Hormones Flashcards

1
Q

Describe the 1st experiment on hormones

A

Loss of function: castrate chickens.

  • if you castrate, they will develop without the wattle/tail and be non agressive/won’t mount.
  • if you reintroduce testes when young into the abdomen (no innervation) it restores appearance and behavior.
  • if you reintroduce later in life, no effect, no restoration of function.

Activational effects, but timing is critical.
Chemical signals via the blood.

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2
Q

what is a hormone?

A
released primarily by glands Ibut also other tisses) 
into bloodstream (but also locally) 
by animals (but also some alamones in plants) 

Exocrine: out (sweat/tears)
Endocrine: chemical within the body

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3
Q

What are the different crines and mones?

A

Endocrine: into bloodscream
Neurocrine: nervous system standard synapse
Autocrine: hormones and NT. On the same cell, negative feedback mechanisms
Paracrine: release locally, not into bloodstream always. (extracellular fluid in local area) signal weakens and diffuses as it spreads out.

Pheromone: within same species
Allomone: to other species.

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4
Q

What are the general rules of hormone function.

A
  • much slower effects, gradual. (hours-weeks)
  • early exposure can have lifelong effects, whereas NT can just last minutes.
  • No polarity (on off behaviors) but more “increased likelihood” of a behavior (i.e. during mating season reptiles are more likely to engage in sex?)
  • Hormones influence ur behaivor and behavior influences your hormoens. Reciprocal.
  • mulciplicity: different hormoens cause same effects in one target and same horrmones can cause different effects in different targets. Mediated by receptor types.
  • Pulsatile and rhythmic: hormones released to a rhythm (circadian, menstrual), its in little burts with long lasting effects, don’t need a steady drip
  • Hormones interact with other hormones or with cofactors.
  • Hormones need receptors to act (like NT)
  • DOn’t have to be on plasma membrane, can be intracellualr!
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5
Q

Describe the hypothalamus and neuroendrocrine cells.

A

Hth: junction between NS and endrocrine system. HTh contains neuroendocrine cells (neurosecretory).
Where the BBB is less existant/more porous. Need the communication between hypothalamus and bloodstream. Behaves mostly like neurons. Post synaptic potential released hormone instead of transmitter.
Some hormones are also NT (epi and noepi)

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6
Q

What are the types of hormones?

A

Peptides: small proteins/large??
Amine: single amino acid, monoamine can be same as NT (noepi, epi). Only some can cross plasma membrane.
Steroid: 4 ring structure, can pass plasma membrane.

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7
Q

What are the hormone receptor types?

A

At the membrane: GCPR: faster (versus NT where they’re slower) no entry, no pore. only g coupled proteins that run off and do jobs for us. Activating kinases, enzymes, protein complexes. Small signals that cause large signal cascades.

Intracellular: usually near nucleus, TRANSCRIPTION FACTOR so steroid hormone goes through membrane, becomes activated when steroid binds with receptor and become transcription factor. they regulate gene transcripton (up or down) Takes a LOT longer. Steroid hormones can have GPCRs too !!

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8
Q

How do we measure hormones and receptors.

A

Radioactivity: release positrons to be measured
Antibodies: targets like antigens, you can see wehre tis bonding with a fluorescent marker.

Radioimmunoassay: measure hormone levels in the blood. Behavior then blood sample, radioactive antibody that will bind to hormone in the blood.

Autoradiopraphy: brain areas effected by the hromone. Insert radioactive hormone, when it circulates and binds, kill animals and shows where its bound in the brain.

Immunohistochem: stain tissue: immunocytochemistry cells in a sepcific subsection. Use antibody technique. antibody will bind where receptors are.

In Situ Hybridization: target messenger RNA, create complementary strnad, label it, insert into tissue slice, shine light and see wehre that RNA is. See changes in RNA expression in response to events/neg feedback etc..

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9
Q

Where can you find negative feedback mechanisms?

A

Autocrine: neg feedback
Hypothalamus: change in behavior and perceptions sent to hypothalamus.
Pituitary and hypo.
*** becca

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10
Q

Whats the pituitary gland like in GENERAL?

A
NS/endocrine intersection. 
Connected by infundibulum (pit stalk) 
Release hormones (Hth) which cause tropic hormones to be released from pituitary which causes hormones to be released from the gland and then get them to the target!!
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11
Q

Describe posterior pituitary. What do the areas do?

A

HTh has neuroendocrine cells in paraventricular and supraoptic nuclei. Axons travel dwon infundibulum to post pituitary. These Hth axons terminate on capillaries which release OXYTOCIN and ADH (vasopressin/antidiuretic hormone) into the blood. Both paraventricular and supraoptic release both oxy and adh.

oxytocin: uterine contractions, milk letdown, pitocin: artificial oxytocin to induce labour. Sucking and conditioned response to baby crying will induce letdown.

vasopressin: constricts blood vessels and aids in water retention. Special type of calcium L channels inhibited when you drink alcohol which inhibits ADH release, meaning you have to pee a lot - become dehydrated.
L type calcium channels usually used for exocytosis

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12
Q

Describe the anterior pituitary

A

Neuroendocrine cells Terminate at median eminence, HTh release hormones, carried 2mm by the hypophyseal portal veins. When they reach targets in ap, the ap releases tropic hormones into the bloodstream which go to glands to cause further hormone release.

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13
Q

What are the hormones of the anterior pituitary?

A

ACTH: adrenal cortex
TSH: thyroid
LH and FSH: lutinizing and follicle stimulating: testes and ovaries (gonads) (from GnRH at the hypothalamus)
Prolactin: mammary glands. parental behavior and promote lactation.
GH: bones: many things while you’re sleeping mostly.
Somatotropic horone (released from hypothalamus during sleep) INfluence protein metabolism. Related to chronic stress (less GH release)

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14
Q

Describe the adrenal gland

A

Adrenal cortex (80%): get signals from anterior pituitary.

  • releases steroid hormones
  • glucorticoids (cortisol)
  • regulate glucose metabolism
  • mineralocorticoids (aldosterone) ionic balance. Mineral corticoids. Sodium levels in body for aldosterone act on KIDNEYS to stop urination for salt retention.
  • sex steroids (antrostenedione) organizing body hair.
  • MADE ON DEMAND. can’t have them running about in the body cause they can cross plasma membranes.

Adrenal medulla: get signals from direct innervation from ANS (para and sympathetic NS- efferent)
- release amine hormones like epi and noepi.
- increase heart rate, take in more air, blood retained in core, noepi in your brain under stressful events too.
FAST ACTING stress hormones.

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15
Q

What’s the thyroid gland?

A

Release thyroid hormones (around adams apple)

  • thyroxine, triiodothyronine which regulate basic metabolism.
  • and calcitonin: promote calcium storage in bones. If you have thyroid issues, you have bones and calcium retention.

-They are Amines that act like steroids (can cross plasma membrane)
- Iodine is used in the thyroid, changes in diet can change thyroid function (iodized salt)
Regulate growth and metabolism.

Hyperthyroidism: changes in alertness, awakeness, cognition, depression.
Diet is big contributor.

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16
Q

What is the pineal gland?

A

Your third eye (in birds-photoreceptors close to the skull and snakes-parietal eye)
not seat of the soul
- in the midbrain
- get signal from peripheral nervous system (PNS) from SUPERIOR CERVICAL GANGLION
- Releases melatonin for sleeping cycles.
-Release inhibited in presence of light.

  • inhibits/interacts with gonadotropic releasing hormones that cause stimulation of gonads, as days get shorter, less melatonin release, so MORE GNRH and more mating behavior arise!!
17
Q

What are the gonads?

A

Testes and ovaries! Both have one for sex hromone production and one for gamete production.
- GnRH (from hypothalamus) to anterior pituitary which releases FSH/LH to the gonads.
Testes: sertoli cells (sperm)
Leydig cells (androgens)

Ovaries (ova: gametes)
Steroid hormones like progestins and estrogens (progesterone and estradiol).

Kisspeptin: stimulates GnRH (important in puberty onset>

Organizing effects are powerful
Activational effects are more present in rats/lizards, less for humans.

18
Q

Hormones in Behavior?

A

Yes, but more responses are observed in birds and stuff. Cortex supersedes older controls for behavior. More likely that behavior influences hormones (psychosocial dwarfism, when removed, they grow again)

Oxytocina nd vasopressin/adh.
Oxy: mediates behavior in females
Vasopressin: equivalent in males.

Inject oxytocin: rats lay on top of each other.
Remove oxytocin gene in mice: social amnesia, will act like its the first time meeting each other. inject oxytocin and it goes away .
- oxytocin seen in ventral pallidum (part of globus pallidus) main target of nucleus accumbens (where u find the most.

Prarie voles (more oxytocin mate for life) 
Meadow voles: fewer oxytocin/adh shits
19
Q

Is oxytocin the love molecule?

A

no. oxytocin amplifies stress response. if you block it it releives social stress in animals, not just social bonding. If someone is beating u up, oxytocin blocking makes u less stressed.

LInk between early trauma and addiction. Gendered results: men given oxytocin showed less activity in amygdala, and reduced cravings. Oxytocin benefitted men not women.

Oxytocin also increases ingorup bias: train task (oxytocin makes u save people who matter more to you and more ok with murdering outgroup)

20
Q

are pheromoens a thing?

A

not REALLY.
part of olfactory system. VOMERONASAL ORGAN. In animals YES in people NO
1. we have a vomeronasal organ
2. they have no receptors on them
3. never recorded activity
4. genes have become pseudogenes.
THis what happens to things that aren’t valuable to us.

Maybe they’re acting on standard olfacotry system.
- shouldn’t have a concious smell.

McClintock effect: sync menstual cycels, but evidence is weak.

Men’s sweat: not a great thing.

21
Q

Are stress hormones mediating behavior?

A

yes. some of it central (in brain) and other dual pathways.
HPA: hypo pituitary adrencal cortex to release glucocorticoids
Sympathetic nervous system from adrenal medulla to release noepi and epi. quick boy.
Quick acting
(also noepinephrine from locus corelus is released)

influenced by the context of he situation: stooge!!
- schacter: new vitamin (epinephrine) made people shift towards valence of the stooge.

Stress mounts body for a response, and needs to be contextualized.

22
Q

SEX. GENDER, THE GOOD STUFF!

A

Biolcial sex, gender identity, sexual behavior, sexual orteintation (asexuality 1%)., intersex births (2.5%) ambiguous genitals, measure length of phallus

23
Q

Support “sex hormones have potent organizational effects”. How does it vary?

A

Chromosomes aren’t your sex!
- Y chromosome SRY gene (6 weeks) that causes testes formation which release testosterone and antimullerian hormone. T + AMH cause male phenotype.
Female pattern is default (by 8 weeks differentiated)

Abnormalities:
AIS (androgen insensitivity) androgen receptor mutations. No menstruation, sex is painful, vagina is shallow/underdeveloped.
They have SRY, internal testes, but no androgen stuff!

SRY mutations: develop ovaries over testes
SRY hopping: XX male syndrome (sry on an XX chromosome, accidentaly transferred. ur a male)

AMH (or receptor) mutations: female ducts left behind. No degeneration.

High androgen exposure: congenital adrenal hyperplasa: XX fetuses express some male features. Genitals are intersex. Wollfian and mullerian ducts will for.

24
Q

How are differences in sex related to biology, physiology and pathology.

A

AMBIEN (gaba agonist like benzodiazopines)
- metabolism is 2x as fast for men (fundamental sex difference), so they need double the dose.
Same for alcohol

PAIN
-estrogen interacts with metabolism and whatnot and makes them feel pain more and requries less meds for pain cause they break them down faster.

STRESSORS: women more likely to get depression, alziehemers, lung cancers
Men more likely to get addiciton, commit suicide and have parkinson’s disease.

25
Q

Do androgens and estrogens mediate behavior?

A

Non humans: yes. More teritorial and interested in mating in some time periods. testosterone higher in lizards.

Humans: somewhat.

Rats/humans: sexual activity not determined by amount of androgen levels (but need some for the behavior)
Some testosterone is needed for male sexual interest.
It comes back to what it was at before. need for some but doesn’t track beyond that.

Agression and testosterone are related somewhat. Iguanas fight with each other (Do pushups) and songbirds will sing a lot. In humans, not much effect.

vicarous experiments: winning team goes up, loisng team goes down. CHildren accidentaly exposed show higher levels of agression.

26
Q

Are gendered behaviors present?

A
  • biology determined or driven by environment. CHoice of toys depends on what adult gives them usually. Male babies are picked up and held more. girl babies looked at more.

Are they to do with biology or social stuff?

Men: spatial rotation, folding, throwing stuff
Women: perceptual speed, fine motor control, verbal fluency, visual memory.

Some abilities are dissappearing

27
Q

How is sexual orientation described by hormones?

A

Homosexuality in many species.
Rams (preoptic area, 10% of males are gay)
Humans, INAH-3 of preoptic area in hypothalamus for gay men, but the study was done post mortem of people who’d died of aids SO.

Fraternal birth order. 33% more likley each older brother you have. Mothers being exposed to hormones they’ve never had, build a response over time.

Women: higher fetal androgen exposure, and 2D/4D finger digit ratio. Gay women have shorter index finger.