Exam 1 Flashcards

(102 cards)

1
Q

Behavioral endocrinology

A

The study of the interaction between hormones and behavior

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2
Q

Brown-Sequard

A

Brown-Sequard-syndrome; First scientist to work out the physiology of the spinal cord; First to postulate the existence of substances (hormones) secreted into the bloodstream to affect distant organs; removal of the adrenal glands resulted in death; Self-injected with an extract derived from the testicles of dogs and guinea pigs (know as the Brown-Séquard Elixir)- made him feel “younger”

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3
Q

Berthold

A

First recognized experiments in behavioral endocrinology; hen/rooster experiments; testes are transplantable, can develop vasculature, and are important for masculinizing males; proposed that a secretary blood-borne product of the testes was responsible for normal development

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4
Q

Radioimmunoassay (RIA)

A
  1. Antibody is coating the test tube interior
  2. Take known level of the hormone (radioactively labeled) and put it in the vial
  3. Then take unlabeled hormone (in known concentrations) and add it to the vial to compete off the labeled hormone
  4. Measure repeatedly with labeled vs unlabeled hormone to create a curve of radioactivity
  5. Take the unknown level of hormone (blood, etc.) and then dump it in with some radioactivity and match it to the curve to determine the concentration of the hormone in the unknown fluid
    Measures the levels of hormones
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5
Q

Bioassay

A

An analytical method to determine concentration or potency of a substance by its effect on living cells or tissues; used to estimate the potency of agents by observing their effects on living animals or tissues; measures hormone levels

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6
Q

Immunocytochemistry

A

You have a florescent tag on an antibody and you want to know where cells express a certain receptor so you dump the antibody for that receptor on the cell. You can then excite it with light and see where the antibody is glowing on the issue.
Measures the levels of proteins

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7
Q

Behavioral assay

A

An organismal assay used to study the relationship of behavior to the environment or an experimental condition; measures hormone levels

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8
Q

Hormones

A
  • Organic messengers produced and released by endocrine glands; initiated and transported by Golgi apparatus in an endocrine cell; vesicle fuses to Cell membrane of secretory organ and goes into blood stream; binds to target cell
  • Can be long distance. (coordinate physiology and behavior – reproduction; (slower, not as controlled, analog)
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9
Q

Western Blot

A

-Take tissue and grind it all up (to get the proteins out of the cell membranes). Denature w/ detergent. Then, coat the proteins with a chemical that puts a negative charge on them. Put the negatively charged proteins in a gel.
Larger molecules will move through the gel more slowly than the smaller molecules so they all separate based on size. Push the proteins off the gel onto a membrane (kind of like a piece of paper) so you can see the lines and such. Then use the antibody technique with the paper and dump that onto the paper.
-Measures the concentration of receptors, but not where they are/which cells they are in; measures protein levels

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10
Q

Autoradiography

A
  • The use of X-ray (or occasionally photographic) film to detect radioactive materials. It produces a permanent record of the positions and relative intensities of radiolabeled bands in a gel or blot.
  • Measures where hormones are in the brain; measures protein levels
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11
Q

In situ hybridization

A

You tag a probe that gets at an RNA sequence in the cell that makes the protein of interest. The tag will bind to the RNA and it will become fluorescent. Dump the tag on a tissue, and wherever the probes bind, you have dark spots, so you can see where this RNA sequence is; (measure DNA/RNA)

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12
Q

Agonist

A

chemicals that can activate receptors (essentially mimics the function of the hormone)

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13
Q

Antagonist

A

chemicals that can inhibit the receptors (blocks the action of the hormone)

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14
Q

Brown-Sequard Syndrome

A

the hemisection of the spinal cord, resulting in paralysis and loss of proprioception on the same (or ipsilateral) side as the injury or lesion, and loss of pain and temperature sensation on the opposite (or contralateral) side as the lesion.

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15
Q

Berthold Conclusions (hen/rooster studies)

A

1) Testes are transplantable organs
2) Transplanted testes can function and produce sperm
3) Because testes function normally after all nerves are
severed, the are no nerves directing testes function.

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16
Q

Neurotransmitters

A

chemical messengers used by the nervous system; acts across neural synapse; initiated and transported by Ca 2+ and vesicle from a neuron; vesicle fuses to synaptic cleft of target neuron; binds to post-synaptic receptors

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17
Q

Technique: Is this necessary and/or sufficient?

A

Ablation and Replacement (eg. Berthold’s chickens)

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18
Q

Technique: How much hormone is there?

A

Radioimmunoassay (RIA); Enzyme immune assay (EIA)

eg. EIA - pregnancy test

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19
Q

Technique: How much protein is there?

A

Immunocytochemistry(cells)/immunohistochemistry(tissue) (ICC/IHC); Western blot (eg. Auger et al)

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20
Q

Technique: How much DNA/RNA is there?

A

In situ hybridization

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21
Q

Technique: How much hormone is bound to the receptor?

A

In situ autoradiography

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22
Q

Technique: To what extent is a gene involved in phenotype?

A

Optogenetics; transgenic models(knockouts)

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23
Q

Technique: To what extent is a receptor involved in phenotype?

A

Antagonists & agonists (eg. Bales & Carter)

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24
Q

5 main features of endocrine system

A

1) Endocrine glands are ductless
2) Endocrine glands have rich blood supply
3) Hormones, products of endocrine glands, are secreted into the blood stream
4) Hormones can travel in blood to virtually every cell in body
5) Hormone receptors are specific binding sites embedded in membrane or in the cell.

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25
Chemical messenger
Any substance that is produced by a cell that affects the function of another cell
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Cytokine
A chemical messenger that evokes proliferation of other cells, especially in the immune system
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Neurohormone
A hormone produced by a neuron
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Neuromodulator
A hormone that changes (modulates) the response of a neuron to some other factors
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Neuropeptide
A peptide hormone produced by a neuron
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Neurosteroid
A steroid hormone produced by a neuron
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Endocrine vs. Exocrine cells
Exocrine = release substances into DUCTS, endocrine = release substances into BLOODSTREAM
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5 types of mediation
Intracrine, autocrine, paracrine, endocrine, ectocrine
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Intracrine mediation
synthesized in a cell, regulates something within that cell
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Autocrine mediation
synthesized in a cell, released from the cell, acts on that same cell
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Paracrine mediation
synthesized in a cell, released, acts on a nearby cell
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Endocrine mediation
synthesized in an endocrine cell, released into blood stream to act on cells far away
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Ectocrine mediation
one organism releases a chemical signal that affects another organism
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4 classes of hormones
Protein & peptide, Steroid, Monoamines, Lipid-based; (differ in mode of release, how they move through blood, location of target receptor, and the biological/cellular response)
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Hypothalamic signaling to anterior pituitary
Anterior highly vascularized; neural synapses on portal vessels to affect the gland; Hypothalamus->pituitary portal vein(via neurons)->anterior pituitary->endocrine cells-(releasing factor)>systemic circulation
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Hypothalamic signaling to posterior pituitary
Posterior closer to spinal chord; neurons from hypothalamus go directly into posterior pituitary; uses neurosecretory cells that synapse onto blood vessel; Hypothalamus->systemic circulation
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Anterior pituitary hormones: GnRH (gonadotropin releasing hormone)
influences the anterior pituitary to release LH and FSH to affect the gonads
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Anterior pituitary hormones: GHRH/GHIH (growth hormone-releasing/inhibiting hormone)
influences the anterior pituitary to release growth hormones, which affect growth, concentration, memory, and anxiety/emotional distress; affects the liver and cells throughout the body
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Anterior pituitary hormones: CRH (corticotropin-releasing hormone)
influences the anterior pituitary to release ACTH to affect the adrenal cortex to release cortisol (the stress pathway)
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Anterior pituitary hormones: TRH (thyrotopin-releasing hormone)
influences the anterior pituitary to release TSH onto the thyroid to release TH (thyroid hormone), important for metabolism, growth, and reproduction; TH = triiodothyronine (T3) and thyroxine (T4)
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Anterior pituitary hormones: PRH/PIH (dopamine/prolactin inhibitory hormone and prolactin releasing hormone)
influence the anterior pituitary to release prolactin to the breasts, which influences reproduction, growth/development, stimulation of milk production
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Posterior pituitary hormone: vasopressin (AVP; ADH)
aka an antidiuretic hormone, influences the kidneys to retain water
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Posterior pituitary hormone: oxytocin
involved in lactation, prompts the release of milk; uterine muscles/mammary glands
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Protein & Peptide hormones
Soluble in blood - do not need carrier proteins; peptide hormones = only a few amino acids in length, fasting-acting (5-10 mins); protein hormones =polypeptides, many amino acids, slow-acting (20-30 mins); stored in endocrine cells and released by exocytosis; Peptide = Signal transduction - relay molecules in cytoplasm -> amplification
49
Steroid Hormones
Cholesterol(all steroid hormones come from) -> Progestins(progesterone)->Glucocorticoids; Androgens(testosterone)-> Estrogens -steroid hormone properties: fat-soluble, not water soluble, need a carrier protein, can bind to receptor or move into the target cell, slower-acting
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Five classes of steroid hormones
Androgens, estrogens, progestins, mineralocorticoids, and glucocorticoids
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Androgens
Testosterone, androtenedione, dihydrotestosterone (DHT)
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Estrogens
17b estradiol, estrone, estriol
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Progestins
Pregnenolone, progesterone
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Mineralocorticoids
Aldosterone
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Glucocorticoids
corticosterone, cortisol
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Catecholamines
epinephrine, norepinephrine, dopamine
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Biological sex:
Can be determined by environmental factors, social factors, or (in humans and most mammals) chromosomal factors and gonadal differentiation at embryonic weeks 7&8
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Gender:
Can be determined by attitudes, feelings, and behaviors associated with a person’s biological sex
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Androgen insensitivity syndrome (AIS)
Chromosomes XY are present, so the SRY gene leads to the formation of testes. The testes secrete large amounts of testosterone. However, the androgen receptors are not working properly; therefore, the brain structure and external genitalia will be more female-typical. Testosterone is converted to estrogen and they are usually "all female." People with this syndrome are infertile because they have internal testes, a short vagina, and no cervix. Female carriers of this syndrome have one X chromosome with the mutation and one normal X whereas the affected individuals have one X chromosome with the mutation and one normal Y.
60
Congenital adrenal hyperplasia (CAH) syndrome
In this syndrome, the lack of 21-hydroxylase leads to an increase in the amount of adrogens being released from/synthesized in the adrenal glands. This enzyme blocks progesterone conversion to mineralocorticoids, so they are converted to androgens instead. These individuals have XX chromosomes with developed ovaries but the high androgen concentration leads to masculinization of the internal/external genitalia and the brain. This leads to abnormal sexual development in these females; they will have ambiguous genitalia (the males will not). However, both males and females will have early-onset puberty and early growth stoppage.
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Turner syndrome
Chromosomal sex is XO (only one sex chromosome); female-typical. Symptoms include gonadal dysfunction, possibly sterile, high risk for hypothyroidism and high risk for congenital heart disease; characterized by short stature, low-hairline, low-set ears, webbed neck
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Klinefelter's syndrome
Chromosomal sex is XXY; male-typical. Symptoms include hypogonadism and reduced fertility, weak muscles, some breast development
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XYY syndrome
A human male receives and extra Y chromosome; there are no severe symptoms, but they may be taller than average, may have severe acne during adolescence, learning disabilities, and behavioral problems such as impulsivity
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De la Chapelle syndrome
A human male with XX chromosomes. This is a rare condition in which an X chromosome exhibits the Sry gene. Some have hypospadias (urethral opening not at its normal position at the end of the penis) at birth or may have undescended testes. However, most have no symptoms at all.
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Triple X syndrome
A female has chromosomes XXX. Happens in 1 per 1,000 births and the female has no symptoms.
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Tetrasomy X syndrome (XXXX)
A condition where the female has four X chromosomes. Symptoms are highly variable with some severe and others mild; commonly they display learning disabilities or delays.
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Pentasomy X syndrome (XXXXX)
This many X chromosomes lead to more severe symptoms. There is an impact on cognitive functioning and body structure and reduced fertility.
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Dosage compensation
the mechanism by which the imbalance in gene number between the sexes is corrected
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Mary Lyon's hypothesis
Females essentially de-activate one of the X chromosomes via barr bodies
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How is the amount of barr bodies present determined?
Number of X chromosomes minus 1
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Why X inactivation?
The imbalance of gene number between the sexes needs to be corrected to ensure genes from the chromosomes are the same in both sexes. The X chromosome has thousands of genes while the Y only has a few hundred.
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When does X inactivation occur?
In mice: All cells undergo an early, imprinted inactivation of the paternal X chromosome in two-cell or four-cell stage embryos. In the blastocyst stage, the inactivation is reversed such that all Xs are active. Then, each cell independently inactivates one X at random (paternal or maternal).
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Random X inactivation
Occurs in the early female embryo, where both the maternal and paternal X chromosome have an equal chance of becoming inactivated; the cell first counts how many Xs there are and then chooses to inactivate one
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Why is X inactivation random?
to have a better chance to cope with X-linked mutations
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Mechanism for silencing an X chromosome
XIST is a noncoding RNA that silences the chromosome it's activated on. The chromosome will display histone modifications and DNA methylation
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4 properties of XIST
1. does not code for a protein, but produces a 17 kilobase (kb) functional RNA molecule 2. expressed on the inactive X chromosome 3. remains within the nucleolus to coat the chromosome 4. only expressed in cells with at least two Xs
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Testosterone to estradiol
Converted with aromatase
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Alpha-fetoprotein
In the 2nd week of life, the gonads secrete hormones, but this molecule binds it up. estrogen is prevented from reaching the brain, but testosterone is not.
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Sexual dimorphisms have been found in
- Volume of tissue - Cell death - Connectivity - Cell morphology - Expression of protein - Migration - Neurogenesis - Epigenetics
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Sexual dimorphism: Volume of tissue
When you take a stain of the hypothalamus, you'll see a clustering of cells in the SDN (sexually dimorphic nucleus) of the preoptic area, but the cluster is more dense in the males than the females. Testosterone being aromatized in the brain causes this difference (blocks apoptosis)
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Sexual dimorphism: Cell death
Testosterone kills cells in AVPV; females have larger volume in this area; castrated males(before 10 days of age) have similar AVPV sizes to females; differences in testosterone's effect on cell death in SDN and AVPV exist only for a few days during early life
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Sexual dimorphism: Connectivity
Vasopressin system; Males have more vasopressin = more fibers in the BNST and lateral septum (as part of vasopressin connectivity)
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Sexual dimorphism: Cell morphology
- Neuronal spines: Conditions with high levels of testosterone (males) have significantly fewer spines within arcuate nucleus (AC) - Glia: higher levels of testosterone (males) = more complex glia - more fully differentiated astrocytes with longer processes
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Sexual dimorphism: Expression of protein
Males have more progestogen receptors in the MPN, driven by a difference in estrogen concentration
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Sexual dimorphism: Migration
Estrogen affects the rate/localization of neuronal movement such that female brains' neurons travel a lot further/faster than those in male brains and they have a more defined direction
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Sexual dimorphism: Neurogenesis
In the CA3 region of the hippocampus, you'll see many cells being born. During development, males have higher levels of neurogenesis in this region; females injected with estrogen during development will have increase in neurogenesis
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Sexual dimorphism: Epigenetics
Maternal behavior (licking/grooming) in rats guides sexual differentiation of the genome; mothers lick/groom males more than females; females have more estrogen receptors than males - females with additional contact (same as males) will have lower estrogen levels
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DNA methylation
Reduces transcription to silence a gene; "on state" = unmethylated cytosines and active/unwound chromatin; "dim/off state" = methylated cytosines and silent/condensed chromatin
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"Good"/"bad" rat mother behavior study
Good behavior = licking/grooming pups; pups from good moms had high glucocorticoid receptor expression + low anxiety + good stress response; attentive mothers caused methyl marks to be removed = low methylation of GR promoter (non-attentive = high)
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Change in methylation in rat pups from prenatal to a few weeks old
Prenatally, there's low methylation. On postnatal day 1, there is a spike in methylation. Then, if the pup has a high-licking mom, the methylation will decrease but if the pup has a low-licking mom, they methylation will stay elevated
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Diet & epigenome
Exposure to BPA in pregnant rats = pups with yellow coat, obese, tumors, higher rates of diabetes and cancer; BPA causes demethylation of agouti gene (which is normally methylated in healthy pups); Another group of pregnant mothers fed BPA + high choline, folic acid, B12 diet would yield normal pups ->good diet can counteract BPA toxin and increase methylation
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Reversible epigenetic patterns
Castrated male rats = decreased levels of vasopressin and increased methylation; Introducing testosterone reverses the effect ->demethylation
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Sex differences during adolescent development
Females diagnosed more than males with anxiety and depression; depression diagnosis spikes with puberty; anxiety diagnosis increase with age
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Conditioned place preference
3 chamber task: animal put into 1 chamber - another animal added and allowed to play, then removed; animal then moved to different chamber and remain alone; when barriers removed, animal prefers chamber where it played with other animal
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Why study play?
Alters brain development and refines social interactions; brain areas for play = PFC and amygdala; more testosterone in amygdala = more play
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Development of the adolescent brain and its responses to emotional stimuli
Presence of mothers buffered childrens' amygdala response to emotional pictures; teenagers unaffected by presence of mothers; children who grew up w/o parents had faster maturation of brain (PFC) and showed teen-like response to emotional pictures
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Knockout (KO)
You can remove genetic material to create a "knock out" that lacks a certain receptor. Take embryonic stem cells and introduce the mutant gene into the cells. Take the new DNA stem cell and put it into a blastocyst. Take the blastocyst and put it into a host so it can grow into an embryo and be born. When the animal is born, it will have both mutated and non-mutated DNA in it. Then have two "mixed" organisms mate, and then some of their babies will have completely mutated DNA (thus be a full-knock out).
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Formation of testes
Y chromosome -> carries SRY gene -> presence of SRY gene increases SOX9 -> formation of testes -> testosterone
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Steroid receptor function
Located inside cells, in the cytosol or the nucleus; steroids lipid-soluble, so they penetrate cell membrane to bind with these receptors; when receptors bind with steroid hormone, they migrate to nucleus to regulate gene transcription
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Too much/too little GH =
Too much: oversized body; too little: undersized, depression, poor memory/concentration, anxiety
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Too much CRH =
Suppress appetite, anxiety, boost attention
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Too much/too little TSH =
- Too much: Graves’ disease, rapid heart rate, weight loss, intolerance to heat, increased bowel movements, anxiety - Too little: Slow heart rate, weight gain, intolerance to cold, constipation, depression