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Biopsychology > Exam I > Flashcards

Flashcards in Exam I Deck (258)
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1
Q

What is the purpose of a brain?

A

A brain helps us respond (flexibly, quickly, and with control) to changes in the environment

2
Q

How do we describe behavior?

A

Structure (what, when, which) Function (what happens as a result of the behavior)

3
Q

Tinbergen’s Four “Whys”

A

Proximal Causes (Individual): Mechanism & Ontogeny Ultimate Causes (Species): Adaptive Value and Phylogeny

4
Q

Mechanism

A

One of Tinbergen’s Four Whys. A proximate/individual cause. What is the physiological explanation of the behavior? What in the body or brain changes to initiate the behavior?

5
Q

Ontogeny

A

One of Tinbergen’s Four Whys. A proximate/individual cause. How did the behavior develop over an animal’s lifespan? Is it innate or learned, or both? Is it influenced more by genetics or the environment?

6
Q

Adaptive Value

A

One of Tinbergen’s Four Whys. An ultimate/species cause. What is the evolutionary explanation of the behavior? How does a behavior contribute to reproductive fitness?

7
Q

Phylogeny

A

One of Tinbergen’s Four Whys. An ultimate/species cause. How did the behavior change over the evolutionary history of the species?

8
Q

Empiricism

A

Forming conclusions based on objective observation, control, and replication

9
Q

Somatic intervention

A

We do something to the body and see what happens to behavior (i.e. stimulate brain region, affects movement)

10
Q

Behavioral intervention

A

We do something to behavior and see what happens to the body (i.e. present a visual stimulus, causing changes in electrical activity of the brain)

11
Q

Correlation

A

We determine (mathematically) if a somatic variable and behavioral variable covary

12
Q

Delgado’s charging bull experiment

A

Used radio signal to stimulate caudate nucleus (in the basal ganglia) - framed as a “taming center” but actually just makes you turn left

13
Q

Morgan’s Canon/Occam’s razor

A

A simple explanation is more likely than a complex one

14
Q

DRD4

A

Encodes Dopamine Receptor D4. Most people have 2R/4R repeat on the axon, some have a 7R repeat (changes the shape of the dopamine D4 receptor - doesn’t bind as well). Therefore, it takes more dopamine to get the same response with the 7R repeat. Less activation in the prefrontal cortex and the reward pathway- need more of a stimulus for a good time. Correlated with migration.

15
Q

The levels of analysis

A

Social, organ, neural systems, circut level, celular level, synaptic level, molecular level

16
Q

Applied behavioral neuroscience

A

focuses on understanding and treating dysfunction

17
Q

Natural selection

A

If a trait increases fitness, it is an adaptation and will be passed along to future generations. This requires genetics - a biological mechanism of trait transmission.

18
Q

Sexual selection

A

If a trait attracts a mate, it will be passed on to future generations

19
Q

Mutations

A

Gene change. Single-nucleotide polymorphisms (single base) and tandem repeat variations (portions repeat).

20
Q

Silent mutation

A

Doesn’t affect how the gene is expressed

21
Q

Nonsense mutation

A

Doesn’t code for anything

22
Q

Missense Mutation

A

Change in the expressed gene

23
Q

Frameshift mutation

A

An insertion or deletion or both - more serious

24
Q

Directional selection

A
25
Q

Stabalizing selection

A
26
Q

Disruptive selection

A
27
Q

How can we explain the persistence of apparent genetic disadvantage?

A

There might be advantages (i.e. being a carrier of the sickle cell gene decreases chance of getting malaria)

28
Q

Is evolution?

A

No! Not intentional - doesn’t have a goal

29
Q

Convergent evolution

A

Different species have different ways of solving the same problem (homoplasy)

30
Q

Homoplasy

A

behaviors/characteristics appear similar because they emerged to solve similar problems

31
Q

Homology

A

behaviors/characteristics appear similar because they were derived from common ancestry (i.e. human and bat arms)

32
Q

Analogy

A

behaviors/characteristics evolved separately, but serve the same purpose (i.e. penguin and dolphin flipper)

33
Q

Brains are fairly ____ between species

A

Conserved (they have similar areas)

34
Q

Correlates of behavioral specialization in the brain

A

We can see them. i.e. olfactory bulbs are much bigger in the mouse

35
Q

Why did human brians get bigger?

A

The use of tools to cut meat and cooking of meat- decrease jaw size

36
Q

Bipedalism

A

Walking on two legs. Greater dexterity in forelimbs (detail related activities) but huge restrictions on the morphology of pelvis - harder to pop a baby out (dangerous and requires conspecific help)

37
Q

Effects of big brains on gestation

A

Longer gestation to help develop complex brain. Also a long postnatal developmental period.

38
Q

Direction selection of having a big brain

A

The selection pressure for large brain volume is greater than the selection pressure for small brain volume

39
Q

Coronal sectional plane

A
40
Q

Sagittal sectional plane

A
41
Q

Transverse/Horizontal sectional plane

A
42
Q

Medial versus lateral

A

Medial - more towards the middle, lateral - more towards the outside

43
Q

Anterior versus posterior

A

Anterior - towards the front; Posterior - towards the back

44
Q

Superior- dorsal versus Inferior ventral

A
45
Q

Rostral versus Caudal

A
46
Q

Types of glia

A
47
Q

Astrocytes

A
  1. modulate communication
  2. nutrient transport from blood to neuron (end feet wrap around blood vessels) - form the glymphatic system
  3. supporting myelin coverage of neurons
48
Q

Microglia

A

Act as the brain’s immune system

49
Q

Schwann Cells and Oligodendrocytes

A

Insulate axons (Damage to these cells in multiple sclerosis)

50
Q

The Reticular theory

A

The nervous system is a single continuous network (Camillo Golgi AKA Golgi stain guy)

51
Q

The Neuron Doctrine

A

Cells are functionally, structurally, and metabolically separated from each other, but they communicate across gaps (Santiago Ramon y Cajal AKA art school guy)

52
Q

Golgi Stain

A

Camillo Golgi discovered in the 19th century. Silver chromate (seemingly) randomly stains about 10% of neurons

53
Q

Nissl or Cresyl violet

A

A type of stain discovered by Franz Nissl, in the late 19th century. Stains only cell bodies in the rough ER - utilized for counting.

54
Q

Immunohistochemistry

A

Using antibodies to see proteins

55
Q

In situ hypridization

A

Using complementary RNA strands to see mRNDA

56
Q

Zones in a neuron

A

Input, integration, conduction, output

57
Q

Multipolar neuron

A

The most comon type in which there are multiple dendrites. There are two main types - interneurons and motor neurons

58
Q

Interneurons

A

Type of multipolar neuron. Integrate multiple sources of information

59
Q

Motor neurons

A

Type of multipolar neuron. Control muscles/glands (efferents)

60
Q

Afferent neurons

A

Take information to the CNS

61
Q

Efferent neurons

A

Only take information away from the CNS

62
Q

Bipolar neuron

A

one dendrite. Generally sensory neurons (afferents)

63
Q

Unipolar

A

Touch receptors (afferents)

64
Q

Lipid bilayer

A

Doesn’t let in polar molecules. Has some protein channels.

65
Q

Anterograde versus retrograde transport

A

Anterograde: towards the terminals

Retrograde: towards the soma

66
Q

Microtubules

A

Responsible for the rapid transport of material throughout neurons. They are held together by tau- if tau is damaged then Alzheimers disease can occur

67
Q

Synaptic plasticity

A

Synapses change with experience

68
Q

Two parts of the peripheral nervous system

A

Somatic nervous system & Autonomic Nervous System

69
Q

Somatic nervous system

A

The nerves that send motor commands from the brain to voluntary muscle and send sensory infro from the environment to the brain. Responsible for senses and voluntary muscle movement (i.e. olfactory)

70
Q

Ventral versus dorsal part of the spine (efferent and afferent)

A

Ventral (motor) - efferent

Dorsal (sensory) - afferent

71
Q

Parts of the Autonomic Nervous System

A

Sympathetic & Parasympathetic

72
Q

Sympathetic

A

Part of the Autonomic Nervous System. Sympathetic- speeds things up (Fight/flight). Mostly norepinephrine. Ganglia run alongside the spinal cord.

73
Q

Parasympathetic

A

Part of the Autonomic Nervous System. Parasympathetic - slows things down (primarily acetylcholine) - Rest or digest. Ganglia next to innervated organs (distributed throughout the body).

74
Q

Enteric Nervous System

A

Gut - coordinates digestion (primarily uses serotonin)

75
Q

Central Nervous System

A

Brain and spinal cord

76
Q

Peripherial Nervous System

A

Nervous system outside of the brain and the spinal cord

77
Q

Four lobes of the neocortex and the main sulci and gyruses

A

Lobes: Frontal lobe, parietal lobe, occipital lobe, temporal lobe

Sulci: central (between frontal and parietal lobe (Coronal)); Lateral Sulcus/Sylvian Fissure (between frontal lobe and temporal lobe) (Transverse)).

Gyruses: Both next to the central sulcus. Precentral gyrus (towards front side in the frontal lobe) and Postcentral gyrus (towards back side in the parietal lobe)

78
Q

Corpus callosum

A

Connects the left and right hemisphers of the brain

79
Q

Autonomic nervous system

A

regulates body functions to respond to the environment

80
Q

Built-in protection mechanisms of the brain

A

Chemical protection: blood-brain barrier (Astrocytes and blood vessels)

Physical protection: Meninges (three membranes that line the skull) - Dura mater, arachnoid, & Pia mater

Ventricle: shock protection and circulation

81
Q

Parts of the brain (development)

A
82
Q

Myelencephalon

A

Part of the hindbrain

AKA medula

Autonomic functions: digestion, breathing, heart rate, blood pressure

Includes reticular formation - involved in arousal

83
Q

Metencephalon

A

Part of the hindbrain

Pons- motor control, sensory nuclei, sleep/dreaming

Cerebellum- integration of multimodal signals for motor coordianation (maitenance of posture, fine motor control, motor learning)

84
Q

Mesencephalon

A

Midbrain

Tectum- Superior colliculus, inferior colliculus

Tegmentum- Red nucleus and substantia nigra (sensorimotor); ventral tegmental area (VTA) (reward); Periaqueductal gray surrounds cerebral aqueduct (opiod signaling)

85
Q

Diencephalon

A

Part of the forebrain

Thalamus and Hypothalemus

86
Q

Telencephalon

A

Part of the forebrain

Hippocampus: spatial navigation, contextual memory, memory consolidation, mood (making connection)

Amygdala: classically fear, but really relevance detector

Basal Ganglia:

Neocortex: (includes cerebral commisure - tract of white matter. Largest is corpus callosum - connection)

87
Q

Cytoarchitecture in the neocortex

A

it varies!

88
Q

The limbic system

A

Set of forebrain (telencephalon and diencephalon) structures that serve as the root of emotion/arousal/stress.

Includes: cingulate cortex, hippocampus, amygdala, septal nuclei, mamillary bodies, olfactory bulbs

89
Q

Localization

A

Distinct brain regions have distinct functios; they are domain specific (not as true as we once thought)

90
Q

Connectionism

A

Brain regions are domain-general, and combine to create specific functions

91
Q

Diffusion tensor imaging (DTI)

A

Calculates fractional anisotropy (FA) -diffusion- by looking at movement of water molecules- indicates myelinated axons

92
Q

Manipulating versus measuring the brain to determine localization of function

A

Manipulate: change the structure or change the function (Lesion, electrical stimulation, drug admin, genetic techniques)

Measure: Balancing time-course (function) with resolution (structure) i.e. EEG, MEG, PET, CT, fMRI, MRI, Histology

93
Q

Measure of localization graph (temporal resolution versus spacial resolution)

A
94
Q

fMRI

A

Measures blood oxygen level dependent (BOLD) signal

95
Q

PET

A

Positron emission tomography - measures concerntration of a chosen radioligand i.e. 2-deoxyglocuse - glucose that can’t be metabolized. or Amyloid B - protein implicated in Alzheimers

96
Q

Ex vivo versus in vivo measures of the brain

A

Ex vivo (outside) - histology

In vivo (inside)- measures of density (CT/X-ray) or diffusion (MRI, DTI)

97
Q

Measures of density

A

Study structure of the brain: CT/X-ray

98
Q

Measures of Diffusion

A

Study of the strucutre of the brain: MRI, DTI

99
Q

Study function of the brain via electricty

A

EEG/ERP, MEG, tDCS, TMS, direct stimulation

100
Q

Study function of the brain via metabolism

A

fMRI, PET

101
Q

What kind of signals do neurons communicate with?

A

Chemical and electrical (chemical input to chemical signal to electrical signal to trigger neurotransmitter release- cycle)

102
Q

Positive verusus negative charge

A

Positive- more protons than electrons

Negative- more electrons than protons

103
Q

Electrical potential

A

There is a difference in the positive/negative ions between two places, therefore, there is a potential for movement of ions between those places. Measured by looking at difference (pos and neg). Difference creates an electrochemical gradient

104
Q

Resting potential of neurons

A

At rest, neurons have a negative potential (around -65 mV). B/c there are lots of negatively charged proteins inside the cell.

105
Q

Concentration gradient

A

ions of the same type want to spread out

106
Q

Concentration gradient and electrical gradient of Na+ and Potassium at resting potential

A

Concentration gradient: into the cell for Na+, out of the cell for K+

Electrical gradient: into the cell for K+ and Na+

107
Q

K+ channels versus Na+ channels at rest

A

K+ channels pretty leaky vs Na+ not very permeable

108
Q

Na+/K+ pump

A

maintains resting potential. Binds 3 Na+ from inside and 2 K+ from the outside. With energy they switch places - holding membrane potential at about -65mV

109
Q

Polarized vs depolarized vs hyperpolarized

A

Polarized - different from 0mV

Depolarized - less different from 0mV (happens during excitatory postsynaptic potential (EPSP)

Hyperpolarized: more different from 0mV (happens during inhibitory postsynaptic potential (IPSP)

110
Q

Repolarization

A

returning back to the resting membrane potential

111
Q

Effect of strength and location of stimulus in a neuron

A

Stronger stimulus = stronger response

Decay: Local potential is smaller as you move further from the stimulus site

112
Q

Action potential

A

When you depolarize to a certain threshold (about -40mV)

113
Q

Na+ channels during action potential

A

Voltage-gated Na+ channels open and the concentration and electrical gradients push the molecules into the cell. Spreads depolarization. Next batch opens while previous batch closes b/c time-dependence. Unidirectional process - AP regenerated along axon as it opens up more NA+ channels.

114
Q

What happens to the electrical gradient of Na+ during action potential and what is the effect?

A

It switches (from inside to outside the cell), resulting in the Na+ molecules wanting to leave the cell but they can’t - so K+ molecules move outside of the cell (through voltage-gated K+ channels) w/ the concentration gradient (because concentration and electrical gradients pushing it out)

115
Q

Absolute refractory period

A

Na+ channels are still closed - a second stimulation would not open them (1-2ms)

116
Q

Hyperpolarization during the relative refractory period

A

K+ overshoots the resting membrane potential due to channels- results in hyperpolarization (farther away from 0mV)- hard but not impossible to get a second reaction from a stimulus (need a very large stimulation)

117
Q

Myelination and action potentials

A

Saltatory Conduction: Mylination speeds up action potentials (unmyelinated big toe stub - 4 seconds versus .13 seconds with mylination). B/c action potential jumps between nodes of ranvier - less susceptible to decay

118
Q

How vesicles are docked at the synaptic terminal

A

v-SNARES (vesicle) and t-SNARES (terminal) bind to dock. Then Ca2+ enters from recieving cell, grabbing synaptotagmin, which then binds to SNAREs and the plasma membrane

119
Q

Pre-synaptic, synaptic cleft, and post synaptic›

A
120
Q

Ionotropic versus metabotropic receptor

A

Ionotropic: ligand-gated ion channel

Metabotropic: G-protein-coupled receptor (g-protein can pop off and do other stuff)

121
Q

Ways neurotransmission can be turned off

A

Degradation- enzyme chops up the neurotransmitter so it can no longer bind to the receptor

Transporters- bind neurotransmitter and move it back into the presynaptic cell

Autoreceptors- bind neurotransmitter and trigger downstream effects to stop transmission (activate transporters; turn off CA2+ channels)

122
Q

Gap Junctions

A

maintain electrical signaling without a chemical intermediary

123
Q

EPSP vs IPSP

A

Excitatory postsynaptic potential vs inhibitory postsyaptic potential

124
Q

Graded EPSPs and IPSPs

A

Stronger or longer signal from presynaptic cell = grader change in membrane potential (if sum of depolarizations and hyperpolarizations at axon hillock reaches the threshold of excitation - axon fires an action potential)

125
Q

Integration of PSPs

A

PSP - Postsynaptic Potential

Can combine in time or space

Spatial summation - two PSPs combine at the same location (order of dendrites matters)

Temporal summation- two PSPs occur in rapid succession, one adds to the other

126
Q

Is a single EPSP enough to elicit an action potential?

A

Almost never!

127
Q

Optogenetics

A

Can turn on receptors with lights (action potential)- affects movement

128
Q

Discovery of the first neurotransmitter in 1921

A

Otto Loewi - stimulated a vagus nerve (two jars connected) - acetylcholine

129
Q

What determines a neurotransmitter’s effects?

A

It’s receptors

130
Q

Exogenous substances versus endogenous

A

exo- from outside the body (aka cocaine)

endo- from inside (aka neurotransmitters

131
Q

Types of Acetylcholine receptors and functions

A

Muscarinic (metabotropic & agonist): constrict pupil

Nicotinic (ionotropic and nicotine is an agonist): constriction of muscle fibers

132
Q

Agonist versus antagonist versus inverse agonist

A

Agonist - binds to a receptor and activates it to produce a bio response

Antagonist- block an action of an agonist

Inverse agonist - causes action opposite to that of the agonist

133
Q

Relationship between Neurotransmitter’s effects and location (Dopamine example)

A

Neurotransmitter’s effects are determined by its location.

Dopamine pathways: Nigrostriatal pathway- movement; Mesocorticolimbic pathway (including ventral tegmental area VTA and frontal cortex - connected bia medial forebrain bundle) - reward

134
Q

Parkinsons vs Schizophrenia

A

Parkinsons - not enough - take an agonist i.e. Al-Dopa (risk for additction disorders)

Schizophrenia - too much - take an antagonist - ends up looking like Parkinsons

135
Q

Neuropeptides as neurotransmitters

A

Peptides = protein; neuropeptides can act as neutrotransmitters. Assembled in soma by ribosomes and packaged by golgi aparatus. Most of the time not classical neurotransmitters- typically neuromodulators

136
Q

Neurotransmitters are synthesized where?

A

BOTH in Soma (like neuropeptides) and in the terminal

137
Q

Types of amino acid neurotransmitters

A

Glutamate (excitatory) - have iontropic and metabotropic

GABA (mostly inhibitory) = GABA A + C - ionotropic vs GABA B - metabotropic

138
Q

What is so important about GABA (A)?

A

Different pockets/binding sites - which changes the function (i.e. alcohol, neurosteroids, chloride)

139
Q

Monoamine neurotransmitters

A

One amine

catecholamines- synthesized from amino acid tyrosine. Have a ring. Includes dopaminergic & noradrenergic

Indoleamines- synthesized from tryptophan. Includes serotonergic.

140
Q

Dopaminergic system receptors

A

There are many D1-5

141
Q

Noradreneric system

A

Most in the locus coeruleus (in the midbrain) but projects to the hypothalamus (stress response) neocortex (reward) thalamus (attention) and temporal lobe (memory)

142
Q

Pharmacokinetics

A

what the body does to a drug

143
Q

Route of (drug) administration

A

How the drug gets into the body

144
Q

First-pass effect

A

Drug is eliminated before it reaches circulation

145
Q

Pharmacodynamics

A

What a drug does to the body

146
Q

Dose-response curves

A

How to evaluate the safety and efficacy of drugs. ED50- effective dose for 50% of people vs LD50 - lethal for 50%. Wide therapeutic index is better than a narrow one

147
Q

Tolerance

A

with repeated exposure, it takes more of a drug to be effective

148
Q

Types of tolerance

A

Metabolic - more effective clearence (liver)

Functional - reduced sensitivity to a drug (GABA A - less receptors following repeated exposure to agonist)

Cross-tolerance - if drugs share a mechanisms tolerance to A can lead to a tolerance to B

149
Q

The different ways drugs can impact neurotransmitters

A
  1. Transmitter production
  2. Transmitter release
  3. Transmitter clearance
150
Q

How drugs can impact how neurotransmitters are made and stored

A
  1. inhibit production
  2. block axonal transport
  3. block storage in vesicles
151
Q

How drugs can effect the release of a neurotransmitter

A
  1. block ion channels
  2. change activity of autoreceptors

(Agonist - weed- stimulates hunger by binding to anandamid receptor, which blocks channel, so GABA neuron doesn’t keep response in check)

(Antagonist - caffine - blocks adenosine receptor so norepinephrine continues to be released - makes us less tired)

152
Q

How drugs can interfere with neurotransmitter clearance

A
  1. block reuptake (i.e. SSRIs)
  2. block degradation (stopping enzymes from yeeting in and chopping up neurotransmitters - so they stay longer)
  3. block VMAT (mesicular monoamine transporter)
153
Q

2 Things to consider if a drug is interacting with a receptor

A

Binding affinity- how well does it bind?

Efficacy- how strong is its effect?

154
Q

Classical agonists (neurotransmission)

A

Recreate the effect of the endogenous NT (i.e. LSD - but it stays longer, so other things can’t bind)

155
Q

Partial agonists

A

bind to the receptor but have a lower efficacy than the endrogenous NT; therefore, they are functionally antagonistic (ex: atypical antipsychotic)

156
Q

Indirect agonists/allosteric modulators

A

Bind to the receptor and increase its activity, but binds to different spot than the NT (therefore it is noncompetative) ex: alcohol

157
Q

Inverse agonists

A

Bind to receptor and have an opposite effect of the endrogenous NT

158
Q

Antagonists (neurotransmission)

A

bind to a receptor and prevent the effect of the endrogenous NT

159
Q

Noncompetative antagonists

A

bind to a different site than the endrogenous neurotransmitter and still block its effects (i.e. ketamine)

160
Q

First hints at an endocrine system

A

Came from castration (re-implanting testes), using goat testicles in humans to increase testosterone, etc.

161
Q

Hormone definition

A

A chemical that is secreted by cells in one part of the body and travels through the bloodstream to bind to its own receptor in other part of the body

162
Q

Endocrine

A

Gland sends a hormone through the bloodstream to a receptor

163
Q

Autocrine

A

Gland sends out hormone, works on it’s own receptor

164
Q

Paracrine

A

very local effect (neighbors)

165
Q

Intracrine

A

A prohormone leaves a gland, and turns into the hormone in it’s final location (high local concentration - not lost in the liver)

166
Q

Pheromone

A

Same species to species secretion (i.e. bees to bees)

167
Q

Allomone

A

One species to another secretion (a form of chemical signalling) i.e. bee orchid to bee

168
Q

General properties of hormonal actions

A
  1. gradual effects
  2. makes certain behaviors more/less likely (not an on/off switch)
  3. controlled by environmental stimuli
  4. multiplicity - affect multiple tissues, and a single tissue can be affected by multiple hormones
  5. only affect tissues w/ appropriate receptors
  6. often rhythmic and pulsatile (multiple in one day) (time relationship)
  7. interact with eachother
169
Q

What are the three main classes of hormones?

A
  1. peptide
  2. amine
  3. steroid
170
Q

Neurosteroids

A

steroid hormones made in the brain

171
Q

Peptide hormones

A

Sequence of amino accids, coded for by specific genes (ie. Oxytocin)

172
Q

Amine hormones

A

Derived from a single amino acid (diet) i.e. melatonin, epinephrine, orepinephrine, thyroid hormones

173
Q

Steroid hormones

A

Derived from cholesterol and have a 4-ring structue (estrogens, progestins) - mostly gonadal and adrenal hormones. Tend to be genomic - modulate gene transcription, but can also have nongenomic responses - i.e. second messengers.

174
Q

When steroid hormones are converted into another

A

Intracrine signaling

175
Q

Types of hormone feedback loops

A
  1. Autocrine feedback
  2. Target cell feedback (biological response causes feedback on endocrine cells)
  3. Brain regulation (bio resposne causes feedback on brain i.e. hypothalamus)
  4. Brain and pituitary regulation (feedback on the pituitary and the hypothalamus)
176
Q

Neuroendocrine cells

A

Start many hormonal cascades (triggered by the hypothalamus)

177
Q

How hormones, the brain, and behavior all interact - oxytocin example

A

When you copulate, oxytocin increases, which results in more bonding and spending time together, which increases oxytocin (prarie vole - receptor gene)

178
Q

What does the posterior pituitary release?

A

Oxytocin and vasopressin

179
Q

What does oxytocin do?

A
  1. copulation bonding (reproduction)
  2. stimulates uterus to contract (pushes against cervix- sends signal ] positive feedback loop
  3. mom/baby contact - child rearing
  4. creative problem solving
  5. other human/human connection - “mind reading” and sharing emotions
  6. in-group favortism/ethnocentrism
  7. increase aggression?
180
Q

Anterior Pituitary axis formula

A

Releasing Hormone (Hypothalamus to Anterior Pituitary), Tropic Hormone (AP to target gland), End-product hormone (target gland to everywhere else

181
Q

Hypothalamic-Pituitary-Adreanal (HPA) Axis

A
  1. Corticotropin-Releasing Hormone (CRH) to Anterior Pituity via median eminance
  2. Adrenocorticotropic Hormone (ACTH) from anterior pituitary to adrenal gland
  3. Glucocorticoid and Mineralocorticoid from adrenal gland to target tissues
182
Q

Hypothalamic-Pituitary-Gonadal (HPG) axis

A
  1. Gonadotropin-Releasing-Hormone from Hyp. to A.P. via median eminence
  2. Luteinizing Hormone (LH) and Follicle-Simulating Hormone (FSH) from A.P. to gonads
  3. Estrogens, Androgens, and Progestins from gonads to target tissues
183
Q

Epigenetics and HPA axis

A

Brains of rats raised by inattentive mothers treated with trichostatin A (removes methyl groups) - stress decreases

184
Q

Male HPG Axis

A

GnRH goes to Anterior Pituitary

FSH goes to the Sertoli Cell (sperm)

LH goes to the Leydig Cell (testosterone)

Testosterone goes to the sertoli cell, the anterior pituitary, and to the arcuate nucleus (hippocampus)

185
Q

Peripheral Androgen Effects in males

A

Hair growth, muscle formation, etc.

186
Q

General Takeaways from the female HPG Axis

A
  1. Different hormonal signals from different glands
  2. Signals exhibit both negative and positive feedback (don’t really know how that works)
  3. Multiple pathways, targets, and relationships - reproduction highly sensitive to the environment and development (a lot can go wrong)
187
Q

Which organs/gland secrete which hormones in the female HPG Axis?

A

Hypothalamus: GnRH

Ant. Pit: LH and FSH

Follicle: Estradiol

Corpus Luteum: Progesterone

188
Q

Different species and HPG Axis

A

They differ! (i.e. Rodent- 4 days)

189
Q

What do estrogen receptors do in the brain?

A
  1. increase growth factors
  2. promote cell proliferation
  3. promote plasticity
  4. neuroprotective
  5. Neuromodulation
  6. Modulation of reproductive behaviors
190
Q

What does androgen do in the brain?

A
  1. converted to estradiol
  2. converted to DHT (Modulation of social behaviors like reproduction and territorial aggression)
191
Q

What does progesterone do in the brain?

A
  1. converted to allopregnanolone (GABA A Agonist)
  2. Neuroprotective
  3. Neuromodulation
192
Q

Organizational reproductive hormone actions

A

Persist in the absence of sex hormone

193
Q

Activational reproductive hormone

A

Effects disappear when the hormone does (i.e. mounting in mice)

194
Q

Organizational reproductive hormones

A

Effects persist in the absence of sex hormone. Occurs during development.

195
Q

What three things can cause attraction?

A

Chemical stimuli

Visual stimuli

Auditory stimuli

196
Q

Pheromones

A

chemicals released by one animal and detected by a conspecific (same species) resulting in a change in behavior - Vomeronasal Organ (VNO) - Flehmen response

197
Q

Does attraction in humans change b/c of circulating hormones?

A

Maybe. Women like less masculine faces on birth control. Women like more masculinized faces and bodies when fertile, but only for hookups.

198
Q

Stages of sexual behavior

A
  1. Sexual attraction
  2. Appetitive behavior (female is proceptive)
  3. Copulation (female is receptive)
  4. Postcopulatory behavior
199
Q

What does sexual behavior require?

A

Combo of social signal (pheromone) and endocrine signal (hormone)

200
Q

Female pathway for mating behaviors

A

VMH- PAG- medullary reticular formation - spinal cord (top-down hormonal, social, and botom-up tacticle signals into response)

  • sensitive to circulating E2 and P4
201
Q

Male pathway for mating behavior

A

mPOA- midbrain - basal ganglia- motor input (erection)

sensitive to circulating T (via conversions to E2)

Integrates hormonal and social signals

202
Q

Relationship between gonadal steroids and sexual behaviors

A

Gonadal steroids activate sexual behaviors but don’t change their intesnsity

(i.e. testosterone in rats)

203
Q

Conditioned Place Preference

A

Do you return to the location where you banged? Rewarding (rats)

204
Q

Refractory period

A

need time after mating

205
Q

Coolidge effect

A

refactory period is shorter if there is a different female aroud (i.e. Sooty the rodent)

206
Q

Non-reproductive mating

A

(Copulations outside of fertility, same-sex, other stimulation). Humans do it but so do most social species!

207
Q

Activated parts of the brain during sex

A
  1. Cortex
  2. Ventral striatum (anticipation)
  3. Hypothalamus (ventromedial nucleus -females, medial preoptic area - male sexual behavior)
  4. Amygdala (identifying partners)
208
Q

Sex drive differing via gender study

A

Changing the methods- do you want to meet another stranger for sex?

209
Q

How are gametes found

A

through meiosis (XX - XY)

210
Q

When do male and female embryos begin to differentiate?

A

6 weeks

211
Q

How are male and female embryos differentiated?

A

SRY protein (from Y chromosone)- induces the gonad to develop into a testis. If none- develops into an ovary

212
Q

Wolffian ducts

A

Become male - vas deferens, seminal vesicles. etc.

213
Q

Müllerian ducts

A

become fallopian tubes

214
Q

Testis secretion and exteral genitalia

A

Testis secretes Testosterone and AMH (Anti-Müllerian hormone) - AMH regresses Müllerian ducts, while T promotes development of Wolffian ducts. T metabolized into dihydrotesterone DHT - scrotum ad benis

215
Q

What does “typical” male development require?

A

SRY

T - develop Wolffian ducts

DHT - act on adrogen receptors to promote external genitalia

216
Q

What does “typical” female development require?

A

Absence of androgen

217
Q

What happens if there is no expression of SRY?

A

Turner Syndrome - lack of Y chromosome - wide neck, mental disability, toes not developed

218
Q

What happens if there is no Testis-derived T to develop Wolffian ducts?

A

Androgen Insensitivity Syndrome- generally female phenotype despite the XY genotype

219
Q

What happens if there is no DHT?

A

“Güevedoces” AKA “Penis at twelve” - cannot make DHT from T

Internal reproductive tract develops male, but phenotypically female at birth

Develop male secondary sex characteristics at puberty

220
Q

Male, female, male roduct fetuses

A

slighly masculinized

221
Q

How can there be androgen in female development?

A

-Congenital Adrenal Hyperplasia (CAH)

Instead of being adrenal hormones, they get pushed into gonadal hormones

Look male - used to be the ruler to measure penises

222
Q

Sensitive period of reproductive brain development

A

2nd/3rd trimester in humans

223
Q

Full expression of reproductive behavior requires both ________ & _________ effects

A

organization/activational

224
Q

What does estradiol do to the rodent brain?

A

It masculinizes it

225
Q

What are sexually-dimorphic nuclei? Give an example

A

When brain regions are different in males and females (i.e. song nuclei exists in male zebra finches only)

226
Q

Women and test scores

A

Corresponds with culture (not biology) - corresponds to measures of women’s emancipation

227
Q

Can we see gender in the human rain?

A

Potentially. The Bed Nucleus of the Stria Terminalis (BNST) - larger in men regardless of gender assigned at birth (but also what about the hormone therapy?)

228
Q

Monkeys playing with “boy” toys vs “girl” toys

A

Male monkeys played more with boy toys- maybe not socialized

229
Q

Can we see sexual orientation in the human brain?

A

INAH-3: Straight men, gay men, women

230
Q

Biomarkers of sexual orientation

A

Otoacoustic emissions (straight women to straight men spectrum) - clicks made by hair cells

2D/4D ratio- larger for straight women, smaller for straight men, gays inbetween

231
Q

Biological determinants of sexual orientation

A

Genetics (via twin studies)

Older brother effect - maternal immune hypothesis

232
Q

What makes embryonic stem cells so unique?

A

They are totipotent - they can become any cell of the body

233
Q

cell-cell interactions

A

The fate of a cell is determined, in part, by chemical signals it gets from the cells around it (location!)

234
Q

Embryonic ectoderm development

A
235
Q

Teratogen (and 2 examples)

A

Substance that interferes with normal development

  • Alcohol - fetal alcohol syndrome
  • Thalidomide - skeletal malformations
236
Q

Phenylketonuria (PKU)

A

Lack an enzyme that breaks down phenylalanine - but thats okay as long as you exclude it from your diet in the beginning.

237
Q

Schizophrenia and pregnancy complications

A

Schizophrenia is highly genetic - but also combines with preganancy complications

238
Q

Neural development process (6 stages)

A
  1. Neurogenesis - cells created
  2. Cell Migration - cells move
  3. Cell Differentiation - change shape to become specific type of cell
  4. Synaptogenesis - neurons form connections
  5. Cell death - unnecessary cells are removed
  6. Synapse rearrangement - unnecessary synapes regress and useful new synapses are formed
239
Q

Where does neurogenesis occur?

A

In the ventricular zone (near the central canal of the neural tube)

240
Q

How to keep tract of new cell divisions?

A

BrdU - same function of “T”

241
Q

How does cell migration occur?

A

New neurons move along radial glial cells away from the center of the neural tube (towards the marginal zone)

242
Q

How can cells be prevented from cell migration, and what is the effect?

A

Reelin knockout - neurons stay attached to radial glia and don’t get to their destination :( - wobbly mouse

Lissencephaly AKA smooth brain - can’t make it to destination (b/c of dysfunctional cytoskeleton)

243
Q

Induction (and example)

A

When chemical signals from nearby cells turn on/off different genes to influence a cell’s development - aids in differentiation.

Notochord in the Ventra releases sonic - creates motor neurons (vs bmp - don’t become motor neurons)

244
Q

How does synaptogenesis happe?

A

Cell adhesion molecules - chemoattractants and chemorepellents - guide the growth cone

245
Q

How does neuronal cell depth happen?

A

CA2 rushes into cell, then mitochondria, mitochondria releases diablo, diablo steals IAPs away from caspases - so they can destroy the cell

246
Q

Neurotrophic factors

A

A form of chemical signaling that tells neurons not to die - if you collect a lot of them you won’t die.

247
Q

Epigenetics

A

our cells control how genes are expressed - which can impact behavior

248
Q

Methylation & Epigenetics

A

It is difficult for transcription factors to bind to genes with a methyl group

249
Q

Inattentive mom rats and HPA access

A

Pups with inattentive moms (regardless of genetics) - have greater methylation. This means less negative feedback of HPA axis - continues to be activated

250
Q

Methylation & PTSD

A

Methylation leads to hypercortisolemia- methylation (and childhood trauma) are protective against PTSD

251
Q

When does synaptic pruning occur?

A

Throughout adulthood

252
Q

Fragile X Syndrome

A

Tandem repeat varient on the X chromosome reults in instability of DNA

253
Q

Rotating frog eyes 180

A

They think the fly is on the wrong side- therefore, axons from retina reconnect based on their previous connections

254
Q

How is axon regenration guided?

A

Chemically (chemoffinity hypothesis) and experientially guided (fine-tuned)

255
Q

Amblyopia

A

Can lead to permanent eye damage if there is a lack of stimulation during the sensitve period - inactive synapses regress

256
Q

Hebbian Synapses

A

Cells that fire togetehr wire together!

257
Q

Ocular domance vs monocular deprevation vs one-eye deviated

A
258
Q

What do we learn as a child that are hard to aquire later (in regards to vision?)

A

Gestalt principles and monocular depth cues