Regulation and reproduction Flashcards

1
Q

What is membrane potential?

A
  • electric charge difference
    • across membrane
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2
Q

What is resting potential?

A
  • imbalance of positive and negative charges across membrane (-70mV)
  • no signal
  • inside negative, outside positive
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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
  • leakages
    • voltage gated channels = open at certain electrical potential value
      • closed are leaky
        • more K+ leaks outside
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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
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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
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6
Q

What is axon hillock?

A
  • junction between cell body and axon
    • plasma membrane composition changes
      • voltage-gated channels
  • initiates electric impulse
    • small amounts of Na+ accumulate there
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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
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8
Q

What is repolarisation?

A
  • at action potential
    • Na+ closes — K+ open
    • K+ outside
      • charge drops
      • K+ and Na+ at wrong sides
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9
Q

What is hyperpolarisation?

A
  • K+ channels close
    • slow
  • potential inside drops further than resting state
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10
Q

What happens at the absolute refractory period?

A
  • after action potential
    • Na+ channels can’t open
  • no action potential
    • prevents backflow
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11
Q

What happens at relative refractory period?

A
  • hyperpolarisation
    • harder to reach threshold potential
    • stronger stimulus needed (more Na+)
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12
Q

How is action potential propagated forward?

A
  • depolarisation
    • opens channels in next part of axon
      • signal goes forward
  • 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)
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13
Q

What is myelin?

A
  • coats nerve fibres
  • phospholipid bilayer
    • Schwann cells deposit myelin
      • 20 or more layers
  • gap: node of Ranvier
  • saltatory conduction
    • impulse jumps from node to node
      • quicker
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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)
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15
Q

How does a signal move?

A
  • neurotransmitters send signals across synapses
    • from signal to receiver cell
      • receptors on post-synaptic cell
    • diffusion
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16
Q

What are the steps of synaptic transmission?

A
  1. impulse propagated along pre-synaptic neuron
    • reaches axon terminal
  2. depolarisation of membrane
    • voltage-gated channels of Ca2+ open
      • Ca2+ inside
  3. Ca2+ influx causes vesicles with neurotransmitters to move
    • fuse with membrane
  4. neurotransmitter is released to synaptic cleft
    • exocytosis
  5. neurotransmitters bind to post-synaptic receptors
  6. Na+ channels open
    • Na+ into the cell
      • threshold potential
  7. neurotransmitter degraded by enzyme or back into pre-synaptic membrane by a transporter or reuptake pump
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17
Q

How are neurotransmitters in axon terminal?

A
  • produced in cell body
    • in vesicles
      • transported to axon terminal
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18
Q

What happens after synaptic transmission?

A
  • vesicles fuse with pre-synaptic membrane
    • enlarged
  • neurotransmitter reuptake
    • endocytosis
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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)
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20
Q

How is acetylcholine produced?

A
  • pre-synaptic cell
    • combining choline (diet) with acetyl group (aerobic respiration)
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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
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22
Q

How is knowledge about synaptic transmission applied?

A
  • neuronal and mental diseases
    • Selective Serotonin Reuptake Inhibitor (SSRI) = antidepressants
  • neuroactive toxins
    • neonicotinoids (pesticide)
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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
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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
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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
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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

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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
  • 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
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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
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29
Q

What is an example of second messengers?

A
  • water soluble — spread signal fast
    • Ca2+ and cyclic AMP (cAMP)
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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
    • cAMP (cyclic adenosine monophosphate) activates protein kinase enzymes
      • glycogen breakdown and inhibit glycogen synthesis
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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
  • 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
  • posterior pituitary
    • oxytocin and ADH
  • hormones synthesised in neurosecretory cell in hypothalamus
    • the end of axons
      • impulse stimulates secretion
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
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
  • 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
  • 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
  • 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
43
Q

What are the types of diabetes?

A
  • type I
    • early onset
      • autoimmune (destruction of beta)
    • no insulin
    • skinny complexion
  • 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
  • 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
  1. before birth
    • oogonia formation
    • meiosis arrested at prophase I
      - primary oocyte (follicle)
  2. 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
  3. fertilisation
    • meiosis II completed
      - ovum
      - maturation of gamete
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)
    • small cells in the gaps = interstitial cells (Leydig cells)
52
Q

What are the steps of spermatogenesis?

A
  1. mitosis (puberty)
    • spermatogonium —> primary spermatocyte
  2. meiosis I
    • primary spermatocyte —> 2 secondary spermatocytes
  3. meiosis II
    • secondary spermatocytes —> 2 spermatids
  4. 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
  • 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
  • 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
  • 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)
61
Q

What are different fertilisation types?

A
  • internal (terrestrial animals)
    • gametes would dry
      • close proximity
  • 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
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
  • 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
  • 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
  • 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
  • intramuscular injections of FSH and LH daily for 10 days
    • follicle development
      • higher concentration, more follicles = superovulation
  • 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)