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PSYC 211 > Final Exam pre Midterms > Flashcards

Final Exam pre Midterms Flashcards

1
Q

Split Brain Surgery

A

Done to alleviate epileptic seizures. Sever the corpus callous. The hemispheres can’t communicate directly with one another. Coordinated movement is still possible thanks to the brainstem and spinal cord.

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2
Q

Corpus callosum

A

The bundle of white matter tracts connecting the left and right hemispheres.

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3
Q

Cerebral Hemispheres

A

Consciously process sensory information and initiate purposeful movement.

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4
Q

Lateralized function of cerebral hemisphere

A

Left brain:
- Control of muscles on right half of the body
- Couple language comprehension, speech, writing
- Processing right half of visual field
Right brain:
- Control of muscles on left half of the body
- Limited language, small ‘dictionary’
- Processing left half of visual field

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5
Q

Vision and the Hemispheres

A

When focusing on a fixation point, vision is divided into a left and right visual field:
The left visual field is processed by the right half of each eye. The right visual field is processed by the left half of each eye.
Nasal half of visual information (half closer to the midline) crosses over at the optic chasm.
Left hemisphere of brain processes right visual field. Right hemisphere processes left visual field.

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6
Q

Gazzaniga’s Interpreter Theory

A

In experiments with split brain patients, researchers give a visual command to the nonverbal right brain. Then ask the patients to verbally explain why they had done that thing. The left brain would create a story to explain the behaviour. Gazzaniga theorized that this is how unified conscious experience arises. Our behaviour is out of our control (no free will). The left brain develops a meaningful narrative through which we can understand our experiences.

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7
Q

Atoms

A

Every element is a type of atom. Atoms can and to form molecules. If an atom or molecule has a charge, it is an ion.

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8
Q

CHNOPS

A

Carbon, Hydrogen, Nitrogen, Oxygen, Phosphorus, Sulfur

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9
Q

The CHNOPS elements form 5 main molecules

A

Water, sugar, fat (lipids), nucleic acids, amino acids.

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10
Q

RNA

A

Single stranded chain of nucleic acids. Fragile. Ribozymes: Subgroup of RNA that catalyze chemical reactions. Thought to give rise to first life on Earth.

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11
Q

DNA

A

Double stranded chain of nucleic acids. Stable. In eukaryotes, stored safely in the nucleus. Primary storage of genetic info today.

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12
Q

Cell membrane

A

Phospholipid bilayer. Hydrophilic (water loving) phosphate head. Hydrophobic (water hating) lipid tail. The structure makes diffusion across the membrane difficult - a good thing if you want an enclosed cell.

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13
Q

Prokaryotic Cells

A

Single cell organisms. Cell membrane filled with cytoplasm (salty, nutrient filled liquid inside a cell). DNA, RNA, and ribosomes floating around.

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14
Q

Eukaryotic Cells

A

Single- or multi-cell organisms. Contains organelles like mitochondria and nucleus. Can now store DNA and create energy.

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15
Q

Protein Synthesis

A
  1. A segment of DNA in the nucleus is unraveled and a complementary strand of RNA is created (mRNA) - Transcription.
  2. mRNA leaves the nucleus
  3. Ribosome latches onto mRNA, recruits tRNA to bring in complementary amino acids - Translation.
  4. Amino acids are added to a growing chain that eventually breaks off and folds into a protein.
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16
Q

What is a neuron

A

A specialized type of cell that is electrically excitable. Neurons send electrical and chemical signals that permit fast communication.

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17
Q

Reticular Theory (Golgi)

A

Believed that the brain was a physically connected network

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18
Q

Neuron Doctrine (Cajal)

A

Believed that the brain was composed of individual cells communicating.

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19
Q

Soma

A

Cell body. Location of the nucleus and other organelles.

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20
Q

Dendrites

A

Sites for receiving chemical or sensory input.

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21
Q

Axon

A

Electrical signals (action potentials) are sent down the axon. Only one axon, but that axon can branch many times.

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22
Q

Axon terminals

A

End of axon, where the action potential triggers the releases of neurotransmitter.

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23
Q

Phospholipid Bilayer

A

Cell membrane. Ions cannot move across it. Hydrophilic (water loving) phosphate head. Hydrophobic (water hating) lipid tail. Inside: Cytosol (salty like solution filled with potassium, chloride, and sodium).

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24
Q

What makes a cell specialized?

A

All cells within an organism have the same DNA. Not all cells read the same sections of DNA. A section of the DNA (the gene) codes for a certain protein (strings of amino acids). Other sections of DNA define what cells should read the gene and when. Neurons are filled with proteins that determine the cell’s role.

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25
Q

How do neurons communicate - Electrically

A

Relies on membrane potential (Vm = difference in charge between inside and outside of cell). Within a cell.

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26
Q

How do neurons communicate? - Chemically

A

Relies on neurotransmitter release from axon terminal onto other neurons. Between cells.

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27
Q

Ions

A

Molecules carrying electrical charge.
Cations (+): Na+, K+, Ca2+, Mg+
Anions (-): Cl-

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28
Q

Setting the Resting Membrane Potential

A

Inside: 0mV
The outside (extracellular space) will always be 0 mV; it is the baseline against which we compare the cell’s internal charge.

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29
Q

Sodium Potassium Pump

A

Sets the concentration gradient (difference in amount of an ion present in one area vs another); sends Na+ out of cell, K+ into cell. Sets resting membrane potential.

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30
Q

What determines where ions want to go?

A

Diffusion: Ions want to be spread out from other like ions. If many of the same ions are close together (e.g. all within the cell), there is a pressure to spread away.
Electrostatic force: Ions want to be spread out from similarly charged ions. Opposite charges attract, similar charges repulse.

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31
Q

Potassium Leak Channel

A

Allows K+ to move freely in / out of cell; K+ leaking out sets negative Vm (-70mV). Sets resting membrane potential.

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32
Q

What starts an action potential?

A

We now have a negatively charged cell - positive ions want to come in because of electrostatic pressure. Sodium ions also want to come in to move down the concentration gradient. Some depolarizing stimulus (e.g., neurotransmitters released from another cell, sensory stimulus), then receptor binding opens ion channels, allowing initial influx of Na+.

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33
Q

Voltage-Gated Sodium Channel

A

Opens when the cell is slightly depolarized (-40mV); ball and chain blocks pore, inactivates channel after opening. During action potential.

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34
Q

Voltage-Gated Potassium Chanel

A

Opens during the upswing of the action potential (0mV); responsible for the return to baseline Vm. During action potential.

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35
Q

Action Potential Stage 1 - Baseline

A

Vm: -70mV
What’s Happening: Na+/K+ pump changes ion concentrations; K+ leak channel brings K+ out.
Diffusion: Na+ wants in, K+ wants out.
Electrostatic Force: Na+ wants in

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36
Q

Action Potential Stage 2 - Stimulus

A

Vm: -40mV
What’s Happening: External input depolarizes cell; a few VG Na+ channels open.
Diffusion: Na+ wants in, K+ wants out.
Electrostatic Force: Na+ wants in

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37
Q

Stage 3 of Action Potential - Upswing

A

Vm: Increasing towards peak
What’s Happening: Tons of VG Na+ channels open: VG K+ channels begin to open
Diffusion: Na+ wants in, K+ wants out.
Electrostatic Force: Na+ wants in, K+ wants out

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38
Q

Stage 4 of Action Potential - Peak

A

Vm: +40mV
What’s Happening: VG Na+ channels are plugged by ball and chain; VG K+ channels still opening.
Diffusion: Na+ wants in, K+ wants out
Electrostatic Force: K+ wants out

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39
Q

Action Potential Stage 5 - Downswing

A

Vm: Decreasing towards hyper polarization
What’s Happening: VG K+ channels open
Diffusion: Na+ wants in, K+ wants out
Electrostatic Force: K+ wants out

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40
Q

Action Potential Stage 6 - Hyperpolarization

A

Vm: -80mV
What’s Happening: Some VG K+ channels are still open, K+ leaves, sends Vm. more negative than baseline.
Diffusion: Na+ wants in, K+ wants out.
Electrostatic Force: Na+ wants in

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41
Q

Action Potential Stage 7 - Return to Baseline

A

Vm: -70mV
What’s Happening: VG K+ channels close; Vm set by Na+/K+ pump and K+ leak channel.
Diffusion: Na+ wants in, K+ wants out
Electrostatic Force: Na+ wants in

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42
Q

Diffusion during action potential

A

The force of diffusion never changes because the relative concentrations never change

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43
Q

Why doesn’t the action potential travel backwards?

A

An action potential involves an influx of positive charge into the cell. The influx of positive ions pushes other positive ions away (down the concentration gradient). Previously active voltage-gated Na+ channels are in refractory period (ball is clogging the pore), influx of positive ions cannot reopen them.

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44
Q

Myelination

A

Wrapping an insulating layer of fat around segments of the axon. Propagating the action potential can be slow and axons can be long, myelination makes this more efficient.

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45
Q

Glia - Astrocytes

A

Janitors of the cell. Break down and clean up waste. Provides scaffolding for other cellular functions.

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46
Q

Glia - Microglia

A

Provide immune support. Regulate cell development and response to injury.

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47
Q

Glia - Oligodendrocytes

A

Create myelin, wrap it around nearby axons. Can provide sheath for 50 axons. Schwann cells - equivalent in peripheral nervous system.

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48
Q

Glia - Ependymal cells

A

Line the ventricles. Circulate cerebrospinal fluid.

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49
Q

Saltatory Conduction

A

Insulation means the ions inside myelinated axon segments are insensitive to charge differences outside. Positive charge quickly travels down axon and is repropagated at nodes of Ranvier.

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50
Q

Nodes of Ranvier

A

Unmyelinated segments of membrane at which the action potential is repropagated.

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51
Q

Voltage-Gated Calcium Channel

A

Ca2+ into the cell triggers neurotransmitter release. At axon terminal.

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52
Q

Two main types of receptor

A
  1. Ionotropic: Ion channels. Direct, fast effect on cell potential. Excitatory EPSP: Na+ permeable. Inhibitory IPSP: Cl- permeable.
  2. Metabotropic: G-protein coupled receptors. Can act indirectly on ion channels. Slower modification of cell excitability.
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53
Q

Excitatory Postsynaptic Potential (EPSP)

A

Na+ permeable. Does not always induce an action potential in the postsynaptic neuron.

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54
Q

Inhibitory Postsynaptic Potential (IPSP)

A

Cl- permeable. does not always prevent an action potential in the postsynaptic neuron.

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55
Q

How do neurotransmitters get removed? - Reuptake

A

Reuptake proteins transport neurotransmitter back across the membrane of the presynaptic cell. Neurotransmitter can then be repackaged into vesicle for another round of release.

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56
Q

How do neurotransmitters get removed? - Enzymatic Deactivation

A

Enymes (proteins dedicated to destruction) break down neurotransmitter in the synapse.

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57
Q

How do neurotransmitters get removed? - Diffusion

A

Released neurotransmitter moves down its concentration gradient, away from initial release site.

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58
Q

Metabotropic Receptors

A

Metabotropic receptors have lots of different effects on the cell - depends on the receptor and the signalling cascade its activation causes.

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59
Q

G protein coupled receptors

A

G proteins are proteins that use GTP as an energy source for chemical reactions. Logan binding to receptor drives a sequence of events by which the G protein can catalyze chemical reactions around the cell.

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60
Q

Steps of a G protein coupled receptor

A
  1. Neurotransmitter binds and the receptor changes shape, forcing the G protein to let go of GDP from a previous activation.
  2. A nearby GTP molecule can bind to the newly opened site on the G protein
  3. The G protein and its bound GTP will dissociate from the receptor and catalyze chemical reactions.
  4. The G protein will eventually convert GTP to GDP, at which point it will reassociate with the receptor.
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61
Q

Where do synapses form? - Dendritic

A

Neurotransmitter is released into dendrites (either smooth shaft or spines)

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62
Q

Where do synapses form? - Somatic

A

Neurotransmitter is released onto the cell body. These synapses exert great control over whether the cell fires, due to proximity to the axon hillock.

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63
Q

Where do synapses form? - Axoaxonic

A

Neurotransmitter is released onto axon terminal. Can suppress or amplify VG Ca2+ activation if neuron 2 has an action potential. Amount of Ca2+ entry determines how much NT is released.

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64
Q

The Life of a Neurotransmitter

A
  1. Synthesized from a precursor molecule (an amino acid) by enzymes in the axon terminal.
  2. Neurotransmitter is packaged into vesicles by transporter proteins.
  3. Vesicles are released into the synapse through fusion to the membrane (exocytosis)
  4. Some neurotransmitter binds to postsynaptic receptors, some binds to auto receptors to down regulate release.
  5. Neurotransmitter in the synapse is cleared away by reuptake proteins (return neurotransmitter to cell it was released from) and enzymes (degrade neurotransmitter)
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65
Q

Neurotransmitters

A

Made of modified amino acids. Synthesized locally in axon terminals. Secreted from small synaptic vesicles. Activates Ionotropic and metabotropic receptors. Yes reuptake.

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66
Q

Neuropeptides

A

Made of short strings of amino acids. Synthesized in soma, transported down the axons. Secreted from large dense core vesicles. Activates metabotropic receptors. No reuptake.

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67
Q

Lipid-Based Signalling Molecules

A

Made of Lipids (e.g., a chunk of cell membrane). Synthesized as needed (not very clear). Secreted from postsynaptic cell (does not require vesicles). Activates metabotropic receptors. No reuptake.

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68
Q

Drugs - Direct and Indirect

A

Exogenous chemicals that alter cell function at low doses.
Direct: affect activity by binding to postsynaptic receptor.
Indirect: affect activity by interacting with something other than the postsynaptic receptor.

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69
Q

Direct Drugs - Competitive

A

Affect activity by binding to postsynaptic receptor at the same site as endogenous neurotransmitter. Agonist: Full, Partial. Antagonist: Full.

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70
Q

Direct Drugs - Noncompetitive

A

Affect activity by binding to postsynaptic receptor at a different site than endogenous neurotransmitter. Agonist: Full, Partial, Positive Allosteric Modulator. Antagonist: Full, Negative Allosteric Modulator.

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71
Q

Partial Agonists

A

Can cause a net increase or decrease in postsynaptic activity. Depends on baseline activity at the synapse. If there is no receptor binding, the receptor activation is 0%. At a highly active synapse, neurotransmitter is frequently binding to receptors. Neurotransmitter binding causes maximal activation of receptor - at baseline, receptors are activated 100%. The drug has higher affinity, so binds to receptors instead of neurotransmitter, BUT it doesn’t activate them as strongly - receptors are activated 50%.

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72
Q

Positive Allosteric Modulators

A

A positive allosteric modulator amplifies the effect of neurotransmitter binding. Alcohol and benzodiazepines are both examples of positive allosteric modulators for GABA.

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73
Q

Negative Allosteric Modulators

A

A negative allosteric modulator decreases the effect of neurotransmitter binding.

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74
Q

Glutamate

A

Neurotransmitter. Excitatory effect, permits Na+ influx.

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75
Q

Repeat Administration effect on Tolerance

A

Drug effects are lessened due to the body down regulating natural processes that do the same thing. E.g., if dopamine levels are elevated because of regular cocaine use, the body will synthesize less dopamine to bring levels closer to normal.

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76
Q

Repeat Administration effect on Withdrawal

A

Cessation after regular use causes the inverse of symptoms. E.g., stimulant withdrawal causing fatigue, opiate withdrawal causing dysphoria.

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77
Q

Dopamine

A

Neurotransmitter. Reinforcement effect, volitional

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78
Q

GABA

A

Neurotransmitter. Inhibitory effect, permits Cl- influx.

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79
Q

Acetylcholine

A

Neurotransmitter. Attention effect, muscle contraction.

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80
Q

Serotonin

A

Neurotransmitter. Mood, sleep/wake states.

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81
Q

Norepinephrine

A

Neurotransmitter. Arousal effect, attention.

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82
Q

Peripheral Nervous System (PNS)

A

Rest of nervous system besides brain and spinal cord. Myelinated by Schwann cells. Uses the lymphatic system: blood leaks out of vessels through capillary gaps, becomes lymph. Lymph provides nutrients and cleans up waste. Recycled back into bloodstream.

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83
Q

Opioids

A

Neuropeptides. Analgesic, pleasure.

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84
Q

Endocannabinoids

A

Lipid-Based Signaling Molecule Neuromodulation, appetite, memory.

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85
Q

Central Nervous System (CNS)

A

The brain and spinal cord. Myelinated by oligodendrocytes. Does not use lymphatic system: no capillary gaps in blood vessels, protected by blood-brain barrier. CNS makes its own interstitial fluid (cerebrospinal fluid).

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86
Q

Division of the PNS - Somatic

A

Somatic: Sensing the external environment. Controls skeletal muscles. ‘Voluntary’.
Afferents: Sensory signal from eyes, ears, skin to CNS.
Efforts: Motor signals from CNS to skeletal muscles.

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87
Q

Neuraxis

A

Line along the length of the CNS (following the spinal cord and brain). The anatomical directions follow the neuraxis, which is why it gets wonky with humans and our bent heads.

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88
Q

Division of the PNS - Autonomic

A

Sending the internal environment. Controls smooth & cardiac muscle, glands. ‘Involuntary’.
Afferents: Sensory signal from internal organs to CNS.
Efferents: Motor signal from CNS to internal organs. Divided into sympathetic & parasympathetic.
Sympathetic: Fight or flight. Facilitates survival response. Prioritizes processes immediately necessary for survival.
Parasympathetic: Rest and Digest. Facilitates activities during relaxed state. Prioritizes increasing energy stores.

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89
Q

Choroid Plexus

A

Site of CSF production - tissue in all ventricles.

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90
Q

Lateral Ventricles

A

Two large ventricles’ mirrored across the sagittal plane.

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91
Q

Cerebral Ventricles

A

CSF (cerebrospinal fluid) is a nutrient filled solution the brain sits in. It is constantly circulated around the keep the brain healthy and refreshed.

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92
Q

Third ventricle

A

Between the thalamic nuclei; along the midline

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93
Q

Brain Development & Neoteny - 0-1 month

A

Neural tube forms - made of neural progenitor cells.

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94
Q

Fourth ventricle

A

Posterior to other ventricles, between pons and cerebellum.

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95
Q

Cerebral Aqueduct

A

Connects the third and fourth ventricle

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96
Q

Brain Development & Neoteny - 2-4/5 months

A

Asymmetrical division of NPCs: One NPC divides into one NPC and one neuron / glial cell. Neurogenesis = birth of new neurons.

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97
Q

Brain Development & Neoteny - 4/5+ months

A

Apoptosis: programmed cell death.

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98
Q

Brain Development & Neoteny- 1-2 months

A

Symmetrical division of neural progenitor cells: One NPC divides into two identical NPCs. Line the inside of the neural tube / ventricular zone.

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99
Q

The Midbrain - Tectum

A

Unconscious sensory processing.
Superior colliculi: Orient towards peripheral visual stimuli.
Inferior Colliculi: Orient towards peripheral auditory stimuli.

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100
Q

The Hindbrain - Medulla

A

Regulates autonomic, involuntary functions (e.g., coughing, sneezing). Processing internal sensation. Area postrema.

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101
Q

The Hindbrain - Medulla

A

Regulates autonomic, involuntary functions (e.g., coughing, sneezing). Processing internal sensation. Area postrema.

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102
Q

The Hindbrain - Pons

A

Relay between cerebrum and cerebellum. Medulla and pons contain many cranial nerve nuclei.

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103
Q

The Hindbrain - Pons

A

Relay between cerebrum and cerebellum. Medulla and pons contain many cranial nerve nuclei.

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104
Q

The Hindbrain - Cerebellum

A

Coordinate muscle movement and timing. Integrating sensory and motor information.

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105
Q

The Hindbrain - Reticular Formation

A

Regulates overall arousal state.

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106
Q

The Forebrain - Thalamus

A

Control of arousal and sleep/wake states. Similar function to pons: relay ascending sensory info to cortex, relay descending motor info to spinal cord.

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107
Q

The Midbrain - Tegmentum

A

Coordinating reflexive species-typical behaviours. E.g., pain, threat response.

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108
Q

The Forebrain - Hypothalamus

A

Control of autonomic nervous system. Control of the endocrine system - similar to medulla, but medulla signals with axonal projections, hypothalamus signals via hormones in bloodstream.

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109
Q

Limbic System

A

Hippocampus: Episodic memory formation.
Amygdala: Emotion recognition and processing.
Cingulate cortex: Connecting limbic structures

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110
Q

The Forebrain - Cerebral Cortex

A

Sheet of grey matter that folds into:
1. Sulci: small grooves, central sulcus: divides rostral and caudal brain.
2. Fissures: large grooves, longitudinal fissure: divides the two hemispheres, lateral fissure: divides frontal and temporal lobes.
3. Gyri: ridges between sulk / fissures

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111
Q

Four lobes of the cerebral hemisphere and their controls

A
  1. Frontal: Movement
  2. Parietal: Touch information
  3. Occipital: Visual information
  4. Temporal: Auditory information
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112
Q

Basal Ganglia

A

Involved in movement, motivation, and learning. Receives input from the forebrain and dopamine neurons in the midbrain. Damage results in movement problems.

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113
Q

Studying the Brain (structure, correlations, causality)

A

We can understand structure through imaging the brain, we can make correlations by recording neural activity during behaviour, we can understand causality by manipulating activity and observing what behaviour is produced.

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114
Q

CT - computerized tomography

A

Utilizes X-rays to image brain structure. Structural purpose. Cheap, fast, noninvasive. Poor spatial and temporal resolution.

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115
Q

fMRI - functional magnetic resonance imaging

A

Same as MRI, but utilizing the difference in magnetic fields around oxygenated vs non oxygenated blood to measure activity. Correlational purpose. Good temporal and spatial resolution, noninvasive. Expensive.

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116
Q

MRI - magnetic resonance imaging

A

Utilizes radio waves emitted from magnetically aligned water molecules. Different density of different substances create image. Structural purpose. High spatial resolution, noninvasive. Expensive.

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117
Q

Studying the Rodent Brain - Calcium Imaging

A

Ca2+ flows into the cell following an action potential. We can express a fluorescent molecule that is brighter when bound to calcium. The amount of fluorescence is a proxy for neuronal activity.

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118
Q

DTI - diffusion tensor imaging

A

Same as MRI, but changes in direction speed of radio wave emittance from water molecules resolves resolves axon tracts. Structural purpose. High spatial resolution for microstructure of axon tracts. Expensive.

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119
Q

PET - positron emission tomography

A

Radioactive molecule is injected, can record use of that molecule via energy emission. Correlational purpose. Can make any isotope radioactive - image whatever you want. Expensive, isotopes must be synthesized within hours of imaging.

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120
Q

Studying the Rodent Brain - Neuronal Tracing

A

Inject a molecule to stain pre- or post-synaptic connections.
Retrograde: Trace afferents (cells innervating cell of interest). Fluorogold.
Anterograde: Trace efferents (cells innervated by cell of interest). PHA-L

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121
Q

Macroelectrode EEG

A

Conductive discs placed on scalp record electrical changes in the brain. Correlational purpose. cheap, non-invasive, high temporal resolution. Meaning of waves is difficult to interpret, low spatial resolution.

122
Q

Studying the Rodent Brain - Optogenetics

A

Steroataxic surgery to inject virus into specific brain region, place implant. Viruses causes certain cell population to express opsins (light sensitive channel). Shining specific wavelength of light via implant can activate opsins. Different opsin can be excitatory or inhibitory. Measure behavioural effect.

123
Q

Studying the Rodent Brain - Microelectrode EEG

A

Metal wires inserted into the brain record changes in electrical activity. Corresponding to actions potentials in nearby neurons. Can record from hundreds or thousands of neurons simultaneously. Can record while animals are awake and moving. Can be chronic (recording for over extended period) or acute (recording briefly).

124
Q

Viral Mediated Gene Delivery

A

Viruses are excellent at delivering DNA into cells, that’s their whole job. We can remove the virus’ DNA and insert foreign DNA into a virus (like an opsin or fluorescent protein). The virus will infect whatever cells are nearby. By putting a promotor for a specific cell type before the DNA, we can target expression to a specific population.

125
Q

Studying the Rodent Brain - Pharmacological Manipulation

A

Deliver drugs into specific brain region via cannula. Measure behavioural effect of drug administration. Can compare same animal’s behaviour with and without drug onboard.

126
Q

Studying the Rodent Brain - Electrical Stimulation

A

Implant electrode into specific region of brain. Electrically stimulate at certain times to increase activity in region - ALL cells within region. Measure behavioural effect.

127
Q

Studying the Rodent Brain - Microdialysis

A

Take samples of extracellular fluid from a brain region. Measure concentration of molecules. Can correlate levels of certain molecules (e.g., neurotransmitter) with behaviours. Low temporal resolution.

128
Q

Studying the Rodent Brain - Excitotoxic Lesion

A

Injecting glutamate receptor agonist (kainic acid) causes excitotoxicity (cell death from over activation). Does not kill passing axons.

129
Q

Studying the Rodent Brain - Reversible Lesion / Sham Lesion

A

Reversible Lesion: Inject drugs that temporarily inactivate a region or population (e.g., GABA receptor antagonist, voltage gated Na+ channel blocker).
Sham Lesion: Placebo / control procedure that involves all steps of real lesion besides the inactivating step (ensuring effects of lesion are not due to other aspects of process).

130
Q

Studying the Rodent Brain - Radio Frequency Lesion

A

Radiofrequency current applied through a metal wire in the brain. Burns surrounding tissue, ablating it. Cannot target specific cell types / parts of cells - will ablate axons passing through lesioned area.

131
Q
A
132
Q

Studying the Rodent Brain - Stereotaxic Surgery

A

Procedure to place implants, inject drugs, lesion brain areas. Rodent is anesthetized, head fixed, and the skull is levelled relative to bregma (the site of convergence of multiple skull plates).

133
Q

Sensation vs Perception

A

Sensation: How cells detect stimuli in our environment and transduce them for neurotransmitter release.
Perception: Interpretation of external stimuli.

134
Q

Sensory transduction

A

Process by which sensory stimuli are transducer (converted) into receptor potentials.

135
Q

Receptor potential

A

Graded change in the membrane potential of a sensory neuron caused by sensory stimuli.

136
Q

Sensory neuron

A

Specialized neuron that detects a particular category of physical events (sensory stimuli). E.g., photoreceptors transduce light into receptor potentials.

137
Q

Light Detection: Opsin Proteins

A

Sensitive to light by binding to retinal, the molecule that absorbs photon energy. All opsin have inhibitory metabotropic receptors.

138
Q

Two types of photoreceptors

A
  1. Rods: One type of rod
  2. Cones: Three types of cones (red, green blue).
    Each rod and cone has their own opsin protein.
139
Q

Tritanopia

A

No functional blue cone opsins - visual acuity is not noticeably reduced since blue cones are not very sensitive to light.

140
Q

Protanopia

A

No functional red cone opsins (X-linked, more common in males).

141
Q

Deuteranopia

A

No functional green cone opsins. (X-linked, more common in males.)

142
Q

Achromatopsia

A

No functional cones at all.

143
Q

Saccadic vs Pursuit Eye Movements

A

Saccadic: Rapid, jerky shifts.
Pursuit: Follows moving objects, smooth.

144
Q

Fovea (also called the Macula Lutea)

A

Only contains cone cells. One to one connection of photoreceptors to bipolar cells to ganglion cells. High resolution. Colour vision.

145
Q

Peripheral Vision

A

More rod than cone cells. Convergence to multiple cells. Low resolution. Faint light and shapes.

146
Q

Photoreceptors

A

No action potentials. Graded glutamate release anywhere between -40mV to -70mV. Leaky sodium ion channels are open in the dark and already depolarized. Release more glutamate in the dark than in the light.

147
Q

Horizontal Cells

A

Regulates adjacent photoreceptor and bipolar cells.

148
Q

Bipolar Cells

A

There are ON bipolar cells and OFF bipolar cells. No action potentials. Graded glutamate release depending on the membrane potential.

149
Q

Bipolar cells: ON

A

Dark: Sodium channels open –> depolarized. Photoreceptors release more glutamate. ON bipolar cells have inhibitory metabotropic glutamate receptors. ON Bipolar cells inhibited by glutamate.
Light: Sodium channels close –> hyper polarized. Photoreceptors release less glutamate. ON bipolar cells are less inhibited.

150
Q

Bipolar Cells: OFF

A

Dark: Sodium channels open –> depolarized. Photoreceptors release more glutamate. OFF Bipolar cells have excitatory glutamate receptors. OFF Bipolar cells excited by glutamate.
Light: Sodium channels close –> hyper polarized. Photoreceptors release less glutamate. OFF bipolar cells hyper polarize.

151
Q

Amacrine Cells

A

Regulate the excitability of adjacent bipolar and ganglion cells.

152
Q

Ganglion Cells

A

Have action potentials and are excited by glutamate. Have on-off receptive fields for light and colour.

153
Q

Ganglion Cells: Receptive Fields

A

Receptive fields: Area of the visual space (relative to a fixation point) where light is capable of changing the activity of a neuron.

154
Q

Anatomy of the eye - Lateral Geniculate Nucleus (LGN)

A

A nucleus in the thalamus; many RGCs project here and then LGN neurons project to the visual cortex.

155
Q

Anatomy of the eye - Left visual field

A

Left visual field goes to the right hemisphere. Each hemisphere gets input from both eyes.

156
Q

Anatomy of the eye - Right. visual field

A

Right visual field goes to the left hemisphere. Each hemisphere gets input from both eyes.

157
Q

Anatomy of the eye - Superior colliculus

A

Involved in controlling fast reflexive movements in response to light.

158
Q

Anatomy of the eye - Hypothalamus

A

Regulates sleep/wake cycles

159
Q

Visual Processing in the Cortex

A

V1 neurons have larger receptive fields and respond to various orientations of light. This helps identify borders, edges, and corners. Primary Visual Cortex –> Dorsal stream to parietal lobe.
Primary visual cortex –> Ventral stream to temporal lobe.

160
Q

Agnosia

A

A problem in sensory association areas, not sensory modalities.

161
Q

Akinetopsia

A

Disability in movement perception.

162
Q

Cerebral Chromatopsia

A

Denying colour perception.

163
Q

Prospagnosia

A

Inability to recognize people by their faces.

164
Q

Monocular vision

A

Use of one eye for vision. Humans rely on monocular cues to perceive depth and distance when not using both eyes. Some cues: relative size, amount of detail, relative movement, 2D images).

165
Q

Binocular vision

A

Use of both eyes. The slight difference in the images perceived by each eye is the basis for the depth perception mechanism known a stereopsis. Retinal disparity: key visual cue in binocular vision that enables the brain to perceive depth.

166
Q

Predictive Coding Theory

A

Every level of visual processing is affected by predictions of what is interpreted at lower levels and a feedback error signal to correct future predictions. Predictions from high level –> Error signal from low level –> repeat

167
Q

Loudness / Pitch / Timbre

A

Loudness: Amplitude of the sound wave
Pitch: Frequency of the soundwave
Timbre: Complexity of the soundwave

168
Q

Outer ear anatomy

A

Pinna: funnel sound
Ear Canal

169
Q

Middle ear anatomy

A

Ossciles: Malleus, Incus, Stapes
Tympanic membrane

170
Q

Inner ear anatomy

A

Cochlea, Oval window

171
Q

The cochlea

A

The basilar membrane in the cochlea stretches with sound. Sounds make the ossicles vibrate against the cochlea. The vibrations make the fluid inside the cochlea move. Fluid (endolymph) moves with sounds, and deforms the basilar membrane: High pitch sound - deformation of the base of the membrane. Low pitch sound - deformation at the tip of the membrane.

172
Q

Organ of corti anatomy

A

Basilar membrane and tectorial membrane. Outer and inner hair cells.

173
Q

Organ of corti - outer hair cells

A

Attached to the tectorial membrane. Acts as a muscle to adjust the flexibility of the tectorial membrane.

174
Q

Organ of corti - inner hair cells

A

Transmit auditory information to the brain. Sway back and forth as the basilar membrane and the endolymph moves. Without them = deaf.

175
Q

Hair cells

A

Vibration in the basilar membrane makes the cilia rub and bend against the tectorial membrane. The stretching of tip links opens ion channels. Information from inner hair cells ascends to the brain.

176
Q

Ear to Brain Pathways

A

Temporal lobe: primary auditory cortex.
Thalamus: synapse in the medial genicular nucleus
Midbrain: synapse in the inferior colliculi
Medulla: synapse in the superior olivary nuclei
Medulla: synapse in the dorsal and ventral cochlear nuclei
Cochlear Nerve
Primary auditory cortex: tonotopic organization (organized by frequency)
Parietal lobe: dorsal/where pathway
Frontal lobe: ventral/what pathway

177
Q

Pitch - Place coding

A

Moderate to high frequency. Position of the active hair cell on the basilar membrane indicates the pitch. Higher frequencies = base of basilar membrane. Lower frequencies = tip of the basilar membrane.

178
Q

Pitch - Rate coding

A

Low frequency, correspond to how much neurotransmitter are released. Inner hair cells: transmit information to the brain. Outer hair cells: change sensitivity of the tectorial membrane to vibration –> tune sensitivity & frequency selectivity of inner hair cell.

179
Q

Sound Perception: Loudness

A

Loudness: number of hair cells that are active. Loud sounds: tip link stretches to their max and break, temporary loss of hearing, prevent excitoxicity.

180
Q

Sound Perception: TImbre

A

Timbre: specific mixture of fundamentals and overtones that different instruments emit when the same note is played. Fundamental frequency: correspond to the pitch of the sound (e.g., 100Hz).
Overtones: multiples of the fundamental frequencies (e.g., 200Hz, 300Hz, 400Hz).

181
Q

Spatical Localization - Phase Difference

A

Low frequency sounds. Timing difference between the ears.

182
Q

Spatial Localization - Level Difference

A

High frequency sounds. Loudness difference between ears.

183
Q

Spatial Localization - Timbre Differences

A

Changes in timbres between differences in location of the sounds.

184
Q

Music - Amusia

A

The characteristics of music (melody, rhythms, and harmony) and how you perceive it (pleasant, unpleasant) are processed in different regions of the auditory association cortex.
Amusia: cannot perceive music, and understand speech, can recognize emotions but would not be able to tell if it’s a consonant/dissonant music.

185
Q

Vestibular System

A

Sense of motion, orientation, and gravity.
Semi-circular canals: filled with fluid, fluid moves with head rotation.
Ampullas: contains the cupula - gelatine that moves with head rotation, movement displaces and activates hair cells.
Utricle & Saccule in vestibular sacs: contain otoconia - heavy mineral that moves in linear motion.

186
Q

Exteroceptive system

A

Cutaneous sense. Information about outside of the body.

187
Q

Interoceptive system

A

Organic sense. Information about inside of the body.

188
Q

Proprioceptive system

A

Kinesthesia. Information about the position of the body.

189
Q

Somatosensory receptors - Free nerve endings

A

Temperature & Pain. Epidermis layer (outer).

190
Q

Somatosensory endings - Meisner Corpuscles

A

Light touch, edge contour, brail-like (only in glabrous skin). Epidermis layer (outer).

191
Q

Somatosensory endings - Merkel’s Disk

A

Precise information about touch, skin indentation. Dermis layer (middle).

192
Q

Somatosensory endings - Ruffini Corpuscles

A

Stretches, finger position. Dermis layer (middle).

193
Q

Somatosensory endings - Pacinian Corpuscles

A

Skin vibration. Hyperdermis layer (bottom).

194
Q

Temperature

A

Mediated by free nerve endings. Poorly localized information. Temperature gated ion channels. Can be activated by ligands: capsaicin for heat receptors / menthol for cold receptors.

195
Q

Pain

A

Mediated by free nerve endings. Poor localized information. Nociceptors. Respond to intense pressure or extreme temperatures.

196
Q

From the Body to the Brain - Dorsal Column

A

High Spatial Resolution. Fine touch, kinaesthesia. Ascend ipsilaterally and first synapse in medulla. Cross over to the contralateral side and ascend to the thalamus.

197
Q

From the Body to the Brain - Spinothalamic Tract

A

Low spatial resolution. Crude touch, temperature, pain. First synapse in the spinal cord and cross over to ascend controlateraly to the thalamus.

198
Q

From the body to the Brain - Thalamus

A

Dorsal column and spinothalamic tract synapse before projecting to the primary somatosensory.

199
Q

From the Body to the Brain - Midbrain

A

Dorsal column and spinothalamic tract join together.

200
Q

Tactile Agnosia

A

Disorders of the somatosensory association cortex. Cannot verbally identify object by touch alone. Can draw objects from touch alone.

201
Q

Phantom Limb

A

Sensation of pain coming from a limb that has been amputated. The Somatosensory cortices is confused by noisy signals from the axons that have been cut.

202
Q

Somatotopic map

A

The primary somatosensory cortex is organised in a somatotopic map

203
Q

6 types of taste receptors

A

Sweet, Bitter, Unami, Salt, Sour, Fat

204
Q

Taste Receptors - Sweetness

A

Sugar. Single metabotropic receptor. Rewarding.

205
Q

Taste Receptors - Bitterness

A

Different molecules. 50 metabotropic receptors. Aversive.

206
Q

Taste Receptors - Unami

A

Glutamate. Single metabotropic receptor. Rewarding.

207
Q

Taste Receptors - Saltiness

A

Sodium ions. Ion channel permeable to sodium.

208
Q

Taste Receptors - Sourness

A

pH level. Ion channel permeable to free protons.

209
Q

Taste Receptors - Fat

A

Fatty acids. Metabotropic and fatty acid transporters.

210
Q

Taste Buds

A

Groups of 20-50 taste receptor cells sensitive to one particular tasting –> express the same taste receptor protein.

211
Q

Taste Receptor cells

A

Do not have action potential –> release neurotransmitters in a graded fashion. Replaced every 10 days –> directly exposed to the surface.

212
Q

Primary gustatory cortex

A

Organized by taste within people. Not a consistent organization across people,

213
Q

Odorants

A

Volatile substances that activate olfactory receptors. 400 types of odorant’s. 10 000+ different types of doors –> one odourant can activate multiple receptors.

214
Q

Olfactory Receptor cells

A

Located in the olfactory epithelium (tissue of the nose). Express one type of receptors. Synapse in glomeruli (process one type of cell meaning one type of odour).

215
Q

Olfactory information

A

Only sensory information that does NOT go through the thalamus. Goes to the primary olfactory cortex in temporal lobe + amygdala.

216
Q

What are Pheromones

A

Chemical released by one that affects behaviour of another animal (can signal attraction, danger, etc…). Can be inherently good or bad.

217
Q

Vomeronasal Organ

A

Process pheromones. Activated by sniffing of mouth / anogenital region. Contain metabotropic vomeronasal receptors. Not present in humans, apes & birds.

218
Q

Accessory Olfactory Bulb

A

Necessary for the effects of pheromones.

219
Q

Lee-Boot Effect

A

Female mice without male urine present –> slowing down/stopping of estrous cycle

220
Q

Whitten Effect

A

Female mice with male urine present –> synchronization of cycles.

221
Q

Vandenbergh Effect

A

Female mice with male urine present –> earlier onset of puberty.

222
Q

Bruce Effect

A

Unfamiliar male scent –> termination of pregnancy.

223
Q

Volumetric thirst

A

Caused by low extracellular fluid volume (hypovolemia - low blood flow). Signalled by renin (hormone released by kidney). Low blood flow –> kidney –> angiotensinogen (angiotensin I, angiotensin II)

224
Q

Osmometric thirst

A

Keep track of intracellular fluid volume. Induced by increase in solute outside cell. Signalled by osmoreceptors (detect changes in cell size). Water moves where salt concentration is the highest.
Isotonic: Normal cell (salt inside and outside cell). Hypotonic: swollen cell (salt in cell). Hypertonic: shrunken cell (salt outside cell).

225
Q

AV3V region

A

Neurons in the AV3V region of the hypothalamus can be sensitive to angiotensin/osmoreceptors/both. Drinking hypertonic saline (inducing thirst) –> activates AV3V + anterior cingulate cortex. Anterior cingulate cortex + cold sensors in mouth and stomach –> rapid mechanism, responsible for the conscious sensation of thirst.

226
Q

Short term reservoir of energy

A

High glucose level –> put glucose in storage. Low glucose level –> increase glucose levels. Glucose (simple sugar, fuel for cells, in blood) —-> Insulin —-> Glycogen (polysaccharide (chains of sugar), stored in liver and muscles, short term storage of energy)
Glycogen —> Glucagon —> Glucose.

227
Q

Short term reservoir of energy - CNS

A

CNS + cells outside CNS can use glucose: cells outside the CNS can only use glucose transporter when insulin is present (meaning when there is excess glucose).
When glucose is rare (no insulin), glucose goes in priority to the brain.

228
Q

High glucose level –> put glucose in storage

A

Pancreas releases insulin. Insulin transforms glucose into glycogen to be stored in liver and muscles. The excess glucose can be used to both cells in the CNS and outside of the CNS.

229
Q

Low glucose level –> increase glucose levels

A

Pancreas releases glucagon. Glucagon transforms glycogen into glucose. glucose can only be used by cells in the CNS.

230
Q

Long term reservoir of energy - When you eat food

A

Fat is stored in adipose tissues in the shape of triglycerides. Fatty acids are transformed into triglycerides by insulin.

231
Q

Long term reservoir of energy

A

Low blood glucose level. Pancreas releases glucagon –> glucagon breaks triglycerides into fatty acids –> fatty acids are used by the cells outside the CNS.
Livers breaks triglycerides into glycerol –> glycerol is transformed into glucose –> glucose is used by cells inside the CNS.

232
Q

Putting it all together - food in digestive system

A

High blood glucose = release of insulin by pancreas. Glucose is stored as glycogen in the livers by insulin. Fatty acids are stored in adipose tissue as triglycerides. Glucose is used as a source of energy by the brain + cells outside CNS.

233
Q

Putting it all together - Empty digestive system

A

Low blood glucose = release of glucagon by pancreas. Glycogen is transformed into glucose by glucagon and used as a source of energy by the brain. Triglycerides are broken down into glycerol and fatty acids. Glycerol are transformed into glucose which is used by the brain only. Fatty Acids are used as a source of energy for cells outside the CNS.

234
Q

Signals leading to hunger

A

Empty Duodenum –> Ghrelin –> Brain = Hunger

235
Q

Anticipatory satiety from gastric signals

A

CCK and PYY are anticipatory (happens after you eat, but before food is digested). Increasing CCK does not lead to weight loss –> will reduce meal length but people compensate by eating more often. GLP-1 agonist can lead to weight loss.

Duodenum Post-Eating –> CCK, GLP-1 –> Brain = Satiety, Stop the meal

236
Q

Satiety & gastric signals

A

High blood-glucose level: Pancreas release insulin. Insulin crosses the blood/brain barrier. Neurons in the hypothalamus detects it and inhibits hunger.
Pancrease –> insulin –> hypothalamus = inhibit hunger.
High levels of glucose and fatty acids: liver signals satiety through the 10th cranial nerve (vagus nerve).
Liver –> Vagus nerve = inhibit hunger

237
Q

Long term satiety

A

The body weight of most people and animals is regulated over a long-term basis. If an animal is force-fed, it will reduce its food intake once it is permitted to choose how much to eat to go back to a set point. This indicates the presence of a long-term satiety mechanism.
Adipocyte (Fat cell) –> produce leptin –> decrease hunger, increase sensitivity of hypothalamic neurons to short term satiety signals.

238
Q

Putting it all together - hunger/satiety signals

A
  1. Your duodenum is empty. The stomach releases Gherkin which makes you hungry and you start to eat.
  2. You eat food. The stomach calms down. The duodenum releases CCK and PYY. You stop your meal.
  3. The food is digested and the nutriments are absorbed by the blood. The pancreas releases insulin, which sends a satiety signal to the hypothalamus. The liver does the same through the vagus nerve.
  4. As you eat, you build up fat cells (adipocytes). Fat cells releases leptin, which signal to your brain that you have enough fat (no need to eat anymore).
239
Q

Leptin Deficiency

A

Cannot produce leptin –> body think its staring. Leads to obesity. Treated with leptin injection.

240
Q

Satiety Brain Mechanism

A

Leptin –> stimulates the POMC / Alpha-MSH neurons in the arcuate nucleus of the hypothalamus (inhibited by ghrelin) –> stimulate oxytocin neurons in the paraventricular nucleus of the hypothalamus (signals that body has enough fat) –> inhibits hunger

241
Q

Hunger brain mechanisms

A

Ghrelin –> stimulates ARGP/NPY Neurons in the arcuate nucleus of the hypothalamus (activate hunger, inhibited by leptin) –> inhibit oxytocin neurons in the paraventricular nucleus of the hypothalamus (low firing rate –> intense hunger, excess activity does not prevent hunger induced by other signals, it is mainly involved in signalling intense hunger due to low leptin levels) –> signals hunger

242
Q

Prader Willi Syndrome

A

Loss of PVN Oxytocin neurons due to deletion of genes on chromosomes 15 –> no sensation of satiety. Born without interest in eating, low muscle mass. Between 2-8 y ears old: permanent sensation of starving to death. Have no satiety signal to stop eating/throw up –> eat until they rupture their stomach. Average life expectancy = 30 years.

243
Q

Hypoglycaemia

A

Low glucose levels (lack of sugar, excess insulin, drugs that inhibit glucose metabolism): stop insulin secretion (prevent glucose from being stored) –> make the liver produce glucose –> slow down energy expenditure / health growth and reproduction related system = hunger. Override energy homeostatic mechanism –> will promote feeding even if you have high leptin/insulin level.

244
Q

Lipoprivation

A

Low fatty acids level (drugs that inhibit fatty acids metabolism, too little body fat): stop insulin secretion (prevent glucose form being stored) –> make liver produce glucose –> slow down energy expenditure/health growth and reproduction related system = hunger.

245
Q

Hyperglycaemia

A

Caused by problem in insulin signalling. Glucose is not taken from blood to fat cells/muscle. Lead to a loss of fat –> decrease in leptin signalling –> intense hunger (even if there is high glucose levels).

246
Q

Obesity

A

Elevated levels off fat. Leptin resistance: reduction in leptin’s ability to cross the blood/brain barrier. Reduction in neuronal response to leptin. Reduction in the downstream consequences of leptin-signalling neuron. Harder to feel satiated –> need more leptin (meaning more fat cells) to be satiated.

247
Q

Sex chromosomes

A

Female: XX
Male: XY

248
Q

Sex hormones

A

Androgen (responsible for the development of male characteristics and the regulation of reproductive functions in both males and females). & Anti-mullerian hormone (Plays distinct roles in both males and female reproductive development).

249
Q

Sex-organs

A

Gonads (sexual gland): Ovary (female) / Testes (male)
–> Gamete (sexual cell for reproduction, including 23 chromosome)
Internal reproductive organ (Mullein vs Wolffian system)
External anatomy

250
Q

Sexual Development in Women

A

Primordial gonads –> Ovaries (XX) –> Mullerian System, No Wollfian system, primordial external system.

251
Q

Sexual Development in Men

A

Primordial gonads –> Testes (SRY gene, XY) –> Anti-Mullerian Hormone (mullerian system withers away - defeminisation), Androgens (Wolffian System - masculinization), Androgens (Primordial External System - masculinization).

252
Q

Turner Syndrome & Swyer Syndrome

A

Chromosome: single X (Turner) or XY but dysfunctional Y (Swyer). Gonads: None (sterile). Hormone release: None. Internal Organs: Female. External Organs: Female.

253
Q

Insufficient Anti-Mullerian hormone

A

Chromosome: XY. Gonads: testes. Hormone release: Normal androgen, but anti-mullerian production X or receptors X. Internal Organs: Female & Male. External Organs: Male.

254
Q

Androgen insensitivity syndrome

A

Chromsome: XY. Gonads: testes. Hormone release: Normal anti-mullerian, but androgen production X or receptors Y. Internal Organs: None. External Organs: Feminized to masculinized depending on the degree of severity.

255
Q

Congenital Adrenal Hyperplasia (Androgen)

A

Chromosome: XX. Gonads: Ovaries. Hormone release: Too much androgen. Internal Organs: Female & Male depending on severity. External Organs: Masculinized features.

256
Q

Effect of hormone - organizational effect

A

Effects of sex hormones during the development of the body and brain permanently.
Androgen –> Brain: female typical behaviour X, Male-typical behaviour O.

257
Q

Effect of hormone - Activation effect

A

Effects of sex hormones after puberty (production of hormones, gamete). Response to activation effect depends on body & brain.

258
Q

Hormones - Hypothalamus

A

Kisspeptin –> Gonadotropin-releasing Hormone (GNRH).

259
Q

Hormones - Pituitary Gland

A

Follicle-stimulating hormone (FSH) & Luteinizing hormone (LH).

260
Q

Hormones - Gonad

A

Male: Androgen - Testosterone (Cycle X)
Female: Estrogen - Estradiol (Cycle O)

261
Q

Male sexual process

A

Testosterone X –> Sperm X –> sexual behaviour x (not always)

262
Q

Castrated Male rats

A

Castrated (= testes X) –> male behaviour X, female behaviour O.
Injection of estradiol –> female sexual behaviour (Iordosis)
Injection of testosterone –> male behaviour O

263
Q

Testes O

A

Inject of estradiol –> small effect.
Injection of male hormone –> minimal effect

264
Q

Menstrual Cycle

A

Primates & Human. Menstruation occurred –> shed endometrium. Mating season X - concealed. Sexual desire & behaviour less dependent on cycle.

265
Q

Estrous cycle

A

Most mammals. Menstruation X –> reabsorb endometrium. Mating season - displays signs. Typically sexual behaviour only in estrous phase –> sign alter male’s behaviour.

266
Q

Neural circuits male and female sexual behaviour

A

1) Olfactory bulb & Vomeronasal organ (Input)
2) Medial amygdala
3) ??? (difference between male & Female)
–> mPOA (Male) & VMH (Female)
4) PAG (Periaqueductal gray)
5) nPGI (nucleus Paragigantocellularis)
6) Mating behaviour

267
Q

mPOA (Medial Preoptic Area)

A

Plays essential role in male sexual behaviour. Sexual dimorphic nucleus (SDN) larger in male than female. Injection hormone & electric stimulation –> sexual behaviour in males. Lesion of mPOA doesn’t affect female’s sexual behaviour.

268
Q

VMH (Ventromedial Nucleus of Hypothalamus)

A

Plays essential role in female sexual behaviour. Lesion of VMH –> lordosis X. Injection of hormone & electric stimulation –> sexual behaviour in females.

269
Q

Pair Bonds

A

Oxytocin & Vasopressin: found in blood & brain, elevate during sex, childbirth. Artificial injection: reduce anxiety, form life-long pair bond in prairie voles.

270
Q

How to measure sleep

A

Brain activity –> Electroencephalogram (EEG)
Muscle movement –> Electromyogram (EMG)
Eye movement –> Electro-oculogram (EOG)

271
Q

EEG signals

A

Beta: 13-2-Hz, Arousal
Alpha: 8-13 Hz, Awake
Theta: 4-8 Hz, Drowsy, Early stage of sleep
Delta: <4 Hz, Deepest stage of sleep.
REM sleep also showed desynchronized EEG activity like awake state. During the REM sleep, muscle paralysis occurred.

272
Q

Sleep for survival

A

If sleep is deprived –> Die (metabolism cycle broke).
- feel tired
- cognitive level decreased
- learning ability to decrease & impulsive behaviour increase
- symptom of death: seizure, hallucination, weight loss

273
Q

Species & developmental difference in sleep

A

Sleep pattern depends on species: predators usually show long sleep pattern, prey show short sleep pattern (severe when they have big weight).
Sleep pattern depends on development: baby sleep longer than adults.

274
Q

Why is sleep needed?

A
  1. Recover from mental or physical exertion: but people exercise a lot didn’t sleep more than normal. Heart rate went down but there is no caloric difference between sitting and sleep.
  2. Learning & Memory: Update synaptic connection –> synaptic modification occurred. Amount of slow-wave & REM increase –> memory increase.
  3. Waste removal: remove waste by metabolism during sleep. It cannot be done efficiently in arousal state.
  4. Cerebrospinal fluid (CSF): Circulate brain & remove the waste (e.g., protein) in interstitial space. Glympathic system.
  5. Big animal: total sleep time goes down, large interstitial space & powerful CSF system. Length of each session goes up, remove big-size waste in big brain.
275
Q

Circadian Rhythms

A

Daily change in behaviour and physiological process, following a cycle of approximately 24 hours. Controlled by internal biological “clock” in the suprachiasmatic nucleus (SCN) of the hypothalamus. Light information from retinal helps keep the clock timed to 24 hours - invert light cycle in rats shows inverted pattern of sleep. SCN removal: total amount of sleep X, sleep cycle change.

276
Q

Advanced sleep phase syndrome

A

Mutations PER2. Sleep 4 hours earlier.

277
Q

Delayed sleep phase syndrome

A

Mutations PER3. Sleep four hours later.

278
Q

Sleep molecule - Adenosine

A

One of the molecules in the brain. Accumulate during wake, removed during sleep. Caffeine is related to adenosine.

279
Q

Sleep molecule - Others

A

Serotonin (raphe nuclei in the hindbrain).
Norepinephrine (locus coeruleus in the hindbrain).
Acetylcholine (throughout the brain).
Orexi & Histamine (hypothalamus).

280
Q

Sleep/Wake Flip-Flop Circuit

A

Neurons in the ventral lateral pre optic area (vIPOA) of the hypothalamus promote sleep. Electrical stimulation of this area causes drowsiness and sometimes immediate sleep. Lesions suppress sleep and cause insomnia. vIPOA neurons inhibit wake-promoting neurons. But this area receives inhibitory inputs from the same regions in inhibits. This kind of reciprocal inhibition characterizes a flip-flop circuit; both regions cannot be active at the same time and the switch from one state to another is fast. The animal is awake when the arousal, wake-promoting system is more active than the vIPOA neurons. The animal is asleep when vIPOA neurons are more active than the wake-promoting arousal system.

281
Q

The sleep molecule hypothesis (adenosine version)

A

There are adenosine receptors on many neurons throughout the brain. Extracellular adenosine builds-up during the day. Sleep-promoting vIPOA neurons are activated by adenosine signalling. Arousal-promoting acetylcholine (ACh) neurons are inhibited by adenosine signalling. The influence of adenosine signalling during the day can be masked by other regulators of sleep and arousal, such as SCN neiron activity. But at some point, when the clock of SCN neurons aligns with the build-up (or clearance) of sleep promoting molecules, the whole network flip-flops and the animal transitions into (or out of) sleep.

282
Q

Orexin

A

Also known as hypocretin. A peptide produced by neurons in the lateral hypothalamus (LH). Orexin neuron activity promotes wakefulness. Motivation to remain awake activates orexin neurons. Most forms of narcolepsy are associated with the absence of orexin neurons.

283
Q

Insomnia

A

Difficulty falling asleep after going to bed or night. When symptom becomes severe: Fatal familial insomnia & sporadic Fata insomnia. Neurodegeneration around thalamus, hypothalamus and brain stem.

284
Q

Narcolepsy

A

Excessive daytime sleepiness. Neurodegeneration of orexin neuron.

285
Q

Non-REM related Parasomnias

A

Sleep disorder occur during non-REM sleep. Brain caught in between sleeping and waking –> behaviour like arousal state: walking, talking, usually found in children / short duration. Sleep terror: overwhelming feeling of terror upon waking, panic & scream, even harm themselves, usually found in PTSD.

286
Q

REM sleep behaviour disorder

A

Sleep disorder occur during non-REM sleep. Their muscles do not become paralyzed during REM - imitate the behaviour of their dreams. Often found in patients with neurodegenerative disorders.

287
Q

Non-Associative Learning - Sensitization

A

Strong stimulus result in weighted response to other stimuli. Painful intense electrical shock increase the response of Aplysia.

288
Q

Non-Associative Learning - Habituation

A

Repeated stimulus evokes reduced response to repeated stimulus. Repeated light touch decreases the response of Aplysia. Smaller response in motor neuron since presynaptic neuron release less NT.

289
Q

Synaptic Plasticity

A

Refers to changes in the strength between two neurons. how big or small is the response in a postsynaptic neuron when a presynaptic neuron has an action potential (regardless of whether the response is depolarization or hyper polarization)? If the postsynaptic response is depolarization, it is an EPSP (excitatory postsynaptic potential).

290
Q

How LTP Occurs

A
  1. Presynaptic side releases glutamate
  2. Glutamate binds to the NMDA receptor. If the post synaptic cell is depolarized, then NMDA receptor lets Ca2+ flow in the cell.
  3. Ca2+ activates CAMKII (enzyme)
  4. CAMKII leads to an increase in AMPA receptors on the post-synaptic side. AMPA: inotropic excitatory glutamate receptor # of AMPA increase –> increased response.
291
Q

Associate Learning (Associate long-term potentiation)

A

Classical Conditioning: Play a tone every time you blow the air puff into the eye of rat. Later the rat will associate tone and air puff. then it will close its eyes without an air puff when the tone plays.

292
Q

Hebb’s Rule: Fire together, wire together

A

When neuron 1 is activated by air puff, it depolarizes post synaptic cell. When neuron 2 is activated by tone at the same time –> post synaptic cell was already depolarized –> LTP occurred –> Synapse will be strengthened.

293
Q

Types of Memory

A

Sensory memory: Initial sensation of environmental stimuli.
Short term: Limited to a few items (seconds to minutes). Tips for longer time: rehearsal and chunking.
Long term: Relatively permanent, consolidated STM to LTM.
- Nondeclarative memory/Unconscious Memory (implicit, procedural): Do not require conscious retrieval - operate automatically, motor learning, perceptual learning, classical conditioning.
- Declarative memory/Consciously accessible memory (explicit, declarative): Memory of event and facts, episodic: recollection of specific episode, include time, space context, semantic: facts, general information without context.

294
Q

Perceptual Learning

A

Pattern recognition system: enable to recognize & identify objects. People can recognize changes in familiar stimuli. Neocortex. Implicit memory.

295
Q

Motor Learning

A

Learning to make a sequence of movement. Get feedback from joints, eyes, ears, etc –> improve & optimize. Cerebellum, thalamus, basal ganglia, & motor cortex. Implicit memory.

296
Q

Relational Learning

A

How distinct perceptual objects relate to each other - describe the scene. Stimulus-stimulus learning (relationships among stimuli). Hippocampus: short-term to long-term memories, dysfunctional hippocampus –> cannot get new declarative memory. Declarative memory (semantic & episodic) –> explicit.

297
Q

Stimulus-Response Learning

A

Learning to perform particular behaviour when particular stimulus is present - establish a connection between perceptual and motor circuit. Operate conditioning: form of learning in which a reinforcing or punishing outcome follows a specific behaviour in a specific situation.

298
Q

Classical Conditioning (Pavlovian Learning)

A

Association between two stimuli (unconditioned and conditioned).
1) Unconditioned stimulus evokes reflexive behaviour - unconditioned response
2) When CS and US presents at the same time repeatedly
3) When CS evokes UR without US, then we call it classical conditioning –> we call response by CS only as CR

299
Q

Operant Conditioning (Instrumental Conditioning)

A

Learning from the consequence of actions: reinforcement (increase behaviour), punishment (decrease behaviour), positive (get something), negative (remove something).
Steps: Exploratory behaviour (don’t know the consequence - animals decision), result from the exploratory behaviour, change the likelihood of action.

300
Q

Neural circuit of instrumental coding

A

Direct transcortical connections: cerebral cortex to other area, behaviour with consciousness. Basal ganglia (collection of nuclei in forebrain): behaviour becomes habitual response (without conscious, automatic) based on the result & repeated behaviour. Striatum: synapse strengthens based on dopamine, dopamine indicates the animal’s motivation or value of result.

301
Q

Amnesia

A

Memory deficit caused by brain damage or disease. Anterograde amnesia: inability to form new information after disease, but have intact memory from before (Korsakoff’s syndrome & Confabulation).
Retrograde Amnesia: Inability to remember events that occurred before the disease.

PSYC 211 (4 decks)

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