to and come from the kidney

A

renal artery + renal vein

100
Q

key functional unit of kidney

2 types of kidney

A

nephron

  1. cortical (shorter loops)
  2. justamedullary (long loops that go into renal medulla)
101
Q

different steps of nephron function

A
  1. filtration - blood pressure forces filtration of water and solutes
  2. reabsorption - valuable substances returned to the blood
  3. secretion - addition of toxins and ions to urine
  4. excretion - urination
102
Q

hypo-osmotic vs. hyper-osmotic

also iso-osmotic

A

hypo: low solute concentration
hyper: high solute concentration
(NOT WATER CONCENTRATION)

103
Q

how does a nephron work?

A

renal arteries –> blood goes into glomerulus –> some of it becomes filtrate –> proximal tubule –> loop of Henle (descending loop –> ascending loop) –> distal tubule –> collecting duct

104
Q

what is the structure of glomerulus? how does glomerulus work?

A

glomerulus surrounded by Bowman’s capsule

afferent arteriole –> glomerulus –> filtrate + efferent arteriole

105
Q

the direction of water (and some filtrate) flow in filtration and reabsorption and secretion in nephron

A
  1. filtration: blood –> lumen/filtrate
  2. reabsorption: lumen/filtrate –> blood (active/passive transport)
  3. secretion: blood –> filtrate (toxins and nitrogenous waste)
106
Q

how are ions and water reabsorbed in nephron?

A

key point is the osmolarity gradient in kidney loops of Henle

  1. proximal tubule, iso-osmotic
  2. descending loop, increasing osmolarity (becomes more concentrated) - water reabsorbed
  3. ascending loop, decreasing osmolarity (becomes less concentrated) - ions reabsorbed
  4. distal tubule, dilute
  5. collecting duct, increasing osmolarity (becomes more concentrated) - water and urea reabsorbed
107
Q

2 regulators of the concentration of urine

A
  1. osmolarity (determines how much water can be reabsorbed) - high osmolarity dependent on urea (reabsorption in collecting duct)
  2. the number of water channels, aquaporins
108
Q

how to maintain osmolarity (as a response to increasing blood osmolarity)

A
  1. blood osmolarity increases
  2. hypothalamus osmosensors –> generates thirst
  3. hypothalamus posterior pituitary gland secretes antidiuretic hormone (ADH or vasopressin, neuroendocrine signaling) –> opens up more water channels to allow for greater water reabsorption
109
Q

how does ADH work to increase water reabsorption?

A

ADH –> ADH receptor (on collecting duct cells, GPCR) –> adenylyl cyclase activated –> second messenger cAMP –> cascade to protein kinase A –> drives storage vesicles with aquaporin to fuse to the apical surface of the cell (exocytosis) –> more aquaporins

110
Q

why do younger premature babies not display RDS?

A

smaller premature babies have not developed surfactant and have possible other medical conditions
bigger premature babies have developed surfactant, and the lack thereof becomes apparent

111
Q

how is urea produced? and how does kidney process it?

A

urea is produced as a byproduct of protein digestion
urea is filtered through glomerulus, reabsorbed in distal tube to help generate the osmolarity gradient, and the remaining urea is excreted with urine

112
Q

2 types of hormones

A 
water solubles (stored vesicles, stable in blood, bind to surface receptors)
lipid solubles (released without vesicles, bind to plasma in blood, bind to receptors inside the cell)
113
Q

endocrine vs. exocrine glands

A
  1. endocrine: secrete hormone into the blood
  2. exocrine: specialized epithelial cells that secrete chemicals into lumen or outside of body (chief cells, salivary glands, etc)
114
Q

hormones produced by the posterior pituitary

A

ADH (kidney tubules)

oxytocin (mammary glands, uterine muscles)

115
Q

2 ways to regulate blood pressure

A
  1. by changing the diameter of the arteries (vasoconstriction and vasodilation)
  2. by changing blood volume (increasing volume of extracellular fluid increases blood volume, thus blood pressure)
116
Q

renal regulation of blood volume/pressure (2 ways)

RAAS pathway = renin-angiotensin-aldosterone system

A

blood volume/pressure drops
INCREASE PRESSURE
1. JGA (juxtaglomerular apparatus) around renal arteries detects decrease and releases an enzyme called renin
2. renin initiates a series of steps that leads to generation of hormone - angiotensin II
3. angiotensin II binds to muscle around arteries –> increase blood pressure
OR INCREASE BLOOD VOLUME
3. angiotensin II binds to adrenal gland –> releases hormone aldosterone
4. aldosterone binds to distal tubule and increases reabsorption of water and ions –> increase blood volume

117
Q

what is the difference between the ADH and RAAS systems?

A

ADH is triggered by loss of water, hypothalamus sensor

RAAS is triggered by loss of volume, JGA sensor

118
Q

high blood pressure drugs

A
  1. ACE inhibitors: ACE is used to convert renin to angiotensin II (less angiotensin II leads to vasodilation and drop in blood volume –> blood pressure lowered)
  2. ARBs = angiotensin receptor blockers
  3. aldosterone inhibitors (diurectics, helps people lose water)
119
Q

where is growth hormones produced?

A

anterior pituitary gland

120
Q

what does growth hormones do?

A
  1. stimulates protein synthesis and growth of muscles and connective tissues
  2. stimulates production of insulin-like growth factors
  3. overproduction or underproduction leads to body size differences
121
Q

what system does IGFs signaling use? and what is its general mechanism?

A

IGF (insulin-like growth factor) –> RTK receptor –> phosphorylation/dimerization –> phosphorylation cascade –> activates transcription factor –> transcription and proliferation of mRNAs

122
Q

what 2 kinds of immune systems are there?

A
  1. innate: early response, generic response, no memory, all animals and plants
  2. adaptive: later response, responds to particular features of pathogens, maintains “immunological memory”, only in vertebrates
123
Q

two defenses in the innate immunity?

A
  1. barrier defenses (physical barrier, skin, mucous, secretions)
  2. internal defenses (phygocytic cells - lymphocytes, neutrophiles)
124
Q

how to white blood cells battle pathogens?

A

by phagocytosis (internalization of pathogens)

125
Q

what are the steps of phagocytosis?

A
  1. pseudopodia surround pathogens
  2. pathogens engulfed by endocytosis
  3. vacuole forms
  4. fusion between vacuole and lysosome
  5. pathogens destroyed
  6. debris from pathogens released
126
Q

what is the inflammatory response

A

physiological response to harmful stimuli (positive feedback loop)
1. mast cells and macrophages sense presence of foreign bodies, releases histamines and cytokines. Capillaries dilate and cytokines make capillaries “leaky” so that neutrophils can come out of the capillaries.
(positive feedback: more leukocytes –> more cytokines –> more leukocytes)
2. neutrophils digest pathogens and cell debris.

127
Q

how do phagocytes recognize pathogens?

A

phagocytes have Toll-like receptors (TLRs)

TLRs recognize PAMPs (pathogen-associated molecular patterns) - molecules specific to broad range of pathogens

128
Q

2 kinds of responses of adaptive immunity

A
  1. humoral response: antibodies defend against infection in body fluids
  2. cell-mediated responses: cytotoxic cells defend against infection in body cells
129
Q

2 important classes of cells in adaptive immunity

A

B and T lymphocytes

130
Q

what is antigen?
antigen receptor and antibodies?
epitope?

A

antigen: molecules on pathogen that elicits T or B cell response
antigen receptors and antibodies: proteins that bind antigens
epitope: portion of antigen recognized by antigen receptor

131
Q

how do B cells help with immunity?

A
  1. an antigen receptor on an immature B-cell binds to a part of the pathogen
  2. B-cells are activated and begins to secrete antibodies
  3. antibodies bind to pathogens and send signaling to phagocytes to engulf. Or they can also neutralize the pathogen.
  4. some of the B cells become memory cells
132
Q

how do helper T cells help with immunity

A
  1. some phagocytotic cells present a fragment of a pathogen to extracellular space –> antigen presenting cells (use of MHC molecule –> MHC/antigen combination)
  2. helper T-cells bind to MHC/antigen combination (recognizes a specific motif)
  3. helper T-cells are activated
  4. helper T-cells promote antibody secretion by B cells
  5. helper T-cells activate cytotoxic T-cells (cell-mediated immunity)
133
Q

how do cytotoxic T cells kill infected cells

A
  1. activated cytotoxic T-cells bind to MHC/antigen complex

2. cytotoxic T-cells secrete perforins (poke holes) and granzymes (break down proteins)

134
Q

how do cancer cells (which are antigen-presenting cells) hide from immune system?

A

cancer cells protected by immunosuppression by hijacking immune checkpoints

135
Q

structure of neurons

A

dendrites, cell body, axon
dendrites receive stimuli
axon conducts impulses from cell body

136
Q

3 types of neurons and their differences

A 
sensory neurons (sensors in dendrites, long axon, cell body at middle of axon)
interneurons (contact with a lot of cells, integrate sensory neuron information)
motor neurons (transmit output)
137
Q

what is the basis of nervous signaling?

A

by membrane potential (electrical potential different across the membrane)
cytoplasmic - negative pole (resting: -70 mV)
extracellular - positive pole

138
Q

what allows for resting potential

A

concentration gradient is the key

  1. ion pumps (active transports, K+ and Na+)
  2. ion channels
139
Q

2 forces control the movement of ions

A
  1. diffusion: down a concentration gradient

2. electrical gradient

140
Q

What is Nernst potential

A

the membrane potential at which the net movement of ions is 0 (diffusion force and electrical gradient force are balanced)
E_{ion} = 62*log(C_{out}/C_{in})
E in mV, C in mM

141
Q

relative concentration of K+ and Na+ inside and outside the membrane

A

inside: K+ high, Na+ low
outside: K+ low, Na+ high

142
Q

at rest, what channels are mostly open?

A

K+ channels

143
Q

changes in membrane potential are driven by channel gating, and what causes gating?

A
  1. sensory stimulation (photons, touch, temperature)
  2. chemical signals (neutrotransmitters)
  3. voltage changes (action potential)
144
Q

what causes hyperpolarization?

A

stimuli that increase membrane permeability to K+

neurons are inhibited by hyperpolarization

145
Q

what causes depolarization?

A

stimuli that increase membrane permeability to Na+

neurons are excited by depolarization

146
Q

what causes action potential?

A

triggered by a depolarization that reaches the threshold

same amplitude 100 mV, short duration, propagates without dissipating

147
Q

how do neurons communicate with one another

A

presynaptic cell –> synapses –> postsynaptic cell

  1. presynaptic membrane contains synaptic vesicles (containing neurotransmitters)
  2. action potential reaches the end of axon, Ca2+ channel (voltage-gated) opens up, Ca2+ comes in, driving the fusion of vesicles membrane with cell membrane
  3. neurotransmitters released from the vesicles across the synaptic cleft through diffusion, binding to ligand-binding ion channels
  4. action potential carries on in postsynaptic cell
148
Q

synapses can be excitatory or inhibitory, how?

A

excitatory: Na+ influx in postsynaptic cell
inhibitory: K+ or Cl- influx in postsynaptic cell

149
Q

what is the syndrome associated with lack of inhibitory synapses?

A

epilepsy

150
Q

major neurotransmitters

A 
acetylcholine
glutamate (excitatory)
norepinephrine
dopamine
serotonin
151
Q

what are the 2 primary divisions of nervous system?

A
  1. central nervous system (brain + spinal cord)

2. peripheral nervous system (nerves + ganglia)

152
Q

afferent vs. efferent

A

afferents bring information into CNS

efferents carry information out of CNS

153
Q

2 branches in efferents

A
  1. autonomic nervous system

2. motor system (control of skeletal muscles)

154
Q

how are skeletal muscles controlled by nervous system?

A

(neuromuscular junction)

  1. action potential travels along the length of the axon to the axon terminal
  2. voltage-gated calcium channels open and calcium diffuse into the terminal
  3. calcium influx causes synaptic vesicles to release acetylcholine via exocytosis
  4. acetylcholine diffuses across the synaptic cleft and binds to acetylcholine receptors, which contain ligand-gated cation channels
  5. ligand gated cation channels open
  6. Na+ entry, K+ exit
  7. the membrane potential reaches threshold –> propagation
155
Q

what are the 3 components of autonomic nervous system?

A
  1. sympathetic division (fight or flight)
  2. parasynpathetic division (rest and digest)
  3. enteric division
156
Q

differences between sympathetic and parasympathetic branches

A
  1. function: “fight or flight” vs. “rest and digest”
  2. activated by different brain circuits and efferents emerge from different locations of spinal cord
  3. effects on target organs are mediated by different neurotransmitters (epinephrine vs. acetylcholine)
  4. effects neutrotransmitters depend on the different receptors that are on the target organ (but both are categorized within GPCRs)
157
Q

where do most parasympathetic efferents emerge?

sympathetic?

A

para: upper part of spinal cord/brain stem
sym: lower part of spinal cord

158
Q

what neurotransmitters are released in sympathetic division?

parasympathetic?

A

sym: epinephrine or norepinephrine
para: acetylcholine

159
Q

epinephrine (and norepinephrine) signaling through GPCR in a contractile cell

A
  1. epinephrine binds to beta-adrenergic receptor (a GPCR)
  2. GPCR activated, GTP transferred to adenylate cyclase
  3. second messenger cAMP activates protein kinase A
  4. PKA phosphorylates sarcoplasmic reticulum, calcium channel –> increased Ca2+ in cell
  5. stronger contraction of contractile fibers
160
Q

effects of sympathetic and parasympatheic division on the heart

A
  1. activation of beta-adrenergic receptors on pacemaker cells increases heart rate
  2. activation of ACh-GPCR on pacemaker cells slows the heart rate
  3. activation of adrenergic receptors on cardiac muscle cells increases strength of contraction
161
Q

what are muscles made of

and how do they contract?

A

muscle fibers
inside: myofibrils (protein filaments)
myofibrils composed of sacromeres
sacromere contain think filaments (myosin) and thin filaments (actin)
thick and thin filaments slide past each other –> muscle contraction

162
Q

what signals the contraction of sacromeres

A

release of Ca2+ from the endoplasmic reticulum caused by action potential

163
Q

what are sensory neurons

A

specialized cells that convert stimulus energy to changes in membrane potential

164
Q

what are the 5 senses?

A
  1. vision/sleep-wake cycle
  2. audition
  3. offaction
  4. gustation
  5. somatosensation
165
Q

types of sensory receptors

A
  1. photoreceptors
  2. chemoreceptors
  3. mechanoreceptors (vibrations)
  4. thermoreceptors
  5. nociceptors (pain)
166
Q

steps in sensory transmission

A
  1. stimulus
  2. transduction of stimulus into change of membrane potential in sensory neuron
  3. action potential generation in sensory afferent
  4. interpretation of stimulus in CNS
167
Q

how do we tell the intensity of the stimulus?

A

the frequency of membrane potential

168
Q

what are photoreceptors? and what are they made of?

A

specialized neurons: dendrites –> outer segments composed of disks
modified GPCRs - rhodopsin (rod shaped)
signaling molecule: retinal cis –> trans conformation change excited by photon

169
Q

how do photoreceptors work?

A

signling cascade

  1. light activates rhodopsin
  2. transducin (a G protein) activated and binds to phosphodiesterase
  3. phosphodiesterase hydrolyzes cGMP to GMP (on sodium channel)
  4. GMP falls off sodium channel, sodium channel closes
  5. membrane hyperpolarization
170
Q

how does color blindness happen?

what is it more prevalent in males?

A

humans are trichromats - we have 3 opsins (3 different GPCRs, which are activated at different wavelengths –> see different colors)
both red and green opsins are on X chromosome –> more common in males

171
Q

what kind of ion channels do thermoreceptors use?

A

transient receptor potential (TRP) channels
they are gated by a lot of stimuli
when activated, they allow the passage of Na+ or Ca2+
–> depolarization of membrane
different TRP channels at different temperatures

172
Q

TRP thermoreceptors respond to both temperature and chemicals

A

e.g mint binds to cold thermoreceptors

capsacin binds to hot thermoreceptors

Bio 1A (2 decks)

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