Exam I Flashcards
(258 cards)
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”
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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
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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
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Forming conclusions based on objective observation, control, and replication
9
Q
Somatic intervention
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We do something to the body and see what happens to behavior (i.e. stimulate brain region, affects movement)
10
Q
Behavioral intervention
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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
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We determine (mathematically) if a somatic variable and behavioral variable covary
12
Q
Delgado’s charging bull experiment
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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
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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
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Social, organ, neural systems, circut level, celular level, synaptic level, molecular level
16
Q
Applied behavioral neuroscience
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focuses on understanding and treating dysfunction
17
Q
Natural selection
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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
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If a trait attracts a mate, it will be passed on to future generations
19
Q
Mutations
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Gene change. Single-nucleotide polymorphisms (single base) and tandem repeat variations (portions repeat).
20
Q
Silent mutation
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Doesn’t affect how the gene is expressed
21
Q
Nonsense mutation
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Doesn’t code for anything
22
Q
Missense Mutation
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Change in the expressed gene
23
Q
Frameshift mutation
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An insertion or deletion or both - more serious
24
Q
Directional selection
A
25
Stabalizing selection
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Disruptive selection
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How can we explain the persistence of apparent genetic disadvantage?
There might be advantages (i.e. being a carrier of the sickle cell gene decreases chance of getting malaria)
28
Is evolution?
No! Not intentional - doesn't have a goal
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Convergent evolution
Different species have different ways of solving the same problem (homoplasy)
30
Homoplasy
behaviors/characteristics appear similar because they emerged to solve similar problems
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Homology
behaviors/characteristics appear similar because they were derived from common ancestry (i.e. human and bat arms)
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Analogy
behaviors/characteristics evolved separately, but serve the same purpose (i.e. penguin and dolphin flipper)
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Brains are fairly ____ between species
Conserved (they have similar areas)
34
Correlates of behavioral specialization in the brain
We can see them. i.e. olfactory bulbs are much bigger in the mouse
35
Why did human brians get bigger?
The use of tools to cut meat and cooking of meat- decrease jaw size
36
Bipedalism
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)
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Effects of big brains on gestation
Longer gestation to help develop complex brain. Also a long postnatal developmental period.
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Direction selection of having a big brain
The selection pressure for large brain volume is greater than the selection pressure for small brain volume
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Coronal sectional plane
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Sagittal sectional plane
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Transverse/Horizontal sectional plane
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Medial versus lateral
Medial - more towards the middle, lateral - more towards the outside
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Anterior versus posterior
Anterior - towards the front; Posterior - towards the back
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Superior- dorsal versus Inferior ventral
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Rostral versus Caudal
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Types of glia
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Astrocytes
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
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Microglia
Act as the brain's immune system
49
Schwann Cells and Oligodendrocytes
Insulate axons (Damage to these cells in multiple sclerosis)
50
The Reticular theory
The nervous system is a single continuous network (Camillo Golgi AKA Golgi stain guy)
51
The Neuron Doctrine
Cells are functionally, structurally, and metabolically separated from each other, but they communicate across gaps (Santiago Ramon y Cajal AKA art school guy)
52
Golgi Stain
Camillo Golgi discovered in the 19th century. Silver chromate (seemingly) randomly stains about 10% of neurons
53
Nissl or Cresyl violet
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
Immunohistochemistry
Using antibodies to see proteins
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In situ hypridization
Using complementary RNA strands to see mRNDA
56
Zones in a neuron
Input, integration, conduction, output
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Multipolar neuron
The most comon type in which there are multiple dendrites. There are two main types - interneurons and motor neurons
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Interneurons
Type of multipolar neuron. Integrate multiple sources of information
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Motor neurons
Type of multipolar neuron. Control muscles/glands (efferents)
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Afferent neurons
Take information to the CNS
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Efferent neurons
Only take information away from the CNS
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Bipolar neuron
one dendrite. Generally sensory neurons (afferents)
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Unipolar
Touch receptors (afferents)
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Lipid bilayer
Doesn't let in polar molecules. Has some protein channels.
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Anterograde versus retrograde transport
Anterograde: towards the terminals
Retrograde: towards the soma
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Microtubules
Responsible for the rapid transport of material throughout neurons. They are held together by tau- if tau is damaged then Alzheimers disease can occur
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Synaptic plasticity
Synapses change with experience
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Two parts of the peripheral nervous system
Somatic nervous system & Autonomic Nervous System
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Somatic nervous system
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)
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Ventral versus dorsal part of the spine (efferent and afferent)
Ventral (motor) - efferent
Dorsal (sensory) - afferent
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Parts of the Autonomic Nervous System
Sympathetic & Parasympathetic
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Sympathetic
Part of the Autonomic Nervous System. Sympathetic- speeds things up (Fight/flight). Mostly norepinephrine. Ganglia run alongside the spinal cord.
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Parasympathetic
Part of the Autonomic Nervous System. Parasympathetic - slows things down (primarily acetylcholine) - Rest or digest. Ganglia next to innervated organs (distributed throughout the body).
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Enteric Nervous System
Gut - coordinates digestion (primarily uses serotonin)
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Central Nervous System
Brain and spinal cord
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Peripherial Nervous System
Nervous system outside of the brain and the spinal cord
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Four lobes of the neocortex and the main sulci and gyruses
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)
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Corpus callosum
Connects the left and right hemisphers of the brain
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Autonomic nervous system
regulates body functions to respond to the environment
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Built-in protection mechanisms of the brain
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
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Parts of the brain (development)
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Myelencephalon
Part of the hindbrain
AKA medula
Autonomic functions: digestion, breathing, heart rate, blood pressure
Includes reticular formation - involved in arousal
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Metencephalon
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)
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Mesencephalon
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
Diencephalon
Part of the forebrain
Thalamus and Hypothalemus
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Telencephalon
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
Cytoarchitecture in the neocortex
it varies!
88
The limbic system
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
Localization
Distinct brain regions have distinct functios; they are domain specific (not as true as we once thought)
90
Connectionism
Brain regions are domain-general, and combine to create specific functions
91
Diffusion tensor imaging (DTI)
Calculates fractional anisotropy (FA) -diffusion- by looking at movement of water molecules- indicates myelinated axons
92
Manipulating versus measuring the brain to determine localization of function
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
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Measure of localization graph (temporal resolution versus spacial resolution)
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fMRI
Measures blood oxygen level dependent (BOLD) signal
95
PET
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
Ex vivo versus in vivo measures of the brain
Ex vivo (outside) - histology
In vivo (inside)- measures of density (CT/X-ray) or diffusion (MRI, DTI)
97
Measures of density
Study structure of the brain: CT/X-ray
98
Measures of Diffusion
Study of the strucutre of the brain: MRI, DTI
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Study function of the brain via electricty
EEG/ERP, MEG, tDCS, TMS, direct stimulation
100
Study function of the brain via metabolism
fMRI, PET
101
What kind of signals do neurons communicate with?
Chemical and electrical (chemical input to chemical signal to electrical signal to trigger neurotransmitter release- cycle)
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Positive verusus negative charge
Positive- more protons than electrons
Negative- more electrons than protons
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Electrical potential
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
Resting potential of neurons
At rest, neurons have a negative potential (around -65 mV). B/c there are lots of negatively charged proteins inside the cell.
105
Concentration gradient
ions of the same type want to spread out
106
Concentration gradient and electrical gradient of Na+ and Potassium at resting potential
Concentration gradient: into the cell for Na+, out of the cell for K+
Electrical gradient: into the cell for K+ and Na+
107
K+ channels versus Na+ channels at rest
K+ channels pretty leaky vs Na+ not very permeable
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Na+/K+ pump
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
Polarized vs depolarized vs hyperpolarized
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)
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Repolarization
returning back to the resting membrane potential
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Effect of strength and location of stimulus in a neuron
Stronger stimulus = stronger response
Decay: Local potential is smaller as you move further from the stimulus site
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Action potential
When you depolarize to a certain threshold (about -40mV)
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Na+ channels during action potential
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
What happens to the electrical gradient of Na+ during action potential and what is the effect?
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)
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Absolute refractory period
Na+ channels are still closed - a second stimulation would not open them (1-2ms)
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Hyperpolarization during the relative refractory period
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)
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Myelination and action potentials
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
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How vesicles are docked at the synaptic terminal
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
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Pre-synaptic, synaptic cleft, and post synaptic›
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Ionotropic versus metabotropic receptor
Ionotropic: ligand-gated ion channel
Metabotropic: G-protein-coupled receptor (g-protein can pop off and do other stuff)
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Ways neurotransmission can be turned off
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)
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Gap Junctions
maintain electrical signaling without a chemical intermediary
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EPSP vs IPSP
Excitatory postsynaptic potential vs inhibitory postsyaptic potential
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Graded EPSPs and IPSPs
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)
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Integration of PSPs
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
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Is a single EPSP enough to elicit an action potential?
Almost never!
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Optogenetics
Can turn on receptors with lights (action potential)- affects movement
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Discovery of the first neurotransmitter in 1921
Otto Loewi - stimulated a vagus nerve (two jars connected) - acetylcholine
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What determines a neurotransmitter's effects?
It's receptors
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Exogenous substances versus endogenous
exo- from outside the body (aka cocaine)
endo- from inside (aka neurotransmitters
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Types of Acetylcholine receptors and functions
Muscarinic (metabotropic & agonist): constrict pupil
Nicotinic (ionotropic and nicotine is an agonist): constriction of muscle fibers
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Agonist versus antagonist versus inverse agonist
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
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Relationship between Neurotransmitter's effects and location (Dopamine example)
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
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Parkinsons vs Schizophrenia
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
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Neuropeptides as neurotransmitters
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
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Neurotransmitters are synthesized where?
BOTH in Soma (like neuropeptides) and in the terminal
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Types of amino acid neurotransmitters
Glutamate (excitatory) - have iontropic and metabotropic
GABA (mostly inhibitory) = GABA A + C - ionotropic vs GABA B - metabotropic
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What is so important about GABA (A)?
Different pockets/binding sites - which changes the function (i.e. alcohol, neurosteroids, chloride)
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Monoamine neurotransmitters
One amine
catecholamines- synthesized from amino acid tyrosine. Have a ring. Includes dopaminergic & noradrenergic
Indoleamines- synthesized from tryptophan. Includes serotonergic.
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Dopaminergic system receptors
There are many D1-5
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Noradreneric system
Most in the locus coeruleus (in the midbrain) but projects to the hypothalamus (stress response) neocortex (reward) thalamus (attention) and temporal lobe (memory)
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Pharmacokinetics
what the body does to a drug
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Route of (drug) administration
How the drug gets into the body
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First-pass effect
Drug is eliminated before it reaches circulation
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Pharmacodynamics
What a drug does to the body
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Dose-response curves
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
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Tolerance
with repeated exposure, it takes more of a drug to be effective
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Types of tolerance
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
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The different ways drugs can impact neurotransmitters
1. Transmitter production
2. Transmitter release
3. Transmitter clearance
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How drugs can impact how neurotransmitters are made and stored
1. inhibit production
2. block axonal transport
3. block storage in vesicles
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How drugs can effect the release of a neurotransmitter
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)
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How drugs can interfere with neurotransmitter clearance
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)
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2 Things to consider if a drug is interacting with a receptor
Binding affinity- how well does it bind?
Efficacy- how strong is its effect?
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Classical agonists (neurotransmission)
Recreate the effect of the endogenous NT (i.e. LSD - but it stays longer, so other things can't bind)
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Partial agonists
bind to the receptor but have a lower efficacy than the endrogenous NT; therefore, they are functionally antagonistic (ex: atypical antipsychotic)
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Indirect agonists/allosteric modulators
Bind to the receptor and increase its activity, but binds to different spot than the NT (therefore it is noncompetative) ex: alcohol
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Inverse agonists
Bind to receptor and have an opposite effect of the endrogenous NT
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Antagonists (neurotransmission)
bind to a receptor and prevent the effect of the endrogenous NT
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Noncompetative antagonists
bind to a different site than the endrogenous neurotransmitter and still block its effects (i.e. ketamine)
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First hints at an endocrine system
Came from castration (re-implanting testes), using goat testicles in humans to increase testosterone, etc.
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Hormone definition
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
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Endocrine
Gland sends a hormone through the bloodstream to a receptor
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Autocrine
Gland sends out hormone, works on it's own receptor
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Paracrine
very local effect (neighbors)
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Intracrine
A prohormone leaves a gland, and turns into the hormone in it's final location (high local concentration - not lost in the liver)
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Pheromone
Same species to species secretion (i.e. bees to bees)
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Allomone
One species to another secretion (a form of chemical signalling) i.e. bee orchid to bee
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General properties of hormonal actions
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
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What are the three main classes of hormones?
1. peptide
2. amine
3. steroid
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Neurosteroids
steroid hormones made in the brain
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Peptide hormones
Sequence of amino accids, coded for by specific genes (ie. Oxytocin)
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Amine hormones
Derived from a single amino acid (diet) i.e. melatonin, epinephrine, orepinephrine, thyroid hormones
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Steroid hormones
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
When steroid hormones are converted into another
Intracrine signaling
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Types of hormone feedback loops
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)
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Neuroendocrine cells
Start many hormonal cascades (triggered by the hypothalamus)
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How hormones, the brain, and behavior all interact - oxytocin example
When you copulate, oxytocin increases, which results in more bonding and spending time together, which increases oxytocin (prarie vole - receptor gene)
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What does the posterior pituitary release?
Oxytocin and vasopressin
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What does oxytocin do?
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
Anterior Pituitary axis formula
Releasing Hormone (Hypothalamus to Anterior Pituitary), Tropic Hormone (AP to target gland), End-product hormone (target gland to everywhere else
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Hypothalamic-Pituitary-Adreanal (HPA) Axis
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
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Hypothalamic-Pituitary-Gonadal (HPG) axis
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
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Epigenetics and HPA axis
Brains of rats raised by inattentive mothers treated with trichostatin A (removes methyl groups) - stress decreases
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Male HPG Axis
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)
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Peripheral Androgen Effects in males
Hair growth, muscle formation, etc.
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General Takeaways from the female HPG Axis
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
Which organs/gland secrete which hormones in the female HPG Axis?
Hypothalamus: GnRH
Ant. Pit: LH and FSH
Follicle: Estradiol
Corpus Luteum: Progesterone
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Different species and HPG Axis
They differ! (i.e. Rodent- 4 days)
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What do estrogen receptors do in the brain?
1. increase growth factors
2. promote cell proliferation
3. promote plasticity
4. neuroprotective
5. Neuromodulation
6. Modulation of reproductive behaviors
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What does androgen do in the brain?
1. converted to estradiol
2. converted to DHT (Modulation of social behaviors like reproduction and territorial aggression)
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What does progesterone do in the brain?
1. converted to allopregnanolone (GABA A Agonist)
2. Neuroprotective
3. Neuromodulation
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Organizational reproductive hormone actions
Persist in the absence of sex hormone
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Activational reproductive hormone
Effects disappear when the hormone does (i.e. mounting in mice)
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Organizational reproductive hormones
Effects persist in the absence of sex hormone. Occurs during development.
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What three things can cause attraction?
Chemical stimuli
Visual stimuli
Auditory stimuli
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Pheromones
chemicals released by one animal and detected by a conspecific (same species) resulting in a change in behavior - Vomeronasal Organ (VNO) - Flehmen response
197
Does attraction in humans change b/c of circulating hormones?
Maybe. Women like less masculine faces on birth control. Women like more masculinized faces and bodies when fertile, but only for hookups.
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Stages of sexual behavior
1. Sexual attraction
2. Appetitive behavior (female is proceptive)
3. Copulation (female is receptive)
4. Postcopulatory behavior
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What does sexual behavior require?
Combo of social signal (pheromone) and endocrine signal (hormone)
200
Female pathway for mating behaviors
VMH- PAG- medullary reticular formation - spinal cord (top-down hormonal, social, and botom-up tacticle signals into response)
- sensitive to circulating E2 and P4
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Male pathway for mating behavior
mPOA- midbrain - basal ganglia- motor input (erection)
sensitive to circulating T (via conversions to E2)
Integrates hormonal and social signals
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Relationship between gonadal steroids and sexual behaviors
Gonadal steroids activate sexual behaviors but don't change their intesnsity
(i.e. testosterone in rats)
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Conditioned Place Preference
Do you return to the location where you banged? Rewarding (rats)
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Refractory period
need time after mating
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Coolidge effect
refactory period is shorter if there is a different female aroud (i.e. Sooty the rodent)
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Non-reproductive mating
(Copulations outside of fertility, same-sex, other stimulation). Humans do it but so do most social species!
207
Activated parts of the brain during sex
1. Cortex
2. Ventral striatum (anticipation)
3. Hypothalamus (ventromedial nucleus -females, medial preoptic area - male sexual behavior)
4. Amygdala (identifying partners)
208
Sex drive differing via gender study
Changing the methods- do you want to meet another stranger for sex?
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How are gametes found
through meiosis (XX - XY)
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When do male and female embryos begin to differentiate?
6 weeks
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How are male and female embryos differentiated?
SRY protein (from Y chromosone)- induces the gonad to develop into a testis. If none- develops into an ovary
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Wolffian ducts
Become male - vas deferens, seminal vesicles. etc.
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Müllerian ducts
become fallopian tubes
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Testis secretion and exteral genitalia
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
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What does "typical" male development require?
SRY
T - develop Wolffian ducts
DHT - act on adrogen receptors to promote external genitalia
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What does "typical" female development require?
Absence of androgen
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What happens if there is no expression of SRY?
Turner Syndrome - lack of Y chromosome - wide neck, mental disability, toes not developed
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What happens if there is no Testis-derived T to develop Wolffian ducts?
Androgen Insensitivity Syndrome- generally female phenotype despite the XY genotype
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What happens if there is no DHT?
"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
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Male, female, male roduct fetuses
slighly masculinized
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How can there be androgen in female development?
-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
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Sensitive period of reproductive brain development
2nd/3rd trimester in humans
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Full expression of reproductive behavior requires both ________ & _________ effects
organization/activational
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What does estradiol do to the rodent brain?
It masculinizes it
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What are sexually-dimorphic nuclei? Give an example
When brain regions are different in males and females (i.e. song nuclei exists in male zebra finches only)
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Women and test scores
Corresponds with culture (not biology) - corresponds to measures of women's emancipation
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Can we see gender in the human rain?
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?)
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Monkeys playing with "boy" toys vs "girl" toys
Male monkeys played more with boy toys- maybe not socialized
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Can we see sexual orientation in the human brain?
INAH-3: Straight men, gay men, women
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Biomarkers of sexual orientation
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
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Biological determinants of sexual orientation
Genetics (via twin studies)
Older brother effect - maternal immune hypothesis
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What makes embryonic stem cells so unique?
They are totipotent - they can become any cell of the body
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cell-cell interactions
The fate of a cell is determined, in part, by chemical signals it gets from the cells around it (location!)
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Embryonic ectoderm development
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Teratogen (and 2 examples)
Substance that interferes with normal development
- Alcohol - fetal alcohol syndrome
- Thalidomide - skeletal malformations
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Phenylketonuria (PKU)
Lack an enzyme that breaks down phenylalanine - but thats okay as long as you exclude it from your diet in the beginning.
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Schizophrenia and pregnancy complications
Schizophrenia is highly genetic - but also combines with preganancy complications
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Neural development process (6 stages)
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
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Where does neurogenesis occur?
In the ventricular zone (near the central canal of the neural tube)
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How to keep tract of new cell divisions?
BrdU - same function of "T"
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How does cell migration occur?
New neurons move along radial glial cells away from the center of the neural tube (towards the marginal zone)
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How can cells be prevented from cell migration, and what is the effect?
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)
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Induction (and example)
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)
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How does synaptogenesis happe?
Cell adhesion molecules - chemoattractants and chemorepellents - guide the growth cone
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How does neuronal cell depth happen?
CA2 rushes into cell, then mitochondria, mitochondria releases diablo, diablo steals IAPs away from caspases - so they can destroy the cell
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Neurotrophic factors
A form of chemical signaling that tells neurons not to die - if you collect a lot of them you won't die.
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Epigenetics
our cells control how genes are expressed - which can impact behavior
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Methylation & Epigenetics
It is difficult for transcription factors to bind to genes with a methyl group
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Inattentive mom rats and HPA access
Pups with inattentive moms (regardless of genetics) - have greater methylation. This means less negative feedback of HPA axis - continues to be activated
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Methylation & PTSD
Methylation leads to hypercortisolemia- methylation (and childhood trauma) are protective against PTSD
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When does synaptic pruning occur?
Throughout adulthood
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Fragile X Syndrome
Tandem repeat varient on the X chromosome reults in instability of DNA
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Rotating frog eyes 180
They think the fly is on the wrong side- therefore, axons from retina reconnect based on their previous connections
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How is axon regenration guided?
Chemically (chemoffinity hypothesis) and experientially guided (fine-tuned)
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Amblyopia
Can lead to permanent eye damage if there is a lack of stimulation during the sensitve period - inactive synapses regress
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Hebbian Synapses
Cells that fire togetehr wire together!
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Ocular domance vs monocular deprevation vs one-eye deviated
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What do we learn as a child that are hard to aquire later (in regards to vision?)
Gestalt principles and monocular depth cues
