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Behavioral Endocrinology > Midterm > Flashcards

Midterm Flashcards

1
Q

What do hormones increase the probability of?

A

A behavior occurring

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2
Q

__% of brain is glia

A

90%

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3
Q

How can you strengthen a synapse?

A

By increasing dendritic spines or receptor density

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4
Q

Nigrostriatal pathway

A

active in maintaining normal motor behavior

loss of DA is related to muscle rigidity (Parkinsons)

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5
Q

Mesolimbic pathway

A

DA release causes feeling of reward and pleasure

NT system most affected by addictive drugs

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6
Q

Hormones

A

Chemical messengers released from endocrine glands that travel through the blood stream to influence the nervous system and regulate the physiology and behavior of an organism

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7
Q

Where do hormones come from?

A

hormones are produced by glands and secreted into blood

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8
Q

Where do hormones go?

A

They travel in the blood to target tissues containing specific receptors for the hormones

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9
Q

What do hormones do?

A

By interacting with their receptors, hormones initiate biochemical events that can activate gene expression (via intracellular receptors) or induce fast, non-genomic effects (via membrane receptors)

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10
Q

Main function regulated by secretion of hypothalamus?

A

Control of hormone secretions

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11
Q

Main function regulated by secretion of pineal gland?

A

Reproductive maturation; body rhytms

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12
Q

Main function regulated by anterior pituitary secretion?

A

hormone secretion by thyroid, adrenal cortex, and gonads; growth

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13
Q

Main function regulated by posterior pituitary secretion?

A

water balance; salt balance

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14
Q

Main function regulated by thyroid secretion?

A

growth and development; metabolic rate

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15
Q

Main function regulated by adrenal cortex secretion?

A

salt and carbohydrate metabolism; inflammatory reactions

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16
Q

Main function regulated by adrenal medulla secretion?

A

emotional arousal

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17
Q

Main function regulated by pancreas (islets of Langerhans) secretion?

A

sugar metabolism

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18
Q

Main function regulated by gut secretion?

A

digestion and appetite control

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19
Q

Main function regulated by gonads (testes/ovaries) secretion?

A

body development; maintenance of reproductive organs in adults

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20
Q

Neuronal Transmission

A

electrochemical communication. fast, highly specific. NTs are released over a short range (synapse)

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21
Q

Hormonal Communication

A

long-range, slow, very widespread. coordinates response across whole-organism

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22
Q

2 advantages of global communication for hormones?

A
  1. Developmental: coordinated transformation of all cells in an organism
  2. Coordination of a body’s response to an environmental trigger
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23
Q

Negative Feedback System

A

How hormone production is regulated.

The production of a hormone by the target tissue (e.g cortisol from adrenals) feeds back to the source of the hormone to stop production

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24
Q

Hormone action on the brain

A

A hormone secreted from an endocrine gland travels through the blood stream to target tissues (including the brain)

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25
Q

Steroid hormones & blood brain barrier

A

Steroids are lipophillic (fat loving) and can pass through the phospholipid bilayer

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26
Q

De Novo

A

Brain has all machinery to make hormones

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27
Q

Areas in the brain with dense receptors suggests what?

A

Higher sensitivity to that hormone

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28
Q

For every hormone there are ___ receptors in the brain

A

unique

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29
Q

3 things a hormone does once it binds to a receptor in a brain cell?

A
  1. might change membrane potential, making it easier or harder to start an action potential
  2. could impact gene transcription, mechanism for increasing/decreasing receptor expression
  3. change protein expression (e.g stimulate NT synthesis)
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30
Q

4 behaviors that hormones influence?

A

stress
memory
aggression
depression

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31
Q

6 brain regions in the limbic system?

A 
thalamus
nucleus accumbens
hypothalamus
amygdala
hippocampus
VTA
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32
Q

Odine’s Curse

A

lesion to midbrain region and you lose capacity to do automatic breathing. you die of sleep deprivation

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33
Q

What role does amygdala have in limbic system?

A

fear, anxiety, aggression

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34
Q

What role does hippocampus have in limbic system?

A

turns off stress response

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35
Q

What is the last part of the brain that matures?

A

frontal cortex

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36
Q

What is the best predictor for how large the frontal cortex is in a species? What does this suggest?

A

The average size of their social group

Suggests that this part of the brain evolved for gossip and social intelligence and social behavior

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37
Q

3 classes of evidence to establish hormones-behavior relationship

A
  1. the behavior disappears when the hormone is removed or blocked
  2. replacing the hormone reinstates the behavior
  3. hormone concentrations and the behavior covary (behavior occurs when hormone concentration is high; never or rarely when hormone concentrations are low)
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38
Q

4 levels of analysis as to what causes zebra finches to sing?

A
  1. immediate causation
  2. development
  3. evolution
  4. adaptive function
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39
Q

Ablation & Replacement Steps (Behavioral Endocrinology Techniques)

A
  1. Gland that’s suspected to be the source of a hormone affecting a hormone is surgically removed
  2. The effects of removal are observed
  3. The hormone is replaced by re-implanting the removed gland, or injecting a purified hormone
  4. Determine whether the consequence of ablation is reversed by replacement therapy
    (e. g Berthold’s experiment)
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40
Q

RIA (radioactive immunoassay)

A

A technique for determining antibody levels by introducing an antigen labeled with a radioisotope and measuring the subsequent radioactivity of the antibody component

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41
Q

EIA (enzyme immunoassay)/ELISA (enyzme-linked immunoassay)

A

Both techniques are based on the principle of immunoassay with an enzyme rather than radioactively as the reporter label

Home pregnancy tests use a form of EIA

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42
Q

Immunocytochemistry

A

Identifying neurons that produce a particular hormone or NT

Where in the body is the hormone or hormone receptor?

1st antibody - against NT
2nd antibody - labeled

Technique that uses antibodies to determine the location of a hormone or hormone receptor in body

The range of microscopic techniques used in the study of the immune system

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43
Q

What kind of samples is immunocytochemistry performed?

A

On samples consisting of cells grown in a monolayer or cells in suspension which are deposited on a slide, relies on same enzyme reactions as IHC

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44
Q

Immunohistochemistry

A

Where in the body is the hormone or hormone receptor?

Test to detect antigens (e.g proteins) in cells of tissues by exploiting the principle of antibodies binding to specific antigens

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45
Q

What kind of samples is immunohistochemistry performed?

A

Performed on samples derived from tissues that have been histologically processed into thin sections and the staining process exploits enzymes which catalyze the deposition of a colored staining product at antigenic sites within sample

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46
Q

1) Estrogen receptors could be localized where in the brain?

2) Estrogen receptor colocalized with cells staining for what NT? As well as what 2 receptors containing neurons?

A

1) Both neurons and astrocytes

2) Dopamine, D1A, D2

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47
Q

Autoradiography

A

A technique used to detect a radio labeled substance, such as a hormone, in a cell or organism, by placing a thin slice of the material in contact with a photographic emulsion

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48
Q

Autoradiograph

A

Image on an x-ray film or nuclear emulsion by the pattern of decay emissions (e.g beta particles or gamma rays) from a distribution of a radioactive substance

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49
Q

In Situ Hybridization

A

A technique in which nucleic acid probes are used to locate specific nucleic acids (DNA in chromosomes and RNA in cells)

Not at the protein but at the level of gene expression to identify tissues that show specific protein (hormone, receptor, etc)

Stain for something specific (e.g oxytocin)

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50
Q

Pharmacological Techniques

A

The use of chemical agents that may alter the action or function of a hormone

2 major groups referred to as agonists and antagonists

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51
Q

Agonists

A

Hormone mimics

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52
Q

Antagonists

A

Hormone blockers

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53
Q

2 ways agonists and antagonists can be administered to an animal?

A

Cannulation: Chronic indwelling

Single injection: using a syringe and needle

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54
Q

In general, what are tract tracing methods used to map?

A

A neural circuit

Where does a particular cell project

You see what’s stained after it’s injected

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55
Q

Anterograde tract tracing

A

Inject tracer in cell body, and explore cell’s axonal projections

Let it diffuse along axonal projection to see where it ends up

How a cell body might be producing a certain hormone, where it’s branching off to, etc

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56
Q

Retrograde tract tracing

A

At fiber terminals, and examine location of cell body

Injection is going backward

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57
Q

Knockout/in mice

A

Produce mice in which a specific gene has been deactivated (knocked out)

Use DNA, or a mutant copy of gene you’re interested in

Take cells that have one mutant copy and introduce it into embryo or astrocyte

Through selective breeding paradigms, you can get mice that have wild-type or double knockout

You can make hypothesis about which receptors are used in certain roles

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58
Q

(Knockout/in mice) forms of estrogen receptor knockout mice

A

Wild-type: normal, what you would expect to see

Alpha: less branching; selective knocking out produces change in mammary glands in alpha, but not beta

Beta: looks similar, fully developed duct network

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59
Q

Optogenetics

A

Newer techniques, last 10-15 years.

Both probing and manipulating function of nervous system.

You engineer mice that have a special ion gate that are light activated.

Put ion channels in different neurons, ex) dopamine neurons (whatever you want to manipulate, you can activate or inhibit specific neurons, you can see how activating a specific area it’s called cell specific you can see what effects that has on specific circuit)

Can drive specific cell types, exquisite experimental control over neurons

You can look at multiple layers (e.g lamina throughout cortex)

Beautiful, large scale volume layerts

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60
Q

What is leptin released from (a decade ago)?

A

Adiopose (fat) cells

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61
Q

Leptin mutation in mice that causes obesity

A

Someone discovered there was a mutation in mice that causes extreme obesity, if it develops two copies of this defective gene, they’re homozygous - they become hyperphagic - they over eat & reproductively sterile

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62
Q

Ob gene

A

codes for leptin

travels to CNS to regulate

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63
Q

Intracrine Mediation

A

Intracrine (hormone that acts inside a cell) substances that regulate intracellular events

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64
Q

Autocrine Mediation

A

Autocrine (cell secretes a hormone that binds to autocrine receptor on same cell) substances feedback to regulate the same cell that secreted them

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65
Q

Endocrine Mediation

A

Endocrine cells secret chemicals into the bloodstrem, where they may travel to distant target cells

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66
Q

Paracrine Mediation

A

Paracine cells that secrete chemicals that affect adjacent cells

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67
Q

Ectocrine Mediation

A

Ectocrine substances, such as pheromones, are released into the environment by individuals to communicate with others

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68
Q

Chemical Messenger

A

Any substance that’s produced by a cell that affects the function of another cell

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69
Q

Cytokine

A

A chemical messenger that evokes proliferation of other cells, especially in the immune system

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70
Q

Hormone

A

A chemical messenger that’s released into the blood stream or tissue fluid system that affects the function of target cells some distance from the source

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71
Q

Neurohormone

A

A hormone produced by a neuron

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72
Q

Neuromodulator

A

A hormone that changes (modulates) the response of a neuron to some other factors

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73
Q

Neuropeptide

A

A peptide hormone produced by a neuron

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74
Q

Neurosteroid

A

A steroid hormone produced by a neuron

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75
Q

Neurotransmitter

A

A chemical messenger that acts across the neural synapse

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76
Q

How is the pituitary gland connected to hypothalamus?

A

by median eminence

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77
Q

One important feature of the major endocrine glands?

A

Highly vascularized, they harness the bloodstream to travel

Thyroid is the most highly vascularized in entire body

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78
Q

If you want to control hormones without agonists or antagonists what do you do?

A

speed up or slow down vascular flow

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79
Q

The human pituitary is the size of what?

A

a blueberry, yet it secretes many hormones

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80
Q

Anterior and posterior pituitary have different one?

A

embryonic origins and function

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81
Q

What is called the “conductor of endocrine orchestra”?

A

Posterior pituitary, weighs 1 gram (like a paper clip) yet it controls all major endocrine systems and completely indispensable for life

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82
Q

Together, the hypothalamus and pituitary serve to regulate what?

A

Many peripheral endocrine glands

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83
Q

Where does the hypothalamic nuclei integrate info from? What does it coordinate?

A

other parts of the brain

coordinates physiological, bodily processes

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84
Q

Neurosecretory cells

A

at the base of hypothalamus

very similar to conventional neurons but they release neurohormones, they’re released into blood vessels into pituitary gland

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85
Q

Releasing hormones

A

What hypothalamus releases

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86
Q

Hypothalamus is located at _____ and communicates with the ____ via ___ and ___

A

base of brain

pituitary

blood and neurons (axons)

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87
Q

When projecting to the anterior pituitary, where do hypothalamic axons project? What does it carry?

A

project to portal system which carries releasing factors to the anterior pituitary

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88
Q

How does anterior pituitary cells responds to the releasing factors (RF)?

A

They release their own tropic hormones into general circulation

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89
Q

(Hypo-Anterior PS) Peripheral glands release hormones that have ___ effect

A

Metabolic

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90
Q

(Hypo-Anterior PS) what kind of feedback do peripheral hormones tend to provide to both the hypothalamus and anterior pituitary?

A

Negative feedback

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91
Q

When projecting to the posterior pituitary, where do hypothalamic neurons project axons to?

A

The posterior pituitary (post. pituitary made up of axon terminals)

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92
Q

Posterior pituitary

A

Made up of axon terminals, releases hormones from hypothalamus into blood

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93
Q

What hormones does the posterior pituitary release?

A

Vasopression (AVP or ADH) & oxytocin

Released in response to action potential, causes exocytosis of cell into bloodstrem

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94
Q

Magnocellular neurosecretory cells

A

in hypothalamus - sends axons all the way down to synapse on blood vessels in posterior pituitary

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95
Q

HPG Axis regulates what?

A

sexual development & behavior

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96
Q

HPA Axis regulates what?

A

the stress response

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97
Q

HP Axis for Thyroid helps regulate what?

A

Energy metabolism

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98
Q

Vasopressin

A

Regulates water & sodium balance

Blood pressure, etc

Also activated in a stress response

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99
Q

Oxytocin

A

Hormone related to social behavior

Bonding, trust & relationships

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100
Q

Neuroendocrine Pulsatility

A

Refers to the coordinated, intermittent release of hormones by a population of neurosecretory cells

With chronic stimulation, the hypothalamus is going to release GnRH but the pituitary stops being responsive after a while

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101
Q

What is the largest class of hormones?

A

Protein and peptide hormones

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102
Q

How come protein and peptide hormones travel feely through blood?

A

They’re water soluble

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103
Q

Where are protein and peptide hormones stored? They’re released via what?

A

Stored - endocrine cells

Released via exocytosis

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104
Q

How do protein and peptide hormones show species specificity?

A

They’re structurally heterogenous

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105
Q

What kind of receptors are for protein and peptide hormones?

A

Transmembrane receptors (G-protein coupled receptors; Enzyme-linked receptors)

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106
Q

Hypothalamic hormones that are protein and peptide hormones?

A

GnRH
CRH
TRH
GHRH

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107
Q

Pituitary hormones that are protein and peptide hormones?

A

LH
FSH
ACTCH
Oxytocin

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108
Q

All steroid hormones are synthesized from what?

A

Cholesterol (amino acid sequence is highly conserved among vertebrates)

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109
Q

How come steroid hormones diffuse easily through cell membrane?

A

Small, fat soluble

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110
Q

How do steroid hormones move through blood?

A

Use chaperones bc they’re not water soluble

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111
Q

What kind of receptors are for steroid hormones?

A

Intracellular and membrane receptors

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112
Q

What steroid hormones are secreted from adrenal glands?

A

Cortisol

DHEA

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113
Q

What steroid hormones are secreted from gonads?

A

Testosterone
Estrogen
Progesterone

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114
Q

What steroid hormones are secreted from brain?

A

Neurosteroids

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115
Q

3 things blood concentrations of steroid hormones are governed by?

A
  1. rate of steroid biosynthesis
  2. rate of steroid inactivation (catabolism)
  3. “tenacity” (affinity) of binding between hormone and plasma carrier protein
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116
Q

Steroid hormones are never ___

A

stored

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117
Q

Steroids are released as they’re what?

A

Synthesized

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118
Q

What do steroid hormones bind to in the circulatory system?

A

Water-soluble carrier proteins

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119
Q

Levels of steroid are regulated by what?

A

Control (e.g phosphorylation) of enzymes that convert cholesterol to active hormones

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120
Q

4 Structural Classifications of Hormones

A

Protein/Peptide Hormones
Steroid Hormones
Monoamines
Lipid-Based Hormones

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121
Q

Prohormone

A

a substance that can act as a hormone itself or can be converted into another hormone that has different endocrine properties

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122
Q

Spermatogenesis

A

Production or development of mature spermatozoa

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123
Q

4 things androgens play a role in?

A

Male secondary sex characteristics (e.g body hair in humans, comb size in roosters)

Courtship/copulatory behavior

Aggression

Muscle Mass

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124
Q

What are androgens aromatized (convert into an aromatic structure) into?

A

Estrogens

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125
Q

Levels of a given steroid are regulated by what?

A

The presence of absence of enzymes that convert cholesterol to the active hormone

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126
Q

In the ovaries, enzymes convert testosterone to what?

A

Estrogen

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127
Q

5 estrogen functions

A

formulation of corpora lutea

secondary sex characteristics

bone mass

metabolism

sexual behavior

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128
Q

Corpora Lutea

A

Yellowish mass of progesterone-secreting endocrine tissue that forms immediately after ovulation from the ruptured graafian follicle in the mammalian ovary

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129
Q

Why are androgens and estrogens neither male nor female?

A

All male vertebrates produce some estrogen and progestins; all female vertebrates produce androgens

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130
Q

What is the difference in androgen and estrogen between the sexes?

A

The relative concentration of these circulating hormones

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131
Q

What is the difference in androgens and estrogens between the sexes driven by?

A

The amount of converting enzymes present in the gonads or elsewhere

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132
Q

Where are neurosteroids produced?

A

in the CNS in glial cells

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133
Q

Neurosteroids synthesis

A

Synthesized ‘de novo’ (anew) from cholesterol

Synthesis is independent of steroidogenic activity in other endocrine glands

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134
Q

3 examples of neurosteroids

A

progesterone
pregnenolone
DHEA

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135
Q

Function of Neurosteroids

A

Modulate neurotransmitter receptors or undiscovered hormone receptors (e.g progesterone receptor evident in CNS)

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136
Q

Classic Steroid Hormone Receptors

A

Are intracellular

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137
Q

Hormone-receptor complex

A

Transcription factor
Steroids
Binds to HRE on DNA to initiate gene transcription

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138
Q

3 major domains of steroid hormone receptors?

A
  1. steroid hormone binding site (C-terminal domain)
  2. DNA binding site (central domain)
  3. Site for other DNA binding proteins to attach (N-terminal domain)
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139
Q

Steroid-receptor complex binds to what to evoke what?

A

Binds to specific HRE on DNA to evoke activation or suppression of gene transcription

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140
Q

What guides the steroid-receptor complex to the right HRE?

A

Co-activators

Mechanism unknown

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141
Q

Non-genomic action of steroids (What has a number of findings indicated over the last 10 years?)

A

That steroids produce rapid (<10 min) behavioral effects not accounted for by changes in gene expression

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142
Q

Estradiol example of non-genomic actions of steroids

A

Estradiol’s ability to potentiate dopamine release

Bases of explaining non-genomic effects of steroids

143
Q

Non-genomic

A

Modulating ion channels, interacting with NT receptors, membrane receptors for steroids

144
Q

Genomic Action of Steroids

A

Slow, steroid hormone binds to intracellular receptor in cell -> genome interaction; increased protein synthesis -> latency of hours

e.g drive transcription of new proteins

145
Q

Non-genomic Actions of Steroids

A

Fast, steroid hormone binds to receptor on membrane of cell/intracellular receptors -> increased second messenger and kinase activity -> latency of seconds

e.g alter membrane permeability

146
Q

2 ways hormones can regulate their own production?

A

Positive feedback loops

Negative feedback loops

147
Q

2 ways hormones can up-regulate or down-regulate receptors

A

Homospecific priming (regulate own receptor)

Heterospecific priming (regulate other hormone receptor)

148
Q

Signal Transduction Pathways

A

A set of chemical reactions in a cell that occurs when a molecule, such as a hormone, attaches to a receptor on the cell membrane

Pathway - actually a cascade of biochemical reactions inside the cell that eventually reach the target molecule or reaction

149
Q

All protein hormones share same what?

A

Basic structure

150
Q

2 functional classes of protein and peptide hormone receptors?

A
  1. intrinsic enzyme activity (tyrosine kinase)

2. second messengers (GPCR’s)

151
Q

Enzyme Amplification

A

A series of chemical reactions in which a single hormone has the cascade effect which triggers the production or activation of up to a billion enzymes

152
Q

3 steps of tyrosine kinase receptor activation

A
  1. When receptor is unoccupied, the tyrosine kinase domain is inactive
  2. After binding of hormone, the tyrosine kinase domain changes shape to allow for interactions with protein kinases
  3. ATP phosphorylates (introduce a phosphate group) and activates the protein kinase, which affects cell function
153
Q

GPCRs are an example of a protein receptor that requires what?

A

A second messenger to carry out a hormonal signal

154
Q

Sexual Differentiation

A

The process by which individuals develop the characteristics associated with being male or female

155
Q

Sex Determination

A

the point at which an individual begins to develop as either a male or female

156
Q

5 levels of sex determination

A

Chromosomal sex -> gonadal sex -> hormonal sex -> morphological sex -> behavioral sex (chromosomal points to behavioral)

157
Q

Chromosomal sex of females

A

Homogametic mammals (XX)

158
Q

Chromosomal sex of males

A

Heterogametic mammals

XY

159
Q

Gametic sex of females

A

Ovaries produce eggs (limited #, large, immobile)

160
Q

Gametic sex of males

A

Testes produce sperm (large #, small, mobile)

161
Q

5 things males/females differ in morphological sex?

A
  1. size
  2. external genitalia
  3. coloration
  4. size of horns/antlers
  5. ornamentation
162
Q

Gender Identity

A

Self-ascribed gender in humans

163
Q

Gender roles

A

Culturally based summary of sex-specific behaviors in humans

164
Q

Asexual Reproduction (Parthenogenesis)

A

Asexual reproduction is very efficient

Parthenogenesis: reproduction from an ovum without fertilization, especially as a normal process in some invertebrates and lower plants

165
Q

Why is asexual reproduction rare in vertebrates?

A

Evolutionary answer - sexual reproduction allows for a wide range of genetic diversity; makes a population more likely to be able to adapt to changing conditions

166
Q

Sexual Reproduction

A

The recombination of genetic material allows for genetic variability.. variability on which natural selection can act

167
Q

Sexual reproduction leads to a species being more what?

A

Resistant to a major environmental change

168
Q

Dimorphic

A

Having 2 different forms; usually refers to differences between 2 sexes

169
Q

Polygamous vs. monogamous species & sexual dimorphism

A

Polygamous species (multiple mating partners) show more sexual dimorphism than monogamous species (single mating partner)

170
Q

Males are ___,___, more ___, higher ___

A

larger
stronger
more aggressive
higher mortality

171
Q

Typically, ___ compete, ___ choose

A

males compete

females choose

172
Q

Why do 2 sexes differ in appearance/behavior?

A

Sexual selection - act to favor certain traits among competing sex

173
Q

Bowerbirds & Sexual Selection

  1. Are bowerbirds polygamous or monogamous?
  2. Females select males based on what 2 characteristics?
  3. What do characteristics signal? (Dull feathers = ? Simple bower = ?)
  4. Males competing made them evolve to be ___, more ___, more ___
A
  1. polygamous
  2. males morphological (coloration) and behavioral (bower) characteristics
  3. Characteristics signal gene quality (dull feathers = higher internal parasitic load; simple bower = higher environmental parasitic load)
  4. evolved to be bigger, more colorful, more aggressive
174
Q

Males of polygamous species tend to explore ___ territory

175
Q

Do males of monogamous specie have poorer direction finding skills or spatial aptitude than polygamous males? What’s this associated with?

A

Yes; associated with a dimorphism in hippocampus

Polygamous: hippocampus males > females

Monogamous: hippocampus males = females

176
Q

Sexual Dimorphic Behaviors

A

Behaviors that are different in males & females

Include courting, mating, parental behavior, most forms of aggressive behavior

177
Q

What can play a role in the development and control of sexually dimorphic behaviors?

178
Q

Gonadal Steroid Hormones (How do hormones guide behavioral sex differences?)

A

Organizational and activational effects on brain

179
Q

(Gonadal Steroid Hormones) Organizational (programming) effects on brain

A
  1. Early in development and puberty; irreversible
  2. Differential exposure to hormones act early in development to organize neural circuitry underlying sexually dimorphic behaviors
180
Q

(Gonadal Steroid Hormones) Activational effects on brain

A
  1. in adulthood
  2. temporary; may wane after the hormone is metabolized
  3. differential exposure to sex steroid hormones later in life “activate” the neural circuit previously organized
181
Q

Dynamic Model for Sexual Differentiation

A

Sex differences arise due to the actions of hormones during early development, during puberty, and during adult life. Experience plays an important role, as well, and interacts in an epigenetic fashion with the ongoing influences of hormones at various stages of development

182
Q

When does the first step of mammalian sexual differentiation occur?

A

At fertilization

183
Q

Germinal Ride

A

Gonadal development of the human embryo

Bipotential primordial (exist at beginning of time) gonad 
Can become ovary or testis
184
Q

SRY gene

A

Sex-determining Region of Y chromosome

185
Q

What happens if SRY gene is present?

A

Testis determination factor protein -> testis formation

186
Q

What happens if SRY gene is absent?

A

Ovary formation

187
Q

Wnt4

A

Gene that may be required for ovarian development

188
Q

Hormonal secretions from developing gonads guide what?

A

Development

189
Q

What do mice that are chromosomally XY but do not have the SRY gene develop?

190
Q

XX transgenic mice that have SRY inserted develop what?

191
Q

Accessory Sex Organs

A

The internal organs of the male and female reproductive tract that connect the gonads to the external environment

Mullerian duct system
Wolffian duct system

192
Q

When is the mullerian duct system and wolffian duct system both present in both sexes?

A

During embryonic development

193
Q

When does one system develop and the other regress?

A

During 1st trimester

194
Q

Mullerian duct system

A

Ovaries or absence of any gonads
No MIH or androgen
Female

195
Q

Wolffian duct system

A

Testosterone/androgens and MIH required

Male

196
Q

Defeminization

A

Mullerian duct regression (MIH dependent)

197
Q

Demasculinization

A

Wolffian duct regression

198
Q

5alpha-reductase

A

Standard development of the external genitalia

Converts T to DHT

Present in embryonic genitals in M and F

199
Q

In the standard development of the external genitalia, what happens if unusually high (androgens) are present in females?

A

Some T will be converted to DHT, leading to male external genitalia

200
Q

In the standard development of the external genitalia, what happens if males lack 5alpha-reductase?

A

Males that lack the enzyme have female-typical external genitalia

201
Q

In the standard development of external genitalia, what happens if females lack 5alpha-reductase?

A

Females that lack the enzyme have external genitalia

202
Q

Congenital Adrenal Hyperplasia

A

A genetic deficiency that results in the overproduction of androgens by the adrenal glands

Syndrome has no reported effects on genital differentiation in males but causes various degrees of masculinization of the external genitalia in females, which may lead to erroneous (wrong) assignment of sex at birth

Partial masculinization

203
Q

Complete Androgen Insensitivity Syndrome (CAIS)

A

Anomalous (deviating from what’s normal) sexual differentiation in XY individuals

No functional androgen receptors

Genetic mutation on X chromosome (gene for AR) causes insensitivity to andorgens

Genetic XX females with mutation suffer no ill effects

204
Q

Genetic XY males with Complete Androgen Insensitivity Syndrome (CAIS)

A
  1. Have SRY gene -> gonads are testes, androgen production
  2. Testes produce MIH -> regression of Mullerian duct
  3. No AR, so Wolffian duct is underdeveloped
  4. Individuals have female external genitalia, sexed/reared as girls
  5. No uterus, fallopian tubes, sterile, typical female body shape
205
Q

William C Young studied what?

A

The effects of hormones on sexually dimorphic behaviors

206
Q

Sexually dimorphic mating postures

A

Lordosis in females

Mounting in males

207
Q

(Mating behavior is under the control of gonadal steroid hormones)

  1. Castrate males - ?
  2. T replacement - ?
  3. Does T cause mounting?
  4. T replacement in females - ?
  5. Male vs. female behavior
A
  1. No mounting behavior
  2. Resumes mounting
  3. No
  4. No Mounting
  5. Female behavior “de-masculinized”, male behavior “de-feminized”
208
Q

(Effects of hormones on sexually dimorphic behaviors)

How are these differences in hormonal response mediated hypothesis?

A

Hormonal events early in development must be responsible for the induction of feminine and masculine behavior

209
Q

William C Young’s Experiment on giving pregnant guinea pigs T throughout gestation

A
  1. Large T dose: females had male external genitalia “hermaphrodites”
  2. Small T dose: female genitalia “unmodified”
  3. Animals matured, gonadectomized; administered T; observed mounting behavior
  4. Females primed with T early in development and again in adulthood displayed the male typical behavior (mounting, not lordosis)
210
Q

Prenatal action of hormones causes what?

A

Differentiation/organization of neural substrates for behavior

211
Q

Adult hormones activate what?

A

Activation of previously organized substrates seen in prenatal action

212
Q

Even females whose external genitalia are not physically masculinized demonstrate what?

A

Behavioral masculinization and defeminization

213
Q

Puberty

A

Reproductive maturation guided by a sequence of timed neuroendocrine events

214
Q

Adolescence

A

Transitional period between childhood and adulthood. Psychological, cognitive, social, cultural aspects

215
Q

2 consequences of puberty that are energetically expensive?

A
  1. defense of territory or partner

2. pregnancy and caregiving

216
Q

Puberty begins as an integration of what 3 cues?

A

metabolic
social
environmental

217
Q

Adrenarche

A

Adrenal androgen secretion (DHEAS)

218
Q

Gonadarche

A

Gonadal production of steroid hormones

219
Q

Thelarche

A

Breast development in girls

220
Q

Pubarche

A

Axillary and pubic hair growth

221
Q

Menarche

A

Onset of menstruation

222
Q

What’s the first overt sign of puberty in girls & boys?

A

Girls - thelarche

Boys - testicular enlargement

223
Q

Typical age of puberty onset for girls

A

8-12 years

224
Q

Typical age of puberty onset in boys?

225
Q

The puberty transition lasts how long?

226
Q

Early menarche in girls is a risk factor for what 5 things?

A 
breast cancer
CVD
depression
diabetes
all-cause mortality
227
Q

Early puberty in boys can result in what 2 things?

A

testicular cancer

psychosocial distress

228
Q

When was there a decrease in average age of menarche/thelarche?

A

19th to 20th century

229
Q

Racial/ethnic differences in puberty; what % of non-hispanic caucasians, african americans, hispanics, and asians had start developing breasts by age 7?

A

10% non-hispanic caucasians
23% african american
15% hispanic
2% asian

230
Q

What environmental factors could cause early onset of puberty?

231
Q

What psychosocial factors could cause early onset of puberty?

A

Family stress: maternal depression/absent parent

232
Q

Precocious Puberty

A

<8 years in girls

<9 years in boys

233
Q

Central precocious puberty

A

Early maturation of HPG axis
GnRH dependent
Tumors, chronic sex steroid exposure
60% idiopathic (spontaneously)

234
Q

Peripheral precocious puberty

A

Early hormone production from peripheral glands

235
Q

Delayed puberty

A

> 13 years in girls

>14 years in boys

236
Q

Hypogonadism

A

> 18 years puberty

237
Q

Hypogonadotropic Hypogonadism

A

In CNS
Deficiency in GnRH secretion
Genetic defect in 40% of known cases
Organic causes: tumor, drug use

238
Q

Hypergonadotropic hypogonadism

A

Outside CNS

Defect in the gonads

239
Q

What is the primary mechanism by which the body alters its reproductive status during development?

A

Changing the pulse frequency of GnRH

240
Q

Puberty onset requires finely tuned ____ control of ____ release from neurons in the ___

A

temporal
GnRH
hypothalamus

241
Q

Strong ___ component to the timing of puberty

242
Q

What kind of neurons are central to gonadal maturation?

243
Q

What kind of hormone is kisspeptin?

A

Newly discovered small peptide hormone

244
Q

What gene is kisspeptin encoded by? Binds with high affinity to what receptor?

A 
Kiss1 gene
KISS1R receptor (GPR54)
245
Q

Human and mice with mutated KISS1R have what impaired function?

A

impaired reproductive function

246
Q

Where are neurons that express kisspeptin localized to?

A

hypothalamic nuclei that control GnRH neuron activity

247
Q

What neurons releases kisspeptin and what does this release stimulate?

A

KNDy neurons stimulates GnRH

248
Q

What is kisspeptin essential for?

A

GnRH secretion
LH
ultimately puberty

249
Q

A single injection of kisspeptin in animals leads to a huge increase in what?

A

secretion of gonadatropics

250
Q

Repeated injections of kisspeptin in immature rats advances what?

A

age of puberty

251
Q

Blocking kisspeptin in rats will stop what?

A

estrous cycle

252
Q

Does inhibiting kisspeptin even after puberty block reproductive function?

253
Q

Adiminstering kisspeptin to food-restricted animals stimulaes what?

A

gonadatropins

254
Q

In seasonal-breeding animals, what is kisspeptin controlled by?

A

Duration of daylight

255
Q

During short winter days; ___ kisspeptin, ___ sexual acitivity

A

reduced

no

256
Q

Long summer days; ___ kisspeptin, ___ breeeding

A

increased

stimulates

257
Q

What does artificial injections of kisspeptin in winter stimulate?

258
Q

Clinical Implications of Kisspeptin: Treatment for precocious puberty

A

taking pills with kisspeptin derivative

259
Q

Clinical Implications of Kisspeptin: Treatment for delayed puberty

A

Admin kisspeptin to kickstart the process

260
Q

Clinical Implications of Kisspeptin: Infertility treatment

A

Kisspeptin can start reproductive function in women who have stopped ovulating due to a steroid hormone imbalance

261
Q

Initiation of puberty (Kisspeptin, Kiss1 gene, PcG repressor proteins)

A
  1. kisspeptin stimulates GnRH neurons
  2. Expression is Kiss1gene is suppressed by a complex of proteins: PcG repressor proteins
  3. Epigenetic changes to Kiss1 promotor region releases the proteins and allows gene transcription to proceed
262
Q

MKRN3

A

Inhibits of HPG axis in control of puberty onset

263
Q

Role of environment in age of pubertal onset: What 2 things are thought to be causally linked? What is the inverse correlation?

A

Historical decrease in the age of sexual maturation (especially for girls) and increase in body weight

Inverse correlation between body mass index and pubertal onset in girls1

264
Q

Precocious puberty is 10x more likely in ____

265
Q

Delayed puberty is 5x more common in ___

266
Q

2 peripheral metabolic hormones that have metabolic control of GnRH secretion?

A

Leptin

Ghrelin

267
Q

Where is leptin stored?

A

Adipocytes

268
Q

What is leptin highly correlated with?

269
Q

Leptin (___ factor, permissive signal to ___, signals size of ___)

A

satiety
HPG axis
energy reserves

270
Q

Where is ghrelin?

271
Q

Ghrelin signals ___, inhibits ___

A

signals energy insufficiency

inhibits GnRH pulsatility

272
Q

When does grey matter peak in boys & girls? What’s it followed by?

A

11 - girls
12 - boys
followed by cortical pruning/thinning

273
Q

What mechanisms are responsible for maternal and paternal behavior?

A

Neuroendocrine mechanisms

274
Q

What is parental investment and style based on?

A

The developmental state of offspring at birth and their growth trajectory

275
Q

Maternal care across species zoo incidents example (Binti Jua vs. Harambe)

A

Binti Jua - 8 year old female gorilla, new mom to 17 month old baby, lactating, caregiving/agression

Harambe - 17 year old male gorilla, nonparental dominant male

276
Q

Parental Investment Theory: Parental style/investment varies widely within and between ___

277
Q

Parental Investment Theory reflects an optimal ____ strategy for maximizing ___

A

evolutionary

fitness

278
Q

Parental Investment Theory: Optimal strategy

A

Provide care, but no more than absolutely necessary

279
Q

Parental Investment Theory: Parental investment

A

The extent to which parents compromise their ability to produce more offspring in order to care for the young they have

280
Q

Parental Investment Theory: The sex making the larger investment in feeding/protecting is ___ in selecting mate

281
Q

Parental Investment Theory: The sex that contributes fewer resources to offspring success ___ among themselves to be chosen

282
Q

Parental Investment Theory: Tradeoff between what 2 things?

A

investing in reproduction and parental care

283
Q

Parental Investment Theory: if a single female can sufficiently care for her young, what will male do?

A

make other “reproductive investment” to increase his fitness

284
Q

Parental Investment Theory: What could happen to the fitness of both parents if they both abandon young?

A

both parents could suffer

285
Q

Parental Investment Theory: in most cases, males become involved in parental care only if what?

A

the offspring needs high levels of care from 2 parents

286
Q

Parental Behavior

A

Behaviors performed in relation to one’s offspring that contribute directly to the survival of fertilized eggs or offspring that have left the body of the female

287
Q

Altricial

A

Born or hatched at an early stage of development.
Altricial offspring are generally helpless and require substantial parental care to survive.

Large number of immature young
Mothers may or may not display parental care

288
Q

Precocial

A

Born or hatched at an advanced stage of development. Precocial young require little or not parental intervention for survival

Few number of well-developed offspring
Can survive with little or no parental investment

289
Q

In terms of parental behavior, hormones shape what 3 things?

A
  1. initiation of parental behavior
  2. maintenance and development of parental behavior
  3. termination of parental behavior
290
Q

What kind of animal display an enormous diversity in parental behavior?

291
Q

What kind of parental care if common in bird?

A

Biparental care - equal parental investments

Biparental care is adaptive

292
Q

Parental behavior of birds

A

nest building
incubation
feeding
protection

293
Q

What do immature birds require to survive?

A

continuous food intake

294
Q

Alloparenting

A

caregiving to offspring that is provided by individuals other than their genetic parents

e.g birds

295
Q

North temperate zone birds; Prolactin -> drives what 3 things in many bird species?

A

onset, maintenance, and duration of parental behavior

296
Q

California mouse fathers have increased ___ concentrations

297
Q

In Florida scrub jays, what does prolactin concentrations correlate with?

A

the amount of care provided to the offspring

298
Q

Prolactin in Florida jay scrubs

A

prolactin: breeders > helpers > nonhelpers

299
Q

In Florida jay scrubs, what inhibits prolactin?

A

Stress (corticosterone)

300
Q

4 factors of maternal behavior in marsupials

A
  1. mammary glands
  2. maternal care dominates
  3. developmental stage at birth varies between mammalian species
  4. marsupials: unreliable habitat, can end pregnancy if harsh conditions occur
301
Q

4 factors of maternal care in eutherian mammals

A
  1. placenta
  2. more stable habitat
  3. greater developmental stage at birth
  4. parental care is rare among mammals
302
Q

3 types of maternal care in eutherian mammals (e.g rats)

A
  1. mother provides food care and shelter to altricial young
  2. mother bears precocial young capable of independent activity
  3. neither/semi-precocial young
303
Q

What animal is a rare example of biparental care in mammals?

A

The California mouse

304
Q

Endocrine correlates of mammalian parental behavior (6 hormones)

A
  1. prolactin
  2. prostoglandins
  3. beta-endorphin
  4. oxytocin
  5. progesterone
  6. several estrogens
305
Q

Concaveation (foster pup rat study)

A

In rats, foster pups presented to nulliparous female for several hours a day; female begins to behave maternally

sensitization

all behaviors typically observed in rat dams are observed in “sensitized” females, except maternal aggression

also seen in male rats

not hormonally mediated (occurs after ovariectomy; mediated by dopamine?)

306
Q

Maternal Aggression

A

Serves to protect offspring from predators or intruders

Hormonally regulated

Progesterone

307
Q

(Progesterone & Maternal Aggression)

  1. P treatment ___ aggressive behavior in nulliparous mice
  2. Pregnant females start to show ___ behavior when P levels peak
  3. Pregnancy termination (reduces P) ___ aggressive behavior
  4. P replacement ___ behavior in hysterectomized animals.. but aggression is __ after birth when P levels are low
A
  1. elevates
  2. aggressive
  3. eliminates
  4. restores, high
308
Q

Endocrine correlates of maternal behavior in primates

A

largely unknown

309
Q

Role of experience in maternal behavior in primates?

A

Hormones help establish onset of maternal behavior in first-time mothers but not necessary to stimulate the behavior in experienced mothers

310
Q

Hormones & basic parental behaviors in humans

A

hormones are nether necessary nor sufficient for the appearance of basic parental patterns

311
Q

Maternal behavior in humans

A
  1. adoptive parents, siblings, grandparents, caregivers show attachment
  2. same behavioral pattern; different endocrine profiles
  3. concaveation
312
Q

Oxytocin & role of maternal behavior in humans

A

Mothers with high O levels show higher gaze with infant or polymorphism

313
Q

Expected human fathers display reduced concentrations of what hormones? Increased circulating concentrations of what hormone?

A

reduced - T and cortisol

increased - estradiol

314
Q

What hormone concentration is elevated in fathers just before birth?

A

Prolactin, like California male mice

315
Q

Men who respond to infant cries show ___ prolactin relative to unresponsive fathers

316
Q

What hormone is elevated in fathers?

317
Q

What enhances father-child interactions?

A

intranasal OT

318
Q

Lateral projections from where are critical in rat maternal behavior?

319
Q

How does estrogen promote maternal behavior?

A

By enhancing activity in neural circuit that underlies maternal behavior

320
Q

Neural circuit that underlies maternal behavior

A

MPOA (hypothalamus), BNST, septum

321
Q

What does lesions to MPOA eliminate in rats?

A

maternal behavior

322
Q

Maternal care organizes brain of offspring to respond to what?

A

Environment

Nongenetic transmission of parenting styles

323
Q

Low maternal licking/grooming in rats:

  1. ___ GR in hippocampus
  2. ___ HPA stress response
  3. Offspring become ___ L&G
A
  1. decreased
  2. exaggerated
  3. low
324
Q

High maternal licking/grooming in rats:

  1. ___ GR in hippocampus
  2. ___ HPA stress response
  3. Offspring become __ L&G
A
  1. increased
  2. efficient
  3. high
325
Q

What kind of studies studied nongentic transmission of parenting styles?

A

cross fostering studies

326
Q

What brain regions were activated in response to seeing picture of own child vs. unrelated?

A 
Precuneus
MPFC
OFC
Midbrain
Posterior Cingulate
ACC
Thalamus
DLPFC
Regions associated with motivation, reward, emotion regulation
327
Q

Some ___ behaviors evolved from parental behavior

328
Q

What two kinds of love evoke similar brain activity?

A

maternal and romantic

329
Q

Affiliative behaviors

A

how most primate species communicate affection and reduced group tension

e.g calmly sitting close to each other, touching, mutually grooming, etc

330
Q

Relationship status and oxytocin levels

A

Couples displaying high interactive reciprocity scores

331
Q

What rating did oxytocin enhance of partner’s faces?

A

attractiveness

332
Q

What brain region activity was enhanced when partner’s face was shown? When was it suppressed?

A

NAcc (reward circuit)

Suppressed reward circuitry response to unfamiliar face

333
Q

In what species is pair-bonding adaptive?

A

species whose offspring require biparental care

monogamous

334
Q

What are the proximate means of bringing about cooperation of biparental care/parents staying together?

A

hormones that evoke affiliation

335
Q

Higher levels of oxytocin binding where in the brain for monogamous?

A

NAcc, fronto-parietal cortex, lateral amygdala, thalamus

336
Q

Higher levels of oxytocin binding where in polygamous?

A

Lateral septum

337
Q

Attachment

A

A strong emotional bond between caregiver and offspring, important for subsequent emotional stability

338
Q

___ antagonist reverses partner preference in females (monogamous praire voles)

339
Q

___ antagonist reverse partner preference in males (monogamous praire voles)

A

vasopressin

340
Q

Disrupting ___ signaling disrupts social preference in zebra finches

341
Q

What does oxytocin treatment in dogs promote?

A

social behaviors with other dogs and with human owner

342
Q

Types of Aggression

A 
Predatory
Intermale
Fear-induced
Irritable
Territorial 
Maternal
Instrumental
Predatory attack
Self-defensive behavior
Parental defensive behavior
Social conflict
343
Q

Common lab tests of aggression

A 
Muricide (mouse killing) by cats or rats
Shock-elicited fighting
Isolation-induced aggression
Resident-intruder aggression
Maternal aggression
Brain stimulation-induced aggression (hypothalamus)
Dominance-related behavior
Visible burrow stressor
344
Q

Seasonal variations in what hormone and what behavior coincide?

A

T and aggression

345
Q

When do aggressive behaviors increase? Why?

A

At time of puberty, when the testes become active again and androgens level rise

346
Q

Seasonal changes in aggression may also be mediated by ___ signaling

347
Q

What does low T inhibit?

A

reproductive success

348
Q

What does high T suppress?

A

immune function/survival

349
Q

How come the hormone-behavior relationship (TAggression) is bidirectional?

A

Social experience can affect hormone concentrations

350
Q

Males who lose a fight show ___ T levels; how long does this last?

A

suppressed; many days after defeat (in monkeys this suppression can last for weeks)

351
Q

Winning males in fight had T levels that ___ with 24 hours of victory

A

quadrupled

352
Q

In males, winner of competition show ___ T, & ___

A

high

aggression

353
Q

Androgel

A

GnRH drug

Lowers t

Behavioral Endocrinology (1 decks)

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