Regulation and reproduction Flashcards
1
Q
What is membrane potential?
A
- electric charge difference
- across membrane
2
Q
What is resting potential?
A
- imbalance of positive and negative charges across membrane (-70mV)
- no signal
- inside negative, outside positive
3
Q
What causes resting potential?
A
- inside
- K+
- protein anions (-)
- outside
- Na+
- Cl-
- sodium-potassium pumps (ATP needed)
- for every 3Na+, 2K+ are pumped
- more Na+ on the outside
- for every 3Na+, 2K+ are pumped
- leakages
- voltage gated channels = open at certain electrical potential value
- closed are leaky
- more K+ leaks outside
- closed are leaky
- voltage gated channels = open at certain electrical potential value
4
Q
How do voltage-gated channels work?
A
- Na+
- open at threshold potential (depolarisation)
- Na+ in
- close at action potential
- K+
- open at action potential (repolarisation)
- K+ out
- close after reaching resting potential again
5
Q
How is action potential propagated?
A
- ion movement depolarises one part
- Na+ inside move from depolarised part to not yet depolarised
- Na+ outside move the opposite direction
- difference = -50mV (threshold potential reached) - impulse initiated at one terminal
- passed at other terminal
6
Q
What is axon hillock?
A
- junction between cell body and axon
- plasma membrane composition changes
- voltage-gated channels
- plasma membrane composition changes
- initiates electric impulse
- small amounts of Na+ accumulate there
7
Q
What is depolarisation?
A
- Na+ in axon hillock
- charge grows inside neurone
- plasma membrane depolarisation
- threshold potential is reached (-55mV)
- voltage-gated channels open
- Na+ inside
- more Na+ channels open = positive feedback
- charge changes to 40mV = action potential
- Na+ inside
- voltage-gated channels open
8
Q
What is repolarisation?
A
- at action potential
- Na+ closes — K+ open
- K+ outside
- charge drops
- K+ and Na+ at wrong sides
9
Q
What is hyperpolarisation?
A
- K+ channels close
- slow
- potential inside drops further than resting state
10
Q
What happens at the absolute refractory period?
A
- after action potential
- Na+ channels can’t open
- no action potential
- prevents backflow
11
Q
What happens at relative refractory period?
A
- hyperpolarisation
- harder to reach threshold potential
- stronger stimulus needed (more Na+)
12
Q
How is action potential propagated forward?
A
- depolarisation
- opens channels in next part of axon
- signal goes forward
- opens channels in next part of axon
- local currents
- Na+ inside the cell (depolarised part) move to the polarised part
- Na+ outside the cell (polarised) moves to depolarised part
- this prevents signal from going backwards
- reduces concentration gradient (easier to reach -55mV)
13
Q
What is myelin?
A
- coats nerve fibres
- phospholipid bilayer
- Schwann cells deposit myelin
- 20 or more layers
- Schwann cells deposit myelin
- gap: node of Ranvier
- saltatory conduction
- impulse jumps from node to node
- quicker
- impulse jumps from node to node
14
Q
What is a synapse?
A
- space between the axon terminals of one nerve and dendrites of the other
- or muscles and glands
- fluid-filled gap = synaptic cleft (20nm)
15
Q
How does a signal move?
A
- neurotransmitters send signals across synapses
- from signal to receiver cell
- receptors on post-synaptic cell
- diffusion
- from signal to receiver cell
16
Q
What are the steps of synaptic transmission?
A
- impulse propagated along pre-synaptic neuron
- reaches axon terminal
- depolarisation of membrane
- voltage-gated channels of Ca2+ open
- Ca2+ inside
- voltage-gated channels of Ca2+ open
- Ca2+ influx causes vesicles with neurotransmitters to move
- fuse with membrane
- neurotransmitter is released to synaptic cleft
- exocytosis
- neurotransmitters bind to post-synaptic receptors
- Na+ channels open
- Na+ into the cell
- threshold potential
- Na+ into the cell
- neurotransmitter degraded by enzyme or back into pre-synaptic membrane by a transporter or reuptake pump
17
Q
How are neurotransmitters in axon terminal?
A
- produced in cell body
- in vesicles
- transported to axon terminal
- in vesicles
18
Q
What happens after synaptic transmission?
A
- vesicles fuse with pre-synaptic membrane
- enlarged
- neurotransmitter reuptake
- endocytosis
19
Q
What is a motor neurone?
A
- from central nervous system (CNS) to muscles
- elongated axon - connected to muscle
- neuromuscular junction
- chemical synapse
- neurotransmitter: acetylcholine (cholinergic)
- chemical synapse
- neuromuscular junction
20
Q
How is acetylcholine produced?
A
- pre-synaptic cell
- combining choline (diet) with acetyl group (aerobic respiration)
21
Q
How does cholinergic synapse work?
A
- acetylcholine is released after Ca2+ influx
- ACh binds to Na+ channel receptors
- threshold potential
- shortly bounded: only 1 action potential
- acetylcholinesterase (in synaptic cleft) breaks ACh down into choline and acetate
- choline is reabsorbed by pre-synaptic neuron
- back into ACh
22
Q
How is knowledge about synaptic transmission applied?
A
- neuronal and mental diseases
- Selective Serotonin Reuptake Inhibitor (SSRI) = antidepressants
- neuroactive toxins
- neonicotinoids (pesticide)
23
Q
What are neonicotinoids?
A
- similar to nicotine
- binds acetylcholine receptors
- insects
- acetylcholinesterase doesn’t break it down
- irreversible
- paralysis and death
- not toxic to humans
- more cholinergic synapses in CNS of insects
- bind less strongly to receptors
- imidacloprid = commonly used pesticide
- harmful for honeybees
24
Q
What are hormones?
A
- chemical messengers
- produced by endocrine glands
- homeostasic regulation
- modification of activity of tissues
- transported by blood
- slower but long lasting effects
25
Q
What are the differences between nervous and endocrine system?
A
- nerve impulse vs chemical messenger
- neurons vs blood
- fast vs slow
- carried to specific cells vs throughout body
- muscles / glands vs range of organs affected
26
Q
What are different types of hormones?
A
~ steroids
- receptors in nucleus
- action by transcription regulation
- affect gene expression
- slow
> peptides
- receptors in plasma membrane
- act by signalling cascade
- affect chemical processes and gene expression
- fast
> proteins, glycoproteins, amines or tyrosine derivatives
27
Q
How do steroid hormones work?
A
- cross through plasma and nuclear membrane
- bind to receptors
- ex. sex hormones
- form receptor-hormone complex
- serves as transcription factor (promotion or inhibition)
- produced from cholesterol
- calciferol: intestinal cell membrane
- complex affects expression of calcium transport protein calbindin
- absorption of calcium
- complex affects expression of calcium transport protein calbindin
- cortisol binds in cytoplasm and enters nucleus
- in liver cell: gluconeogenesis
- conversion of fats and proteins into glucose
- decreases expression of insulin receptor
- in pancreas
- in liver cell: gluconeogenesis
28
Q
How do peptide hormones work?
A
- bind to membrane receptors
- triggers cascade reaction, edited by second messengers
- hydrophilic so cannot pass the membrane
29
Q
What is an example of second messengers?
A
- water soluble — spread signal fast
- Ca2+ and cyclic AMP (cAMP)
30
Q
How does epinephrine signalling work?
A
- epinephrine mediates “fight or flight” (first messenger)
- supply of glucose (energy) needed
- in liver binds to G-protein couple receptor
- activation of G-protein
- uses GTP as energy to activate enzyme adenylyl cyclase
- ATP —> cAMP
- uses GTP as energy to activate enzyme adenylyl cyclase
- activation of G-protein
- cAMP (cyclic adenosine monophosphate) activates protein kinase enzymes
- glycogen breakdown and inhibit glycogen synthesis
31
Q
What are the endocrine glands?
A
- pituitary
- pineal
- hypothalamus
- thyroid
- parathyroid
- thymus
- mammary
- adrenal
32
Q
What is the role of hypothalamus?
A
- combines nervous and endocrine system
- control of pituitary gland
- secretion of releasing factors
- stimulate anterior pituitary gland
- carried by portal vein
- stimulate anterior pituitary gland
- negative feedback
- blood solute high
- osmoreceptors in hypothalamus react
- ADH secretion
- blood solute low
- ADH reduced
33
Q
What is the role of pituitary gland?
A
- anterior pituitary
- growths, reproduction, homeostasis
- FSH and LH
- growths, reproduction, homeostasis
- posterior pituitary
- oxytocin and ADH
- hormones synthesised in neurosecretory cell in hypothalamus
- the end of axons
- impulse stimulates secretion
- the end of axons
34
Q
What is thyroxin and its function?
A
- hormone
- regulates metabolic rate (especially in liver, muscle and brain) and helps control body temp
- as the body cools, more thyroxine is produced
- secreted by thyroid gland (neck)
- 4 atoms of iodine
- deficiency of iodine = no synthesis of thyroxin
- 4 atoms of iodine
35
Q
How is temperature controlled by thyroxin?
A
- hypothalamus controls blood temperature
- decrease = signal to thyroid
- metabolic rate in cells increases
- more heat
36
Q
What are the results of thyroxin deficiency?
A
- thyroxine is a hormone regulating metabolism
- deficiency => less metabolism
- less ATP
- imparted muscle work —> fatigue
- imparted neural work —> dizziness, forgetfulness, depression, imparted brain development
- less heat —> feeling cold
- less sugars and lipids used for cellular respiration —> body fat accumulation
- less ATP
- iodine deficiency (hypothyroidism = underactive thyroid)
- cause of thyroxin deficiency
- enlargement of thyroid = goiter
37
Q
How is milk produced and ejected in mammals?
A
- in mammary glands
- prolactin
- anterior pituitary
- development of mammary glands
- milk production
- oestrogen and progesterone increases prolactin
- inhibits effect of prolactin on milk production
- at labour production begins (no oestrogen and progesterone)
- oxytocin
- release of milk
- nursing by infant stimulates prolactin and oxytocin
- contraction of surrounding cells
- ejection of milk
- positive feedback
38
Q
How are growth hormones used by athletes?
A
- produced in anterior pituitary
- targets liver cells
- release of insulin-like growth factor
- stimulates bone and cartilage growth
- increase muscle mass
- short burst of strength
- banned
39
Q
What is melatonin’s function?
A
- feeling of drowsiness, drops body temp
- pineal gland
- controls circadian rhythms
- depend on suprachiasmic nuclei (SCN) in hypothalamus
- control secretion of melatonin by pineal gland
- information about light from retina
- depend on suprachiasmic nuclei (SCN) in hypothalamus
- concentration decreases at dawn
40
Q
What are the causes of jet lag?
A
- three or more time zones
- difficulty in remaining awake and sleeping through night
- fatigue, irritation, headaches
- melatonin can be taken
41
Q
What glands exist in pancreas?
A
- exocrine
- digestive enzymes
- alkaline solution
- endocrine
- hormones
42
Q
How is blood glucose level controlled?
A
- in pancreas
- regions of endocrine tissue: islets of Langerhans
- set point: 5mmol/L
- alpha cells
- glucagon
- blood glucose levels fall
- stimulation of glycogen breakdown into glucose
- released into blood
- stimulation of glycogen breakdown into glucose
- beta cells
- insulin
- blood glucose levels increase
- stimulation uptake of glucose by tissues
- skeletal muscle, liver
- insulin broken down by cells it acts upon = ongoing secretion
- stimulation uptake of glucose by tissues
43
Q
What are the types of diabetes?
A
- type I
- early onset
- autoimmune (destruction of beta)
- no insulin
- skinny complexion
- early onset
- type II
- insulin signal not received by cells (insulin resistant)
- old
- associated with obesity
- disturbance of glucose homeostasis
- bad diet, no exercise
44
Q
What are the treatments for diabetes?
A
- type I (defects in B cells of pancreas)
- insulin injections
- before meal
- implanted devices
- stem cells maybe
- insulin injections
- type II (insulin resistance)
- adjusting diet, exercise
45
Q
What is leptin?
A
- produced by adipose tissue
- glucose uptake
- excess of energetic substrates present
- appetite control centre in hypothalamus
- feeling of satiety
- in mice with recessive on alleles no leptin
- obesity
- objection of leptin decreased mass
46
Q
Why isn’t leptin used to treat obesity?
A
- skin irritation and swelling
- short-lived protein
- rare cases of “low leptin” obesity
- loss of leptin sensibility is more probable
47
Q
What are the functions of reproductive system?
A
- gamete production
- storage
- nourishment
- transport
- fertilisation
- pregnancy
48
Q
What did Harvey do in his experiment?
A
- “soil and seed” theory by Aristotle
- sperm = seed that develops in woman’s uterus with menstrual blood
- dissection of deer’s uterus
- no foetus shown
- hypothesis: foetus development is independent from sex
49
Q
What are the steps of oogenesis?
A
- before birth
- oogonia formation
- meiosis arrested at prophase I
- primary oocyte (follicle)
- after puberty
- each month —> oocyte completes meiosis I and starts prophase II
- first polar body
- secondary oocyte (released at each cycle)
- secondary follicle —> mature follicle
- each month —> oocyte completes meiosis I and starts prophase II
- fertilisation
- meiosis II completed
- ovum
- maturation of gamete
- meiosis II completed
50
Q
What happens to the follicle after releasing of an oocyte?
A
- degenerating follicle = corpus luteum —> corpus albicans
51
Q
Where does spermatogenesis occur?
A
- in testes
- narrow tubes = seminiferous tubules
- outer layer = germinal epithelium
- sperm production begins
- more mature = closer to lumen
- on the wall —> Sertoli cells (large nurse)
- outer layer = germinal epithelium
- small cells in the gaps = interstitial cells (Leydig cells)
- narrow tubes = seminiferous tubules
52
Q
What are the steps of spermatogenesis?
A
- mitosis (puberty)
- spermatogonium —> primary spermatocyte
- meiosis I
- primary spermatocyte —> 2 secondary spermatocytes
- meiosis II
- secondary spermatocytes —> 2 spermatids
- maturation
- spermatozoa = sperm
53
Q
How is sex of the embryo determined?
A
- starting as females
- reproductive hormones: oestrogen and progesterone
- from ovaries and placenta
- reproductive hormones: oestrogen and progesterone
- SRY (sex-determining region Y) gene on Y chromosome
- encoding for TDF (testicle-determining factor)
- TDF triggers development of gonads into testes
- testes produce testosterone
- testosterone : oestrogen ratio high
- further development of male parts
54
Q
How does testosterone work in male development?
A
- pre-natal
- gonads —> testes
- male reproductive organs
- puberty
- production of sperm (primary sexual characteristic)
- secondary sexual characteristics
- enlargement of penis
- pubic hair
- deepening of voice
55
Q
What causes pre- and post-natal development of females?
A
- prenatal
- oestrogen and progesterone
- both sexes
- ratio testosterone : oestrogen matters
- female genitalia development during foetal development
- oestrogen and progesterone
- puberty
- enlargement of breasts
- pubic hair
- underarm hair
56
Q
What are the stages of menstrual cycle?
A
follicular —> ovulation —> luteal —> menstruation
57
Q
What happens during follicular phase?
A
- follicles developing into ovary
- most developed breaks open —> into oviduct
- rest degenerate
- most developed breaks open —> into oviduct
- uterus walls (endometrium) thicken and repair
58
Q
What happens during luteal phase?
A
- wall of follicle releasing egg —> corpus luteum
- endometrium prepares for embryo
- if no, menstruation starts
- corpus luteum breaks down
59
Q
What hormones control menstrual cycle?
A
- pituitary protein hormones
- FSH (follicle stimulating)
- LH (luteinising hormone)
- ovarian hormones
- oestrogen
- progesterone
60
Q
What are the roles of different hormones in menstrual cycle?
A
- FSH
- peak at the end of mentruation
- development of follicles (with oocyte and follicular fluid)
- secretion of oestrogen by follicle wall
- oestrogen
- peak at the end of follicular phase
- repair and thickening of endometrium
- increases FSH receptors —> follicles more receptive to FSH —> more oestrogen (positive feedback)
- high levels —> inhibition of FSH (negative feedback)
- LH secretion
- LH
- sharp peak at the end of follicular phase
- completion in meiosis of oocyte
- partial digestion of follicle wall = opening at ovulation
- development of follicle wall into corpus luteum
- secretes oestrogen (positive feedback) and progesterone
- progesterone
- rise at start of luteal phase
- drops back at the end
- thickening and maintaining endometrium
- inhibits FSH and LH (negative feedback)
- rise at start of luteal phase
61
Q
What are different fertilisation types?
A
- internal (terrestrial animals)
- gametes would dry
- close proximity
- gametes would dry
- external
- bringing egg into proximity with sperm
- risks: predation, temperature, pH
- aquatic animals
62
Q
What happens the first stage of fertilisation?
A
- acrosome reaction
- corona radiata = layer of cells closest to zona pellucida
- zona pellucida = coat of glycoproteins around egg
- acrosome = membrane-bound sac of enzymes
- in sperm head
- digest zona pellucida and corona radiata (+ flagella action)
63
Q
What happens at stage 2 of fertilisation?
A
- membrane on the tip of sperm
- proteins that bind to egg membrane
- first one to get through binds
- fusion of membranes
- sperm nucleus enters = fertilisation
64
Q
What is the cortical reaction?
A
- sperm activates egg
- cortical granules = vesicles near egg membrane
- contents released by exocytosis
- digestion of binding proteins
- no more binding
- zona pellucida hard
> prevention of polyspermy
- digestion of binding proteins
- contents released by exocytosis
- cortical granules = vesicles near egg membrane
65
Q
What happens at stage 3 and 4 of fertilisation?
A
- fusion of plasma membrane of oocyte and sperm
- sperm DNA into oocyte
- meiosis II completed
- mature ovum + polar body
66
Q
What happens at stage 5 of fertilisation?
A
- male and female pronuclei
- chromosomal material decondenses
- in ovum after meiosis
- chromosomal material decondenses
- no distinction in nuclei
- DNA replication in pronuclei
67
Q
What happens at stage 6 of fertilisation?
A
- membranes of pronuclei breakdown
- chromosomes condense
- mitosis
- uses centrioles from sperm
68
Q
What happens during early embryonic division?
A
- no size change
- mitosis (identical cells)
- morula formed
- 4 days after fertilisation
- unqualified division = formation of blastocyst
- 5 days after
69
Q
What is a blastocyst?
A
- unequal mitotic division + migration of cells (making hollow ball = blastocyst)
- 7 days —> blastocysts in uterus (125 cells)
- moved by cilia in oviduct wall
- zona pellucida breaks down
- blastocyst needs external source of food
- sinks into endometrium = implantation
- exchanging materials with mothers blood
- placenta formation
70
Q
What is hCG?
A
- human Chorionic Gonadotropin (hCG)
- produced by early embryo and placenta
- maintains corpus luteum for first week —> progesterone necessary for endometrial activity
- later placenta starts producing progesterone
- corpus luteum degrades
71
Q
What is placenta?
A
- made out of foetal tissue
- contact with maternal tissue
- placental villus (foetal tissue)
- increase with progression of pregnancy (foetus needs food)
- maternal blood in inter-villus
- small distance between maternal foetal blood
- placental barrier = cells between
- selectively permeable
- placental barrier = cells between
- small distance between maternal foetal blood
- foetus also develops amniotic sac
- support for foetus
72
Q
What are the hormones released by placenta?
A
- oestrogen and progesterone
- sustaining pregnancy
- no corpus luteum
- sustaining pregnancy
- danger of miscarriage in the switch
73
Q
What happens at the end of childbirth?
A
- progesterone inhibits oxytocin and contractions of myometrium
- foetal signal to placenta —> no progesterone
- oxytocin
- oxytocin —> contraction of muscle fibres —> stretch receptor signal to pituitary gland to increase oxytocin —> more contractions
- positive feedback
- cervix dilates
- uterine contraction burst amniotic sac (water breaking)
- uterine contractions push baby
74
Q
How does child labour work?
A
- head close to cervix
- amniotic fluid released
- baby into vagina
- baby pushed out
- umbilical cord cut, breathing
- placenta expelled
75
Q
What are the steps of in vitro fertilisation?
A
- step 1: down-regulation
- drug each day –> pituitary stops secretion of FSH and LH
- no oestrogen and progesterone
- suspension of cycle
- drug each day –> pituitary stops secretion of FSH and LH
- intramuscular injections of FSH and LH daily for 10 days
- follicle development
- higher concentration, more follicles = superovulation
- follicle development
- injection hCG to stimulate maturation
- micropipette on ultrasound scanner to take eggs
- incubated
- embryo placed in uterus
- extra progesterone as tablet in vagina (uterus lining maintained)
