Review set 7 Flashcards
TWO major divisions of nervous system
CNS (Central = brain + spinal cord) and PNS (Peripheral = motor/ sensory nerves OUTSIDE of CNS)
Nerves made up of cells called
neurons
neurons:
carry rapid, electrical impulses
Sensory/ Afferent: signals from body TO CNS
Relay (interneurons): signals within CNS
Motor/ Efferent: carry signals FROM CNS to “effectors” (muscles/
glands)
Draw Neuron Structure and identfiy
- Dendrites: short, branched fibers (branching off the cell body)
receive chemical signals (from sensory receptors or other neurons)
and transform them into electrical signals which are sent to cell body
(into neuron) - Cell body (soma): nucleus & cytoplasm + organelles - metabolism and summation of input signals
- Axon: long nerve fibers
carry signals away from cell body to the end of the axon/ axon terminal/ synaptic terminal buttons (where neurotransmitters are released for communication with other neurons or effectors)
LOOK AT THE SLIDE
Schwann cells:
supporting cells that form an insulating layer on the axon called a myelin (mainly lipid) sheath (increases the speed of the signal along axon - saltatory conduction)
Nodes of Ranvier:
spaces in between the Schwann cells (contain membrane proteins - Na+/ K+ channels and pumps)
Neurons and Action Potentials
- Neuron “at rest” maintains resting potential (-70mV charge by sodium-potassium pump: 3Na+ out for every 2 K+ in – active transport)
- Signals/ stimuli received by dendrites
- Cell body “sums” all stimuli together (excitatory and inhibitory)
- IF stimuli “sum” to a more positive charge (more excitatory/ depolarization)
and reach threshold potential (-50mV) an action potential WILL be generated - In an action potential:
Depolarization, Repolarization, Resting potential restored.
Depolarization
(Na+ channels open and Na+ rushes INTO axon, causing more Na+ channels open – domino effect down the axon – membrane potential becomes more POSITIVE)
Repolarization
K+ channels open and K+ rushes OUT of axon – domino effect down the axon – membrane potential becomes more NEGATIVE
resting potential restored
by sodium-potassium pump: 3 Na+ OUT for every 2 K+ IN): This period called refractory period (another action potential cannot be fired until this period is complete)
In myelinated neurons what changes
action potentials travel FASTER down the axon because ion channels ONLY BETWEEN myelinated portions (Nodes of Ranvier) - SALTATORY CONDUCTION
Synaptic transmission
- An action potential arrives at the axon terminal/ synaptic knob (of presynaptic cell)
- Calcium channels open and calcium ions rush INTO the axon terminal/ synaptic knob.
- Calcium ions interact with vesicles (containing neurotransmitter) stored in the axon terminal, causing them to migrate to and fuse with the membrane of the axon terminal/ synaptic knob.
- Neurotransmitter is released (exocytosis) into the synaptic cleft (space between neurons/ neurons and effectors) and DIFFUSES across cleft
- Neurotransmitters bind to protein channels on the post-synaptic membrane (dendrites etc.).
- Protein channels open (due to change in 3 structure) and:
A. Na+ ions rush into the post-synaptic cell (causing depolarization: excitatory due to neurotransmitter Acetylcholine/ Ach) OR
B. Cl- ions rush into the post-synaptic cell (causing hyperpolarization: inhibitory) - Enzymes (such as acetylcholinesterase) break down neurotransmitters (closing ion channels on postsynaptic membrane) and their pieces diffuse back into presynaptic neuron to be assembled into vesicles again
Note: Neurotransmitter NEVER enters a postsynaptic cell!
Acetylcholine causes what?
Ach is released at the neuromuscular junction to trigger depolarization in muscle cell fibers (to cause muscle contraction)
Ach binds to nicotinic/ cholinergic receptors on muscle fibre membranes
Neonicotinoid everything you need to know
bind IRREVERSIBLY (forever) to Ach receptors (nicotinic receptors) on muscle cell membranes in insects (different composition than in humans) and BLOCK NORMAL Ach BINDING Acetylcholinesterase (AchE) is NOT able to break down neonicotinoid pesticides, so they STAY bound to receptors and insects UNABLE to generate their OWN muscle contractions = paralyzed = death Reduce honey bee and bird populations though, so…
Striated Skeletal Muscle Fiber Structure:
- Many nucleii (polynucleated)
- Many mitochondria (lots of ATP needed for muscle contraction)
- Myoglobin (stores oxygen for ATP production)
- Cell membrane (sarcolemma)
- Internal folded membrane structures (sarcoplasmic reticulum – stores Ca2+ ions)
- Myofibrils (divided into sarcomeres = functional/ contractile units: Z line to Z line) made of myofilaments = contractile proteins (actin = thin; myosin = thick)
Actin vs Myosin
Actin vs Myosin
Thin contractile protein filaments - appear as lighter bands vs Thick contractile protein filaments- appear as darker bands
Contain myosin-bidning sites vs Contain “heads” that have actin binding sites
Form helical structures vs Form shaft like structures with protruding “heads”
Regulated by the proteins troponin and tropomyosin vs “heads” are called cross-bridges and contain ATP binding sites, ATPase Enzyme
Diagram a muscle fiber
Check from Ms. Mann slide
Contraction of skeletal muscle
- Action potential from motor neuron sends Ach to muscle cell, which causes sodium ions to rush into muscle fiber, generating muscle action potential
- Muscle action potential causes release of Ca2+ ions from sarcoplasmic reticulum
- Calcium ions bind to troponin on actin filaments, causing it to change shape and move tropomyosin to expose myosin binding sites (on actin filaments)
- Myosin heads hydrolyze ATP and use energy to bind to actin filaments/ form a cross-bridge with actin
- Myosin heads release ADP, causing head to bend forward (SLIDING actin filaments IN toward sarcomere center over myosin
filaments): POWER STROKE = SHORTENS SARCOMERE! - ATP binds to myosin, breaking the cross-bridges
- ATP is hydrolyzed (by enzyme), causing myosin heads to change shape and swivel back, binding to NEXT binding site on actin
- Movement of myosin heads causes actin filaments to SLIDE over myosin filaments – shortening length of sarcomere (distance between Z lines)
Note: Actin and myosin filaments do NOT change their length during muscle contraction (they simply SLIDE PAST EACH OTHER) - This cycle of myosin binding and ATP hydrolysis continues (shortening sarcomere/ contracting muscle) as long as ATP and calcium levels remain high in sarcoplasm (cytoplasm of muscle cell)
Movement of the body requires muscles to work in
antagonistic pairs (such as the biceps and triceps in the elbow joint -a synovial joint)
Draw a Elbow and label it
CHECK IT WITH MS. MANN SLIDE
Cartilage
absorbs compression; reduces friction between bones
Synovial Fluid
Provides nutrients to cartilage; reduces friction
Joint capsule
Surrounds and seals joint cavity, limits range of motion promotes stability
Tendons
Attach muscles (triceps and Biceps) to bones
Ligaments
Connect radius ulna and humerus (bone to bone)
Biceps
Muscles hat contract to provide flexion (bending) of the arm
Triceps
Muscles that contract to provide extension (straightening) of the arm (biceps and triceps are antagonistics)
Humerus
Upper arm bone that provides leverage and attachment for upper portions of muscles of the elbow
Radius
lower arm bone (smaller that acts as lever for the biceps
Ulna
Lower arm bone that acts as a lever for the triceps (triceps attach to it)
Insects have antagonistic muscles for movement too what are those
- Flexor tibiae and extensor tibiae in hind legs
- Flexor tibiae contracts (extensor relaxes), moving femur and tibia closer together; Extensor tibiae contracts (flexor relaxes), extending leg and causing jump!
Draw a male structure from the front and the side and label
Check on ms. mann slide
Testes:
produce sperm and testosterone
Epididymis
Sperm maturation/ motility/ storage
Vas deferens/ Sperm duct
carries sperm to seminal vesicle/ prostate gland
Seminal vesicle:
Adds fructose and mucous
Prostate gland
Adds alkaline fluids
Draw The Female structures from the front and side and label
Check with MS. Manns slides
Ovaires
produce oocytes, estrogen and progesterone
Oviducts
transport oocyte/ embryo to uterus (fertilization occurs here)
Uterus:
embryo implants and develops here (endometrium)
Endometrium:
blood rich lining (nutrients to embryo)
Vagina:
passageway for sperm and baby (protected by cervix)
FSH is secreted from and function
Secreted From: Anterior Pituitary
Function: Stimulates follicular growth, stimulates estrogen secretion from follicles
Estrogen is secreted from and function
Secreted from: Ovaries (developing follicle/ secondary oocyte in follicular phase and corpus luteum in luteal phase
Function: Thickens uterine lining, stimulates LH secretion, inhibits LH and FSH release from pituitary
LH is secreted from and function
Secreted from: Anterior Pituitary
Function: Surge causes ovulation, cause development of corpus luteum
Progesterone is secreted from and function
Secreted from: Ovaries (corpus lueum)
Function: Thickens and maintains uterine lining, inhibits LH and FSH release from pituitary
Look at the graph on MS. manns slide show
Make sure you get it
Oogenesis: In Fetus
- Germline cells divide by mitosis (produce oogonia)
- Oogonia grow into primary oocytes which begin meiosis I (arrested at prophase I until puberty)
In Young Women: - FSH (anterior pituitary) stimulates ONE primary oocyte to develop and complete meiosis I (once a month beginning at puberty) – produces one secondary oocyte (arrested at prophase II until fertilized) and one polar body (smaller, will degenerate – unequal division of cytoplasm)
- Secondary oocyte secretes estrogen (ovary)
- Estrogen inhibits FSH and stimulates lining of uterus (endometrium) to grow/ develop blood vessels and high levels stimulate LH release (surge) and some FSH release
- LH (anterior pituitary) stimulates ovulation of secondary oocyte from ovary and development of corpus luteum in ovary
- Corpus luteum produces and secretes progesterone (thickens and maintains endometrium, inhibits FSH and LH)
Note: No fertilization = declining levels of progesterone; uterine lining sloughs off and FSH/ LH no longer inhibited; cycle begins again
Look at the oogenesis slide on slide show
how you feeling about that
Roles of testosterone in males:
Prenatal development of male genitalia, development of secondary sex characteristics, sperm production, maintaining sex drive (libido)
Spermatogenesis (in SEMINIFEROUS TUBULES
OF TESTES)
- Germline epithelium cells divide (mitosis) to produce spermatogonia (2n)– mature into primary spermatocytes (2n)
- FSH (anterior pituitary) stimulates meiosis I in primary spermatocytes to produce 2 haploid, secondary spermatocytes
- LH (anterior pituitary) stimulates Leydig cells (testes) to secrete testosterone
- Testosterone stimulates meiosis II in secondary spermatocytes, creating 4 haploid spermatids
- Sertoli cells nourish spermatids/ structurally mature them (cause differentiation/ development of tails/midsections)
- Mature (structurally) sperm cells move to epididymis (storage/ motility)
- Seminal vesicle produces fructose/ mucous and prostate gland produces alkaline fluid for semen
Egg: Zona pellucida
barrier to sperm entry (jelly coat)
Egg: Corona radiata
nourish and protect egg (follicle cells)
Egg: Cortical granules
release enzymes to prevent polyspermy
Sperm: Nucleus
Contains chromosomes
Sperm: Acrosome
hydrolytic enzymes to penetrate zona
Sperm: Midpiece
mitochondria (ATP for motility - tail)
Sperm: Tail/ Flagellum
axoneme (microtubules) that bends for movement
Spermatogenesis vs Oogenesis
Location: Testis vs Ovary
Number of Gametes produced: Life long production vs fixed amount
Gametes per germ cell: four vs one
Beginning of Process: Begins at puberty vs Begins during fetal development
Timing of gamete formation: Continuous vs Once a Month
End of process: Fertility is life long but reduces vs fertility stops at menopause
Timing of gamete release: Any time vs monthly cycle
Meiotic divisions: Uninterrupted vs Arrested
Germ line epithelium: Involved in gamete production vs Not involved in gamete production
Fertilization
(External - in water/ spawning/ lots of gametes; Internal - on land/ more protected)
- Biochemical changes to sperm in female reproductive tract (capacitation – destabilizes acrosome cap and removes cholesterol coat for improved mobility)
- Egg sends biochemical signals to attract sperm (to oviduct/ fallopian tube) – chemotaxis
- Acrosome reaction (in oviduct/ fallopian tube): Sperm binds to receptors on egg’s zona pellucida and releases digestive enzymes from acrosome to penetrate
- Membranes of egg and sperm fuse and sperm nucleus and centrioles enter egg (causes release of calcium ions in egg)
- Cortical reaction: Calcium ions cause cortical granules of egg to fuse with egg plasma membrane and release enzymes that destroy sperm-binding sites and harden plasma membrane on egg to prevent polyspermy
- Secondary oocyte completes meiosis II and nucleii of sperm (n) and egg (n) fuse producing diploid zygote (2n)
Mitotic division, blastocyst formation, and implantation
- Rapid mitotic divisions of zygote/ early embryo to form blastocyst (hollow ball of cells – fluid filled cavity in middle called blastocoel, inner cell mass = becomes baby, trophectoderm = becomes placenta and amniotic sac/ fluid)
- Mitotic divisions occur as embryo moves from oviduct to uterus
- Once embryo reaches uterus (~day 5-8) will implant/ embed in uterine lining and begin to secrete hCG
hCG
- hCG (human chorionic gonadotropin) made and secreted by embryo
- hCG maintains corpus luteum (keeps progesterone levels high to thicken cervix and maintain endometrial lining of uterus – for implantation/ nourishment/ growth of embryo)
- placenta eventually takes over maintaining endometrium, making estrogen and progesterone (~8-10 weeks) - hCG levels drop at this point and corpus luteum degrades
Placenta structure and function
Disc-shaped, formed from trophectoderm of blastocyst; umbilical cord connects fetus to placenta (umbilical vein delivers nutrient-rich blood TO baby, pair of umbilical arteries carry wastes away from baby); maternal blood pools in intervillous spaces (NEVER mixes with fetal blood); exchange of gases, nutrients and wastes through chorionic villi (fetus)
Hormonal role: in the exchange of materials between the mother and fetus and it secretes estrogen and progesterone once it is formed
Produces and secretes estrogen (uterine muscle muscle growth/ mammary gland development) and progesterone (maintains uterine lining/ causes development of breast tissue/ inhibits uterine contractions by inhibiting oxytocin) - both inhibit FSH and LH
Birth (parturition)
Walls of uterus stretch (fully grown fetus), causing release of estrogen (estriols) from placenta
- Estrogen inhibits progesterone and increases sensitivity of uterine muscles to oxytocin
- As progesterone levels drop, oxytocin no longer inhibited and released from pituitary
- Oxytocin causes uterine muscle contractions, which constrict baby and baby releases prostaglandins
- Prostaglandins stimulate more uterine contractions
- Uterine contractions cause MORE oxytocin to be released, causing more contractions, more prostaglandins, more contractions, more oxytocin, more contractions etc. (POSITIVE FEEDBACK) until baby is born (Note: oxytocin also causes lactation - milk)
The process of in-vitro fertilization (IVF).
-Stop normal menstrual cycle (drugs), then cause superovulation - give FSH (follicle development) and hCG (follicle maturation), extract many eggs from ovaries, select sperm and prepare (capacitate/ activate), fertilize eggs (outside of body “in glass”), select embryos and implant into uterus, use pregnancy test to assess implantation (does not guarantee viable pregnancy though)
SRY Gene
BOY OR GIRL? SRY gene on Y chromosome codes for protein TDF (testis determining factor); TDF = causes embryonic gonads to become testes and produce testosterone; No TDF = ovaries = estrogen and progesterone
