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Intro to Behavioural Neuroscience McGill (PSYC 211 - 2023 Fall) > Midterm #2 > Flashcards

Midterm #2 Flashcards

1
Q

What is the difference between sensation and perception?

A

Sensation
How cells of the Nervous System detect stimuli in the environment (light, sound, heat…) and how they transduce these signals into a change in the membrane potential and neurotransmitter release.

Perception
Refers to the conscious experience and interpretation of sensory information

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2
Q

What are Sensory neurons?

A

Also known as Sensory Receptors

Specialized neurons that detect a specific category of physical events. They express receptor proteins that are sensitive to a specific feature of the external environment, such as

  • Presence of specific molecules (via chemical interactions) (smell, taste, nausea, pain)
  • Physical pressure (touch, stretch, vibration, acceleration, gravity, balance, hearing, thirst, pain)
  • Temperature (heat, cold, pain)
  • pH (acidity, basicity) (sour taste, suffocation, pain)
  • Electromagnetic radiation (light) (Vision)

Some non-human animals have other senses, such as the ability to detect electrical and magnetic fields, humidity, and water pressure

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3
Q

What is Sensory transduction ?

A

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

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4
Q

WHat is receptor potential?

A

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

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5
Q

What is a sensory neuron?

A

Specialized neuron that detects a particular category of physical events (sensory stimuli).

E.g., photoreceptor (cells) transduce light into receptor potentials

**Not all sensory neurons have axons or action potentials, but they all release neurotransmitter.
- The sensory neurons that do not have action potentials release neurotransmitter in a GRADED fashion, dependent on their membrane potential.
- The more depolarized they are, the more neurotransmitter they release

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6
Q

What is Neural Transduction of Light?

A

Receptor proteins that are sensitive to light

Use four different types of OPSIN PROTEINS to detect light

EACH photoreceptor cell in our eye contains only ONE kind of opsin protein, so we have FOUR DIFFERENT types of photoreceptor cells

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7
Q

What are the four opsin proteins?

A

Rhodopsin opsin (Rod cells express rhodopsin protein)

Red cone opsin (Rod cells express rhodopsin protein)

Green cone opsin (Green cone cells express the green cone opsin)

Blue cone opsins (Blue cone cells express the blue cone opsin)

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8
Q

What are Photoreceptors ?

A

Sensory neuron responsible for vision

Transduce the electromagnetic energy of visible light into receptor potentials

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9
Q

What is an opsin?

A

Light-sensitive protein

Opsin in our eyes gain sensitivity to light by binding a molecule of retinal

Opsins in our photoreceptor cells are all inhibitory metabotropic receptors

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10
Q

What is a retinal?

A

Small molecule

Synthesized from vitamin A

Attaches to opsin protein in our eye

Retinal molecule absorbs the electromagnetic energy of visible light in our eyes

Wavelength of light IT can detect DEPENDS on opsin protein it is attached to

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11
Q

What is visible light?

A

Electromagnetic energy

Wavelength between 380nm and 760 nm

Detect this light using our four photoreceptor cells – 1 rod and 3 cone cells

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12
Q

What do gamma rays do?

A

Can cause cancer and damage if they pass through you

Because it knocks out an electron – stability with it

Damages DNA

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13
Q

What do Ultraviolet waves do?

A

Burns your skin

Slightly ionizing – can cause cancer over time

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14
Q

Describe the red cone opsin.

A

First protein to evolve

Sensitive to light – holding a retinol molecule in the middle of it

“Sweet spot” - very likely to activate around 575nm

Can, but less effective at absorbing light at 500nm and 700nm

Most sensitive to LONG wavelengths

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15
Q

Describe the Blue cone opsin.

A

Second protein to evolve – evolved independently

Most sensitive at 430nm (380nm-540nm)

Having two different light sensitive proteins give rise to color vision

Can distinguish between red and blue

LEAST sensitive to light protein in our eye

Most sensitive to SHORT wavelengths

MUTATION TO THE BLUE CONE OPSIN

Leads to being hard to discriminate colors but DOES NOT affect light sensitivity

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16
Q

Describe the green cone opsin.

A

Most sensitive at 535nm

MOST sensitive to light of all proteins

Most sensitive to MEDIUM wavelengths

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17
Q

What happens (i.e) if red and green light bulbs are too close to one another?

A

When the RED and GREEN light bulbs are TOO CLOSE together, our eyes have a hard time differentiating them making it look like the color YELLOW

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18
Q

What is Brightness?

A

Intensity (luminance, amount)

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19
Q

What is hue?

A

Dominant wavelength (color)

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20
Q

What is Saturation?

A

purity (in terms of composite wavelengths)

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21
Q

What happens if BRIGHTNESS is 0%?

A

Your image will be all BLACK

Hue and saturation have NO IMPACT if there is no brightness

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22
Q

What happens if SATURATION is 0%

A

You are in the middle of the color cone where there is NO COLOR (equal contribution from all wavelengths)

Black and white image

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23
Q

What is Protanopia?

A

Absence of the red cone opsin (1% of males)

People with this inherited condition have trouble DISTINGUISHING colors in the GREEN-YELLOW-RED section of the spectrum

Simple mutations in of the RED cone opsin (1% of males) produce less pronounced deficits in color vision.

Mutations in the RED cone opsin HINDER color vision if they make the red cone opsin act more like the green cone opsin (in terms of what light it can detect).

Red and green opsins come from the “X” chromosomes which is the reason why males are more likely to be colorblind than women

Visual acuity is NORMAL because red cone cells get filled with green cone opsin.

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24
Q

What is Deuteranopia?

A

Absence of the green cone opsin (1% of males)

Visual acuity is normal because green cone cells get filled with red cone opsin

People with this inherited condition have trouble DISTINGUISHING colors in the GREEN-YELLOW-RED section of the spectrum

Simple mutations in of the GREEN cone opsin (6% of males) produce less pronounced deficits in color vision.

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25
Q

What is Tritanopia?

A

Absence of the BLUE cone opsin (1% of the population)

Blue cone cells do not compensate for this in any way, but the blue cone opsin is not that sensitive to light anyway, so VISUAL ACUITY IS NOT NOTICEABLY AFFECTED

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26
Q

What is the Cornea?

A
  • Outer, front layer of the eye
  • Focuses incoming light a fixed amount
  • Lens that focuses the light
  • Can become too thick or too thin – slowly changes over time (Can correct this with glasses)
    Lazer eye surgery can go in and shave a part of the cornea
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27
Q

What is the Conjunctiva?

A

Mucous membrane that lines the eyelid

Outside of eye – fuses with the eyelids

This is the reason that things cannot get behind your eyes – can go up and down but not behind

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28
Q

What is the Iris?

A

Ring of muscle
Contraction and relaxation of this muscle determines the size of the pupil (hole)
Exposes a little hole for the light to get through

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29
Q

What happens to the iris if a room is “dim lit”?

A

Hole contracts and makes hole big so more light can get through

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30
Q

What happens to the iris if a room is “VERY lit”?

A

Bright so the hole becomes smaller so less light gets through

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31
Q

What is the role of the pupil?

A

Determines how much light enters the eye

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32
Q

What is the lens?

A

Several transparent layers

Shape of the lens can change to allow the eye to focus (accomodation)

Adjust in real time to focus on things close or far away

Light passed through the lens and crosses the vitreous humor, a clear, gelatinous fluid.

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33
Q

What is the sclera?

A

Opaque and does not permit the entry of light

Not transparent to light

Light cannot come in from the side only the front

The tough, outer white of the eye

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34
Q

What is the Retina?

A

Interior linning (furthest back part) of the eye

Contains photoreceptor cells (rods and cone cells)

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35
Q

What is the fovea?

A

Central region of the retina

Very little ocmpression of visual information in the fovea

Where the highest visual acuity is

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36
Q

What is the Optic disk?

A

AKA BLIND SPOT
Where optic nerve exits through the back of the eye

Axons leave the eye forming the optic nerve

No photoreceptors – BLIND SPOT

Our eyes are constantly moving so we do not notice our blind spots – we “fill in the blank”

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37
Q

Describe the pathway of light in the retina.

A

Light enters in the ganglion cell layer

From the gagnlion cell layer, it goes through the Bipolar cell layer

To then get to the photoreceptor layer

Which ends up at the back of the eye

Where there are opsin proteins sensing light

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38
Q

How can photoreceptors in the fovea register the exact location of the light, enabling high resolution, color vision?

A

The fovea primarily contains cone cells, each of which connects to a single bipolar cell, which in turn connect to a single ganglion cell.

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39
Q

What occurs in the periphery?

A

In the periphery, many rod cells (containing rhodopsin) converge onto fewer and fewer downstream collections of neurons (bipolar and ganglion cells). With this compression of information, there is little information about the exact location and shape of the light in peripheral vision, but we can easily detect dim light, moving lights, and general shapes.

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40
Q

What does foveal being sensitive to detail and colour mean?

A

High resolution color vision

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41
Q

What does peripheral vision is sensitive to dim light mean?

A

Low resolution grayscale vision

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42
Q

Where and what do cone photoreceptors do?

A

Most prevalent in the central retina

Found in the fovea

Sensitive to moderate-to-high levels of light

Provide information about hue

Provide excellent acuity

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43
Q

Where and what do rod photoreceptors do?

A

Most prevalent in the peripheral retina

Not found in the fovea

Sensitive to low levels of light

Provide only monochromatic information

Provide POOR acuity

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44
Q

Why do people have poor visual acuity in their peripheral vision?

A

Images deficient in high frequency information look unfocused but we can still make out the form

People have poor visual acuity in their peripheral vision where most of light perception is mediated by rod cells

The high visual acuity needed for reading is only possible in the fovea, which is primarily where the cone cells are located

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45
Q

What are the eyes?

A

Eyes are suspended in the orbits

Bony sockets in the front of the skull

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46
Q

What are different movements of the eye?

A

SACCADIC movements
PURSUIT movements

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47
Q

What are Photoreceptor cells?

A

Neurons responsible for the transduction of light

They project to bipolar cells

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48
Q

What are bipolar cells?

A

Neurons that relay information from the photoreceptor cells to ganglion cells

Like photoreceptor cells, bipolar cells also do not have action potentials and release glutamate in a graded fashion dependent on their membrane potential.

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49
Q

What are ganglion cells?

A

The only neurons in the retina that sends axons out of the eye.

They receive information from bipolar cells and project to the rest of the brain

Their axons give rise to the optic nerve, which leaves the retina through the optic disc (i.e., the blind spot of the retina).

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50
Q

What are horizontal cells?

A

Neurons that interconnect and regulate the excitability of adjacent photoreceptor and bipolar cells.

They adjust the sensitivity of these neurons to light in general.

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51
Q

What are Amacrine cells?

A

Neurons that interconnect and regulate the excitability of adjacent bipolar and ganglion cells

There are many different types of amacrine cells, and each have different functions.

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52
Q

Explain the ON/OFF bipolar cells.

A

OFF bipolar cells express ionotropic glutamate receptors, so they are depolarized by glutamate. Because photoreceptor cells release glutamate in the dark, OFF bipolar cells are more active (more depolarized) in the dark than in the light.

ON bipolar cells (depicted to the right) only have inhibitory metabotropic glutamate receptors, so they are uncommonly inhibited by glutamate. Thus, ON bipolar cells are more active (more depolarized) in the light vs the dark.

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53
Q

What are Retinal ganglion cells (RGCs)?

A

Typical neurons. They have action potentials and are generally excited by glutamate.

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54
Q

What are receptive fields - receptive fields of neurons?

A

Involved in visual processing is defined as the area of visual space where the presence of light influences the activity of the neuron (i.e., the part of space in which light must fall to get a response from the neuron).

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55
Q

How do you identify the receptive field of a neuron?

A

We record from the neuron as the animal maintains focus on a central fixation point.

We then shine light in different areas of visual space (e.g., near or far from the fixation point in any direction, usually on a computer screen) to see where the presence of light alters the spiking activity of the neuron.

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56
Q

What happens when the appropriate wavelength of light is in the receptive field of a photoreceptor cell?

A

The cell hyperpolarizes and releases less glutamate onto downstream bipolar cells.

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57
Q

What’s the difference between ON and OFF bipolar cells?

A

An ON bipolar cell, it depolarizes and releases more glutamate.

An OFF bipolar cell, it hyperpolarizes and releases less glutamate.

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58
Q

Why do ON and OFF bipolar cells have different responses?

A

The different responses of the ON and OFF bipolar cells to light in their receptive fields are due to their different glutamate receptors. ON bipolar cells express inhibitory glutamate receptors, whereas OFF bipolar cells express excitatory glutamate receptors.

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59
Q

What is the “center-surround” organization of bipolar cells?

Hint - ON/OFF excited/inhibited by what?

A

ON cells are excited by light in the Center and are inhibited by light in the Surround.

OFF cells are are inhibited by light in the Center and excited by light in the Surround.

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60
Q

What is the Pathwayfor visual information?

A

Visual information is relayed from retinal ganglion cells (RGCs) to the thalamus (lateral geniculate nucleus) to area V1 in the cerebral cortex (primary visual cortex). The receptive fields of V1 neurons in the cerebral cortex are the sum of many RGCs.

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61
Q

What are simple cells (in primary visual cortex)?

A

Sensitive to lines of light, and their receptive fields are typically organized in a center-surround fashion.

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62
Q

What can we call the primary visual cortex?

A

Area V1 or striate cortex

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63
Q

What is the order of layers of receptive fields for visual processing?

A

1- Photoreceptors
2- bipolar cells
3- retinal ganglion cells
4- thalamus
5- primary visual cortex
6- visual association cortex

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64
Q

Why are neurons in V1 special?

A

Neurons in V1 have larger receptive fields than the retinal ganglion cells.

They are most activated when a line of light in a particular orientation is detected in the receptive field.

A line of light is positioned in the cell’s receptive field at different orientations. The cell responds bests when the line is in a particular orientation (vertical in this case).

Some neurons respond best to vertical lines, some to horizontal lines, and some to lines oriented somewhere in between.

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65
Q

What does the visual association cortex include/form?

A

All of the occipital lobe surrounding primary visual cortex

Extends into the parietal and temporal lobes, forming respectively the dorsal and ventral streams of visual information processing.

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66
Q

25% of the cerebral cortex is dedicated to doing what?

A

Processing visual information.

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67
Q

What is the WHAT pathway?

A

The ventral stream starts in primary visual cortex and ends in inferior temporal cortex.

It is involved in identifying form (shape).

It encodes what the object is and its color.

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68
Q

What is the WHERE pathway?

A

The dorsal stream of visual information: starts in primary visual cortex and ends in posterior parietal cortex.

It is involved in identifying spatial location.

It encodes where objects are, if they are moving, and how you should move to interact with them or avoid them.

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69
Q

WHAT IS Monocular vision ?

A

Some V1 neurons respond to visual input from just one eye.

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70
Q

What is Binocular vision ?

A

Most V1 neurons respond to visual input from both eyes.

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71
Q

What is depth perception?

A

There are many monocular cues that can be used to estimate depth, such as relative size, amount of detail, relative movement as we move our eyes, etc.

These are the cues we use to appreciate depth when looking at a 2-dimensional image (e.g., on a photograph or TV screen).

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72
Q

What is stereopsis?

A

The perception of depth that emerges from the fusion of two slightly different projections of an image on the two retinas.

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73
Q

What is disparity?

A

The difference between the images from the two eyes.

It results from the horizontal separation of the two eyes.

It improves the precision of depth perception, which is particularly helpful when trying to quickly plan movements to interact with objects moving in space.

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74
Q

What is Agnosia?

A

Visual agnosia relates to damage located downstream of primary visual cortex (in visual association cortex, or the dorsal visual stream in the parietal cortex, or the ventral visual stream in the temporal cortex).

It is a deficit (problem) in the ability to recognize or comprehend certain sensory information, like specific features of objects, people, sounds, shapes, or smells, although the specific sense is not defective nor is there any significant memory loss.

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75
Q

What is akinetopsia?

A

A type of visual agnosia caused by damage in an area of the dorsal visual stream (in the parietal lobe of the cerebral cortex)

It is a deficit in the ability to perceive movement

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76
Q

What is Cerebral achromatopsia ?

A

Cerebral achromatopsia is a visual agnosia caused by damage to the ventral visual stream.

People with cerebral achromatopsia deny having any perception of color.

They say everything looks dull or drab, and that it is all just “shades of grey”. (People with regular achromatopsia don’t say those things, because they have no conception of color.)

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77
Q

What is achromatopsia?

A

Complete color blindness due to defective cone opsin signaling

Bilateral inherited retinal degeneration affecting all three types of cone photoreceptor cells that results in reduced visual acuity and loss of colour discrimination

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78
Q

What is Prosopagnosia?

A

Failure to recognize particular people by sight of their faces; caused by damage to the fusiform gyrus (fusiform face area)

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79
Q

Which are the only axons that can leave the eye?

A

Only the axons of retinal ganglion cells leave the eye.

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80
Q

The retinal ganglion cells go to the thalamus when they first leave the eye, what occurs here?

A

specifically the lateral geniculate nucleus

which in turn projects to the primary visual cortex in the occipital lobe

Visual information is processed in this pathway to determine WHAT you are looking at.

This pathway creates an internal (mental) representation of your entire visual space (the objects in it, their position, and their attentional value)

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81
Q

What happens when the retinal ganglion cells leave the thalamus and go to the Midbrain?

A

Visual information is used here to control fast visually-guided movements. The midbrain DOESN’T really know WHAT you are looking at, but it knows WHERE light is moving in visual space.

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82
Q

Finally, what happens in the Hypothalamus when the retinal ganglion cells “show up”?

A

Visual information is used here to control circadian rhythms (such as sleep-wake cycles).

The hypothalamus DOESN’T know WHAT you are looking at, but it knows HOW MUCH light is present in your environment.

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83
Q

What is the Somatosensory system?

A

Provides information about touch, pressure, temperature, and pain, both on the surface of the skin and inside the body.

There are three interacting somatosensory systems

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84
Q

What are the three interacting somatosensory systems?

A

Exteroceptive System, Interoceptive System, Proprioceptive System

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85
Q

What is the Exteroceptive system?

A

Cutaneous/skin senses

Responds to external stimuli applied to the skin (e.g., touch and temperature)

Ex. of external stimuli
- Pressure (Touch) Caused by the mechanical deformation of the skin
- Vibrations Occur when we move our fingers through a rough surface
- Temperature Produced by objects that heat or cool the skin
- Pain Can be cause by many different types of stimuli, but primarily tissue damage

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86
Q

What is the Interoceptive system?

A

Organic senses

Provides information about conditions within the body and is responsible for efficient regulation of its internal milieu (e.g., heart rate, breathing, hunger, bladder)

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87
Q

What is the Proprioceptive system?

A

Kinesthesia

System monitors information about the position of the body, posture, and movement (e.g., the tension of the muscles inside the body)

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88
Q

What is the epidermis?

A

The outer most layer of the skin (“above dermis”)

Cells here get the oxygen from the air (not blood)

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89
Q

What is the hypodermis?

A

Deepest layer

Subcutaneous “below the skin”

Sensory neurons are scattered throughout these layers

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90
Q

What is between the epidermis and the hypodermis?

A

The Dermis

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91
Q

What is glaborous skin?

A

“Hairless” skin

Ex. Palms of hands and feet

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92
Q

What is Merkel’s disk?

A

Respond to local skin indentations (simple touch)

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93
Q

What are free nerve endings?

A

Primarily respond to temperature and pain

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94
Q

What are Ruffini’s corpuscles?

A

Sensitive to stretch and the kinesthetic sense of finger position and movement

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95
Q

What are Pacinian corpuscles?

A

Respond to skin vibrations

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96
Q

What are the two categories of thermal receptors?

A

Respond to warmth

Respond to coolness

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97
Q

Can the receptor proteins that are sensitive to temperature only be activated by temperature?

A

Some of the receptor proteins that are sensitive to temperature can also be activated by certain ligands

Ex. Capsaicin molecules activate heat receptors and menthol molecules activate cold receptors

Activated by molecules – ex. Eating spicy peppers

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98
Q

What are free nerve endings?

A

Sensations of pain and temperature are transduced by free nerve endings in the skin

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99
Q

What are nociceptors?

A

There are several types of pain receptor cells – “detectors of noxious stimuli”

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100
Q

What is a high-threshold mechanoreceptors?

A

Type of nociceptors
Pressure receptor cells
Free-nerve endings that respond to intense pressure, like striking, stretching or pinching

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101
Q

Axons from skin, muscles, and internal organs enter the CNS via spinal nerves. What are the are 2 main pathways?

A

The spinothalamic tract
The dorsal column

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102
Q

What is the spinothalamic tract pathway?

A

Poorly localized information (e.g., crude touch, temperature, and pain) crosses over the midline in the spinal cord, just after the first synaptic connection.

This information ascends to the thalamus through the spinothalamic tract

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103
Q

What is the dorsal column pathway?

A

Highly localized information (e.g., fine touch) ascends ipsilaterally through the dorsal column of the spinal cord.

The first synapse in this pathway is in the medulla.

From there the information crosses over to the contralateral side as it ascends to the thalamus.

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104
Q

What is The Somatosensory Homunculus?

A

The somatotopic map is often referred to as the somatosensory homunculus (“little man”)

If there is DAMAGE to any part of the somatosensory homunculus, the specific part that control is disabled

No more sensation there
Mostly on hairless spots

When different sites of primary somatosensory cortex are electrically stimulated, patients report somatosensory sensations in specific parts of their bodies.

The relationship between cortical stimulations and body sensations is reflected in a somatotopic map of the body surface

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105
Q

What is tactile agnosia?

A

Patients with this condition have trouble identifying objects by touch alone

When touching an object, people might think this is that:
pine cone -> brush
ribbon -> rubber band
snail shell -> bottle cap

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106
Q

If patients with tactile agnosia are touching something, how can they accurately represent what they are touching?

A

These patients can often draw objects that they are touching, without looking, and they can sometimes identify objects from their drawings.

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107
Q

What is the phantom limb?

A

A form of pain sensation that occurs after a limb has been amputated
Amputees report that the missing limb still exists and that it often hurts.
One idea is that phantom limb sensation is due to confusion in the somatosensory cortices (primary and association).
The brain gets nonsense signals (in part from the cut axons) and it has difficulty interpreting them.

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108
Q

What are treatments for the phantom limb?

A

Most treatments have proven to be not very effective

Pharmacological, electrical nor behavioral

The “mirror box” has received lots of attention (cheap and easy) but effective

Unclear how effective this is

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109
Q

What are the six different categories of taste receptors that have been identified ?

A

Sweetness
Umami
Bitterness
Saltiness
Sourness
Fat

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110
Q

What do Taste buds do?

A

Contain 20-50 taste receptor cells
Each taste bud is dedicated to processing one type of taste
Meaning that every cell within a taste bud expresses the same taste receptor protein

Taste receptor cells do not have traditional action potentials

They release neurotransmitter in a graded fashion

Taste receptor cells are replaced about every ten days because they are directly exposed to a rather hostile environment

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111
Q

what do primary Gustatory Cortex is in the Insula lobe of the cerebral cortex do?

A

Drives other behaviors

Put sweet taste “ON” as they enter a room, they will want to keep coming in the room

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112
Q

How many different types of odorant receptors are there for humans?

A

Humans express ~400 different types of odorant receptors.
Each one is sensitive to a specific molecule.
Most of odorants are lipid soluble and organic origin
Many substances that meet these criteria have no odor

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113
Q

What is Olfactory epithelium?

A

The tissue of the nasal sinus that sits underneath the skull (the cribriform plate)

Contains olfactory receptors cells.

Each olfactory cell expresses only one type of olfactory receptor protein.

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114
Q

What is Olfactory receptor cells synapse?

A

In glomeruli in the olfactory bulb

In turn sends axons into the brain.

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115
Q

Are odors meant to be good/bad?

A

Odors are largely not hard wired to be innately good or bad.
Unlike tastes

Whether we like or dislike an odor is related to learned associations.

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116
Q

Olfactory information does not relay in the thalamus. Where does it go?

A

It goes directly to primary olfactory cortex in the temporal lobe and the amygdala’

117
Q

What are pheromones?

A

Molecules released by one animal to signal something to another member of the same species.

Behavioral responses to pheromones are largely innate (hard-wired from birth)

118
Q

How are Pheromones used in animals and insects?

A

attract or repel other members of the same species

signal attractiveness and sexual receptivity

mark a path to follow (as seen in ants)

signal danger

119
Q

Where do the initial transduction and processing of pheromones occur in mammals?

A

In mammals, the initial transduction and processing of pheromones occurs in the vomeronasal organ and ‘accessory olfactory bulb’, which are next to but distinct from the regular olfactory epithelium and ‘main olfactory bulb’, which process regular odors.

120
Q

How are pheromones detected?

A

Pheromones are detected by metabotropic vomeronasal receptors

These receptors are only distantly related to the olfactory receptors that detect normal odors, highlighting their different role.

121
Q

What is the Lee-Boot Effect?

A

When female mice are housed together (without any male urine present), their estrous cycles slow down and eventually stop.

122
Q

What is the estrous cycle that occur in animals?

A

Public display unlike a menstrual cycle

Changes behavior and pheromones (changes in male behavior as well)

123
Q

What is the whitten effect?

A

Pheromones in the urine of male mice can trigger synchronous estrus cycles in groups of female mice.

124
Q

What is the Vandenbergh Effect?

A

Earlier onset of puberty seen in female animals that are housed with males

125
Q

What is the Bruce effect?

A

The tendency for female rodents to terminate their pregnancies following exposure to the scent of an unfamiliar male

126
Q

What are saccadic movements of the eye?

A

Rapid, jerky shifts in your gaze from one point to another

Our eyes scan a scene by making saccadic movements

127
Q

What are pursuit movements of the eye?

A

allow us to maintain an image of a moving object

128
Q

What is the difference in the activation of the brain when interpreting emotions from speech depending on whether the subject considers either only the tone or only the literal meaning of words?

A

Tonal analysis is linked with an activation of the right hemisphere, literal analysis is linked with an activation of the left hemisphere.

129
Q

What is loudness

A

Corresponds to the AMPLITUDE or INTENSITY of the molecular vibrations.

130
Q

What is Pitch (tone)

A

Corresponds to the FREQUENCY of the molecular VIBRATIONS.

It is measured in hertz (Hz) or cycles per second

131
Q

What is timbre

A

Corresponds to the COMPLEXITY of the sound.

We use timbre to help identify the SOURCE of the sound wave (through learning processes).

132
Q

What’s the Pinna and what does it do?

A

Sound is funneled through the pinna

The outer ear

133
Q

What is the tympanic membrane

A

Eardrum

Sounds coming down the ear canal cause the tympanic membrane to vibrate.

These vibrations are transferred to the middle ear

134
Q

What is the middle ear and what does it contain?

A

The middle ear is comprised of THREE OSSICLES (small bones)

Malleus
Incus
Stapes.

Vibrations of the ossicles are transferred to the membrane behind the oval window.
These vibrations are transmitted to the fluid-filled cochlea

135
Q

What is the cochlea and its divisions?

A

The inner ear

A long coiled tubelike structure that contains sensory neurons.

Divided into three longtudinal divisions

Scala vestibuli
Scala media
Scala tympani.

136
Q

Pathway of sound in the ear? Faster? Slower?

A

A particular region of the basilar membrane flexes back and forth in response to sound of a particular frequency

High pitched notes – depending on how fast you vibrate the membrane, the membrane bends

Faster – closer to stapes

Slower – deeper in stapes

137
Q

What is the basilar membrane

A

Encodes high notes on the end closest to the oval window (farther from the stapes)

138
Q

What is high frequency

A

When vibrations occur faster / closer to stapes

139
Q

What is low frequency

A

When vibrations occur slower / farther from stapes

140
Q

Cochlea is divided in three longitudinal divisions

A

Scala vestibuli
Scala media
Scala tympani

141
Q

What is the organ of corti

A

The receptive organ

It consists of the basilar membrane on the bottom, the tectorial membrane on the top, and auditory hair cells in the middle

142
Q

What are hair cells?

A

The cells that transduce sound are called hair cells because of their physical appearance.

143
Q

What is cilia

A

Hair-like extensions of hair cells are called cilia

144
Q

What are tip links

A

The cilia of hair cells are connected to each other by tip links

145
Q

Sound waves cause the basilar membrane to move where?

A

Sound waves cause the basilar membrane to move relative to the tectorial membrane
Causes the hair cell cilia to stretch and bend
Movement of the cilia pulls open ion channels which changes the membrane potential of hair cells

146
Q

What are outer hair cells

A

Have cilia that are physically attached to the rigid tectorial membrane.

The cilia of inner hair cells are not attached to anything

They sway back and forth with the movement of the solution

147
Q

What is an insertional plaque

A

The point of attachment of a tip link to a cilium

Each insertional plaque has a single ion channel in it that opens and closes according to the amount of stretch exerted by the tip link.

148
Q

Can loud noise break tip links? What happens to tip links if they break?

A

Loud noises can easily break the tip links that interconnect each cilia.

Hair cells cannot transmit auditory information without tip links.

Fortunately, tip links usually grow back within a few hours.

Tip link breakage generally corresponds to temporary hearing loss (such as after a loud bang or loud concert).

149
Q

Inner vs. Outer hair cells

A

People that do not have working inner hair cells are completely deaf.

People that do not have functional outer hair cells can hear, but not very well.

150
Q

Place Coding

A

Because of how the cochlea and basilar membrane are constructed, acoustic stimuli of different frequencies cause different amounts of movement along the basilar membrane. Higher frequency sounds cause bending of the basilar membrane closest to the stapes, resulting in more hair cell activity in that area

151
Q

Rate Coding

A

Very low frequency sounds are processed using a rate coding system: the rate of neurotransmitter release from the hair cells deepest in the cochlea (furthest from the stapes) determines the perception of low frequency sounds.

Rate coding is used to identify the pitch of low frequency sounds

152
Q

The organ of Corti sends auditory information to the brain via the cochlear nerve.

What is the correct Path of Auditory Information from the Cochlear Nerve?

A

Dorsal and ventral cochlear nerve in medulla
Superior olivary nerve in medulla
Inferior colliculi in midbrain
Medial genicular nucleus in thalamus
Primary auditory cortex in temporal lobe

153
Q

What is ionotopic Representation

A

Like the basilar membrane, the primary auditory cortex is organized according to frequency.
Different parts of the auditory cortex respond best to different frequencies.
This organization, where different frequencies of sound are analyzed in different places of auditory cortex

154
Q

What is amusia?

A

The inability to perceive or produce melodic music.

People with amusia might be unable to sing or recognize the happy birthday song but can often converse and understand speech and recognize environmental sounds.

They can even recognize the emotions conveyed in music, but they will typically be unable to tell the difference between: consonant music (pleasant sounding harmony) and dissonant music (unstable, transitional),

These sounds might alter their emotional state just as they do in other people.

155
Q

Primary auditory cortex

A

Core region: is in the upper section of the temporal lobe, mostly hidden in the lateral fissure.

The belt and parabelt regions refer to auditory association cortex.

Like visual information, auditory information is analyzed in “where” and “what” streams.

156
Q

What is the POSTERIOR (dorsal) auditory pathway involved in?

A

Sound localization

This pathway meets up with the “where” vision pathway in the parietal cortex.

157
Q

What is the anterior auditory pathway involved in?

A

Goes into the frontal lobe, where analysis of complex sounds occur (the “what” are you hearing pathway).

158
Q

Auditory Agnosia

A

Music and language are special, complex forms of auditory processing, and brain damage in auditory association cortex can cause very specific types of auditory agnosia

Other areas of auditory association cortex are involved in the perception of sound as pleasant (consonant) or unpleasant (dissonant), and certain combinations of musical notes can trigger emotions (happy or sad)

159
Q

Vestibular system includes

A

Vestibular sacs
Semicircular canals
Cupula

160
Q

What are the vestibular sacs

A

A set of two receptor organs in each inner ear (utricle & saccule) that detect changes in the tilt of head (gravity)

The utricle & saccule in the vestibular sac respond to the force of gravity and inform the brain about the head’s orientation.

161
Q

What is the Semicircular canals

A

Three ring-like, fluid-filled structures that detect changes in head rotation (angular acceleration)

162
Q

What is the Cupula

A

Gelatinous mass found in the ampulla of the semicircular canals; moves in response to the flow of fluid in canals

163
Q

electroencephalogram(EEG)

A

We measure brain activity by attaching electrodes to the scalp to record an electroencephalogram(EEG).

164
Q

Electromyogram(EMG)

A

We measure muscle activity by attaching electrodes to the chin to record an electromyogram(EMG)

165
Q

electro-oculogram(EOG)

A

Electrodes are also placed near the eyes to measure eye movements via an electro-oculogram(EOG)

166
Q

Beta activity

A

12–30 Hz; typical of an aroused state. It reflects desynchronous neural activity (high frequency, low amplitude oscillations)

167
Q

Alpha activity

A

8–12 Hz; typical of awake person in a state of relaxation

168
Q

Theta activity

A

4–8 Hz; appears intermittently when people are drowsy, and is prominent during early stages of sleep

169
Q

Delta activity

A

<4 Hz; occurs during deepest stages of slow-wave sleep; reflects synchronized low frequency, large amplitude brain activity

170
Q

Rapid eye movement (REM) sleep

A

Also called paradoxical sleep

Is associated with
Desynchronized EEG activity
Rapid eye movements
Dreaming
Muscle paralysis; muscles are totally inactive apart from occasional twitches.
Cerebral blood flow and oxygen consumption increase

171
Q

Correlation between size of animal and time needed for sleep

A

INVERSELY correlated

Larger animals sleep LESS
Their cells are bigger and they need less calories per cell

Smaller animals sleep MORE

172
Q

Main Theories on why animals sleep

A

To recover from physical or mental exertion
Brain Processing
Waste Removal

173
Q

Why is the theory of sleeping to recover from physical or mental exertion debunked?

A

If the function of sleep is to recover from physical or mental exertion, then the amount of time spent exercising and thinking should correlate with total sleep time.

BUT it does not correlate

174
Q

What is the theory of brain processing?

A

Sleep gives the brain an opportunity to reorganize data and archive memories, which perhaps cannot be done efficiently while awake

Learning and memory are clearly impacted by sleep.

175
Q

What is the theory of waste removal?

A

Since total sleep time correlates with body size (as well as brain size, metabolic rate, heart rate, and life span), maybe it is critical for a process that benefits from economies of scale, such as nutrient use or waste removal.

Seems to be some evidence supporting this

176
Q

What is the Glymphatic System?

A

The glymphatic system removes excess proteins and other waste from the interstitial space of the brain.

177
Q

What is the Cerebrospinal fluid (CSF)?

A

Cerebrospinal fluid (CSF) is a clear, colorless fluid that is continually being made in brain ventricles.

CSF circulates around the brain and diffuses into it, into the interstitial space, thus becoming the extracellular solution that surrounds neurons.

As CSF moves through the interstitial space, it clears waste products away before exiting into blood vessels.

178
Q

What is the Circadian Rythm

A

The daily change in behaviour and physiological processes that follows a cycle of approximately 24 hours

Controlled by internal biological clocks

Regular daily variation in light levels keeps the clock adjusted to 24 hours

Rats are normally active at night. If we shift the cycle by a couple hours, the rat’s activity cycle changes as well - the body adapts to this change

179
Q

What is the Suprachiasmatic nucleus (SCN)

A

In hypothalamus

Regulates sleep-cycles cycles.

It receives a direct input from the retina.

180
Q

Lesioning in the SCN

A

Dramatically alters circadian rhythms (such as sleep-wake cycles and hormone secretions).

Alter the length and timing of sleep-wake cycles

Do not change the total amount of time that animals spend asleep

Ex – will sleep the same AMOUNT but take many naps throughout 24 hours (don’t sleep all night like regular people)

181
Q

What is adenosine

A

Part of ATP

Adenosine levels rise in the brain during waking hours and accumulate even more with sleep deprivation.

Adenosine levels fall rapidly during sleep, even during brief intrusions of sleep.
Drowsiness, duration and depth of sleep are strongly modulated by adenosine receptor
Adenosine is likely one of many sleep-inducing molecules in the brain

182
Q

What is Caffeine to adenosine

A

Caffeine, which promotes arousal, is an adenosine receptor antagonist.

183
Q

What are Molecules that increase activity (arousal, alertness, and wakefulness) and decreased activity

A

Serotonin (raphe nuclei in the hindbrain)

Norepinephrine (locus coeruleus in the hindbrain)

Acetylcholine (throughout the brain)

Orexin (hypothalamus)
Orexin and histamine are neuropeptides that are released by neurons in the hypothalamus.

Histamine (hypothalamus)
Histamine receptor blockers (antihistamines) often cause drowsiness

184
Q

Where does the The Sleep/Wake Flip-Flop Circuit happen?

A

Ventral Lateral Proptic Area (vlOPA)
In hypothalamus

185
Q

Where is the Ventral Lateral Proptic Area (vlOPA)

A

In hypothalamus

Neurons here promote sleep.

Electrical stimulation of this area causes drowsiness and sometimes immediate sleep.

186
Q

Lesions of the vlOPA

A

Lesions suppress sleep and cause insomnia.

187
Q

What is 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.

188
Q

How is narcolepsy associated with orexin? Symptoms?

A

Is associated with the absence of orexin neurons

A rare sleep disorder characterized by periods of excessive daytime sleepiness and irresistible urges to sleep, often with the other symptoms described below.
Symptoms
Sleep paralysis
Cataplexy – when complete muscle paralysis suddenly occurs when someone is awake

189
Q

What is insomnia

A

Difficulty falling asleep after going to bed or after awakening during the night

190
Q

What is Fatal Familial Insomnia & Sporadic Fatal Insomnia?

A

A very rare disease that involves progressively worsening insomnia, which leads to hallucinations, delirium, confusional states, and eventually death

ProgressivreNeural degeneration in thalamus, hypothalamus, brain stem

191
Q

What are exapmles of disorders associated with Non-REM sleep

A

Sleepwalking, Sleep-talking, Sleep-groaning, Sleep-crying, Sleep- eating, Sleep-masturbating, Sleep-teeth grinding
Sleep Terrors
REM Sleep behavior disorder

192
Q

What is the result of Disorders Associated with Non-REM Sleep (Non-REM Sleep Parasomnias)

A

Occur during non-REM sleep or during transitions out of sleep.

The brain seems to get caught in between a sleeping and waking state.

Many people are unaware they exhibit this behaviour.

193
Q

What age group is more prevalent for Disorders Associated with Non-REM Sleep

A

Tend to be more prevalent in children (i.e., people can grow out of it).

Episodes can last seconds to minutes or longer.

These states can be caused by certain medications or medical conditions.

194
Q

What are sleep terrors

A

Characterized by overwhelming feelings of terror upon waking.
May include panic and screaming and bodily harm caused by rash actions.
People sometimes have no recollection of these events.
Prevalent in people diagnosed with post-traumatic stress disorder (PTSD).

195
Q

What is REM Sleep behavior disorder?

A

Neurological disorder in which the person does not become paralyzed during REM sleep and thus acts out dreams

It is often associated with more common neurodegenerative disorders such as Parkinson’s disease

196
Q

What is sexual dismorphium

A

Condition where the two sexes of the same species exhibit different characteristics beyond the differences in their sexual organs

Differences may be subtle or exaggerated and can include differences in size, weight, color, behavior and cognition.

Include secondary sex characteristics (i.e., features that occur during puberty)

197
Q

What are Sexual dimorphic behaviors?

A

Behaviors that take different forms, or occur with different probabilities, or under different circumstances across males and females of the same species.

Most striking category of sexual dimorphic behaviors are reproductive behaviors, including courting, mating, parenting, and most forms of aggression.

198
Q

Gametes

A

mature reproductive cells made by gonads (ovaries or testes). They are either ova (egg cells) or sperm

199
Q

What is the Müllerian System?

A

Female internal sex organs

200
Q

What is the Wolfian System

A

Male internal sex organs

201
Q

What is the SRY gene?

A

developpment of testes (Look at the picture)

202
Q

What is the Turner Syndrome?

A

When you only have one sex chromosome (X0).

203
Q

What is the swyer syndrome

A

When you are XY but have a bad SRY gene.

204
Q

What happens if there is Insufficient anti-Müllerian hormone signaling

A

Causes insufficient anatomical defeminization meaning both male and female internal sex organs will develop and get tangled together.

There is often functional external male genitalia.

205
Q

What is the result of the Androgen insensitivity syndrome

A

Results in anatomical defeminization with partial or no masculinization.

206
Q

What happens in severe Androgen insensitivity syndrome

A

In severe cases, no internal sex organs develop.

In these cases, people typically develop normal external female genitalia and identify as heterosexual women, but they will be infertile and have a short vagina.

207
Q

What happens in mild Androgen insensitivity syndrome

A

In mild cases, the external genitalia is fully masculinized.

208
Q

What happens in intermediate Androgen insensitivity syndrome

A

Intermediate cases are associated with ambiguous external genitalia.

209
Q

What are Gonadotropic hormones?

A

Hormones of pituitary gland (follicle-stimulating hormone, FSH, and luteinizing hormone, LH) that have stimulating effect on cells of gonads.

210
Q

Wjat occurs if Congenital adrenal hyperplasia (CAH) is PRESENT AT BIRTH

A

Human adrenal glands, which are present in men and women, typically secrete a small amount of androgens. However, some people’s adrenal glands secrete abnormally large amounts of androgens, which can start either before or after birth.

In males, excess androgen signaling from adrenal glands has minimal effect, since their testes already secrete tons of androgens. However, in females, excess androgen signaling can cause some degree of masculinization of either the body or brain or both.

Depending on the amount of androgen signaling during development, sex organs can become slightly masculinized (e.g., enlarged clitoris, partially fused labia). Brain anatomy and function can also be masculinized. Females with CAH have a higher likelihood of identifying as a man and being sexual attracted to women in comparison to other females.

The implications of this research are that sexual orientation and gender identity might be determined by the timing and effectiveness of androgen signaling in the brain during early development.

211
Q

Ventromedial nucleus of hypothalamus (VMH) is only in the female sexual behavior neural circuitry. What is it?

A

Large nucleus in the hypothalamus that plays essential role in female sexual behavior

Electrical stimulation of VMH facilitates female sexual behavior.

212
Q

Medial Preoptic Area (mPOA) is the male sexual behavior neural circuitry. What happens?

A

Nucleus in the anterior hypothalamus that plays essential role in male sexual behavior.

Electrical stimulation of mPOA in rodents elicits male copulatory behavior.

Within the mPOA, there is an area called the sexually dimorphic nucleus (SDN) of preoptic area. This nucleus is much larger in males than in females.

213
Q

what happens if we decide to lesion the mPOA of female rats

A

Lesioning the mPOA of female rats does not affect their sexual behavior, but it does cause them to ignore their offspring.

214
Q

what are undifferentiated gonads

A

embryonic precursors of ovaries and testes

215
Q

what is the defeminizing effect

A

Effect of anti-Müllerian hormone early in development,
which prevents development of the female-typical internal
anatomy

216
Q

what is the masculinizing effect

A

Effect of androgen hormones early in development, which
triggers development of male-typical anatomy

217
Q

What are androgens

A

male sex hormones

Testosterone is the principal mammalian androgen. It is released
by the testes, and it triggers development of the Wolffian system
(internal male sex anatomy).
Some testosterone is converted into dihydrotestosterone, which
is what triggers development of external male sex anatomy

218
Q

What are Organizational
Effects?

A

Sex hormones influence the development of the body
and brain. These effects are permanent and put you
on a particular trajectory going forward.

219
Q

WHat is Behavioral
defeminization

A

Refers to organizational effect of androgens on
the brain that prevent animals from displaying
female-typical behaviors in adulthood

220
Q

What is Behavioral
masculinization

A

Refers to organizational effect of androgens on
the brain that enables animals to engage in
male-typical behaviors in adulthood

221
Q

Activational
Effects

A

Puberty causes sex hormones to be released by the
gonads, which influence both body and mind. The
production of sperm, ovulation, and general horniness
are all examples of activational effects. How the mind
and body respond to activational hormone signaling in
adulthood depends on how the body and brain were
organized by hormone signaling in utero.

222
Q

What is Kisspeptin?

A

Neuropeptide produced by neurons in the
hypothalamus that initiates puberty and maintains
reproductive ability by triggering release of
gonadotropin-releasing hormone

223
Q

What is Gonadotropinreleasing
hormone?

A

Hypothalamic hormone that stimulates anterior pituitary
gland to secrete gonadotropic hormones

224
Q

What are Gonadotropic
hormones

A

Hormones of pituitary gland (follicle-stimulating
hormone, FSH, and luteinizing hormone, LH) that have
stimulating effect on cells of gonads.

225
Q

What is pair bond formation

A

Formation of long lasting, monogamous-ish pair bonds

In approximately 5 percent of mammalian species, sexually mature
couples tend to form long-lasting, fairly monogamous pair bonds.
Some species of prairie voles form long-term pair bonds. Some don’t

226
Q

What peptides in the brain does the formation of pair bonds relate to

A
  • The formation of pair bonds seems to relate to two peptides in brain:
    vasopressin and oxytocin. (These compounds are released as
    neuropeptides in the brain and as hormones in the blood.) Levels of
    them are elevated during sex, childbirth, and breastfeeding
227
Q

What six different facial expressions can people reliably discriminate?

A

Fear
Anger
Surprise
Disgusted
Sad
Happy

228
Q

Are facial expressions innate?

A

Yes, they are unlearned responses
involving complex muscles movements. The ability to display
emotions and recognize them in others transcends cultural and
linguistic barriers (to some extent).

229
Q

How old do you begin understanding these facial expressions?

A

Babies as young as 36 hours display (mimic) universal facial expressions

230
Q

Is there differences in the display of emotional facial expressions
between congenitally blind, non-congenitally blind, and sighted athletes

A

NO

231
Q

Emotions exist in the abstract: You can cognitively think
about emotions and make your face artificially express
specific emotions (like when people tell you to smile to
look happy or you pretend to be sad). Where is this processed?

A

This aspect of emotions is processed in the neocortex

232
Q

Emotions also exist as a feeling, a raw reflexive response to certain stimuli. Where is this located?

A

This aspect of emotions is processed in the limbic system, most prominently in the amygdala

233
Q

Volitional facial paresis

A

Difficulty in moving facial muscles voluntarily

Caused by damage to face region of primary motor cortex or its subcortical connections

234
Q

Emotional facial paresis

A

Lack of movement of facial muscles in response to emotions in people who have no difficulty moving these muscles voluntarily

Caused by damage around insular cortex or parts of the thalamus

235
Q

Behavioral responses

A

Consists of muscular movements (facial expressions, body language, choreographed movements)

236
Q

Autonomic responses

A

Signaling through peripheral nervous system

Facilitate fight or flight behaviors and provide quick mobilization of energy for vigorous movement

237
Q

Hormonal responses

A

signaling through blood) reinforce the autonomic responses

238
Q

James-Lange Theory of emotion

A

Perception of emotion-eliciting event
e.g., see a bear

Appropriate set of behavioral and physiological responses are triggered
e.g., clench fists, run away, sweating, trembling, increased heart rate

The brain receives feedback from these changes in the peripheral nervous system which, in turn, produces the subjective feelings of emotion
e.g., fear

239
Q

What is the cingulate cortex?

A

a large area that overlies the corpus callosum.

Cingulate means encircling.

This region interconnects many limbic areas of the brain.

240
Q

Where are the hippocampus and amygdala and what do they contain

A

In the temporal lobe of the cerebral cortex.

They each contain several distinct nuclei

241
Q

The Limbic System

A

The cingulate cortex, hippocampus, amygdala, mammillary bodies, septum, and fornix

242
Q

Hippocampus

A

Critical for explicit memory formation

243
Q

Amygdala

A

Critical for feeling and recognizing emotions, particularly fear.

244
Q

Damage to the amygdala

A

Patient S.P. has bilateral amygdalectomy to treat a seizure disorder.
Afterwards she no longer experienced any fear.
She could generate artificial expressions of emotion (including fear) without problem, but she could not identify the emotion of fear even in photos of herself

S.M. is a patient with bilateral amygdala damage.
When shown photographs of faces, she doesn’t look at the eyes.
S.M. can recognise the emotion if she is trained to look at the eyes but she doesn’t do it spontaneously; she has to be reminded every time

245
Q

What is the role of Ventromedial Prefrontal Cortex

A

when myelination occurs, your neural activity goes faster.
The action potential travels faster down an Axon.

It’s not fully myelinated until the teenage years.
And so this is one reason why we think young children have hard times controlling their emotions is because this area of the brain is involved in emotional control and it’s not optimized

246
Q

What are mirror neurons

A

when myelination occurs, your neural activity goes faster.

The action potential travels faster down an Axon.

It’s not fully myelinated until the teenage years.

And so this is one reason why we think young children have hard times controlling their emotions is because this area of the brain is involved in emotional control and it’s not optimized

  • Mirror neurons are thought to be involved in mimicry and empathy.
247
Q

What are the two way of monitoring water levels?

A

Not enough water inside cells (osmometric thirst)
Not enough blood/fluid in our circulatory system (volumetric thirst)

248
Q

What is osmometric thirst

A

Not enough water inside cells

When we drink water, our cells physically expand in size as they absorb water from the interstitial fluid.

When we consume excess salt, our cells physically shrink as they lose water to the salty interstitial fluid. This triggers a type of thirst known as osmometric thirst

249
Q

What is volumetric thirst

A

Not enough blood/fluid in our circulatory system

The heart needs a certain amount of blood to keep beating
People feel an intense thirst after they lose lots of blood because hypovolemia causes volumetric thirst.

Blood flow (blood volume) is monitored by the kidneys.
Low blood flow causes the kidneys to release renin, which triggers a hormone signaling cascade that promotes thirst, among other things

250
Q

What is an isotonic solution

A

similar concentrations of solute on either side of the membrane. The cell will neither gain nor lose water.

251
Q

HypOtonic solution

A

Solute is more concentrated inside the cell than out, so water will enter the cell.

252
Q

HypERtonic solution

A

solute is more concentrated outside the cell than in, so water will leave the cell.

253
Q

Osmoreceptors

A

Neurons that detect changes in cell size.

The membrane potential and release of neurotransmitter from osmoreceptor cells relates to the volume of these cells

254
Q

What is insulin

A

Pancreatic hormone that facilitates

  • entry of glucose into cells of the body for immediate use
  • conversion of glucose into glycogen for short-term storage
  • storage of fatty acids in adipose tissue for long-term storage
255
Q

what is glucagon

A

Pancreatic hormone that promotes

  • conversion of liver glycogen into sugar for immediate use
  • conversion of adipose triglycerides into fatty acids
  • which will be taken up by cells of the body and converted to sugar for immediate use
256
Q

What is grhelin

A

Peptide hormone released by the empty stomach that increases eating

Also produced by neurons in the brain

257
Q

What is gastric favors

A

Short-term satiety (fullness) signals released by the stomach and duodenum immediately after eating, before food has been digested.

258
Q

what are CCK and GLP-1?

A

regulators of digestive processes

They are secreted from the duodenum in response to food intake in proportion to the calories ingested. Their entry of these molecules into the brain correlates with feelings of satiety and inhibits food intake

259
Q

What is CCK

A

causes the gallbladder to release digestive enzymes into the duodenum

260
Q

what is GLP-1

A

Regulates insulin secretion from the pancreas.

261
Q

Which of the following have proven to be more effective for reducing hunger and weight?

a) GLP-1 antagonists
b) GLP-1 agonists
c) CCK agonists
d) CCK antagonists

A

b) GLP-1 agonists

CCK has no evidence for this

262
Q

what is leptin

A

A circulating hormone that is secreted by adipocytes (fat cells).

Is thought to signal the size of peripheral energy stores in the body.

provides a negative feedback signal that decreases hunger

increases the sensitivity of hypothalamic neurons to short-term satiety signals
Exogenous administration of leptin typically decreases meal size in healthy people, but this effect is short-lived.
Leptin makes some neurons more sensitive to satiety peptides such as CCK and less sensitive to hunger peptides such as ghrelin

263
Q

What is Glucoprivation (hypoglycemia)

A

Dangerously low blood-glucose levels (i.e., not enough immediately available sugar in the blood)

Detected by the liver, pancreas, and brainstem

Not enough sugar to support normal brain functions

264
Q

What is lipoprivation

A

Dangerously low levels of fatty acids (i.e., not enough fat on the body or not enough free fat acids in the blood) Detected in the hypothalamus (via leptin) and in the liver

Can be caused by drugs that inhibit fatty acid metabolism

Not enough body fat

265
Q

What is learning?

A

Refers to the process by which experiences change our nervous system and hence our behavior.

Refer to these changes as memories

266
Q

What are memories and types?

A

Memories can be transient or durable, explicit or implicit, personal or impersonal.

267
Q

What is memory retrieval?

A

Accessing memories

268
Q

What is neuronal plasticity?

A

The cellular basis of long-term memory

Refers to the ability of the nervous system to change and adapt

269
Q

To identify neuronal plasticity, what do we typically measure?

A

Intrinsic excitability and synaptic strength

270
Q

What is Intrinsic excitability ? How do we measure this?

A

The number of action potentials a neuron exhibits in response to an influx of positive current

Measurement of intrinsic excitability

determined by the number and type of ion channels (leak channels and voltage-gated channels) expressed by the neuron.

271
Q

What is synaptic strength

A

The amount of positive (or negative) current that enters the postsynaptic neuron when a presynaptic cell has an action potential.

A change in the strength of the synaptic connection between two neurons is called synaptic plasticity.

272
Q

What is synaptic plasticity

A

Refers to changes in the strength of the synaptic connection between two neurons.

When a presynaptic cell releases neurotransmitter, how big or small is the postsynaptic response (regardless of whether it is depolarization or hyperpolarization).

Synaptic plasticity can involve pre- and postsynaptic changes.

273
Q

What occurs in the pre vs. post synaptic changes

A

On the presynaptic side, the amount of voltage-gated calcium channels on the presynaptic membrane influences how many vesicles will be released following an action potential.

On the postsynaptic side, the amount of neurotransmitter receptors influences the sensitivity of the postsynaptic cell to neurotransmitter release

274
Q

What is EPSP (excitatory postsynaptic potential).

A

If the postsynaptic response is depolarization

275
Q

What is habituation

A

Reduced physiological or behavioral responding to a repeated stimulus.

If the siphon is lightly touched, the gill withdraws reflexively.

Repeated light touching of the siphon will reduce the magnitude of this reflex until the Aplysia completely ignores light touches.

276
Q

What is sensitization?

A

Increased sensitivity to a stimulus

In contrast to habituation, in response to painful electrical shocks, the sea slug’s gill withdrawal reflex becomes stronger

277
Q

What is long-term potentiation (LTP)

A

Long-term potentiation increases the strength of the connection between two neurons (i.e., increased synaptic strength).

Repeated high-frequency (tetanic) stimulation of the inputs to a neuron often induces LTP.

For LTP to occur, the release of neurotransmitter must coincide with a substantial depolarization of the postsynaptic cell (normally associated with an action potential)

278
Q

How is nitric ozide (NO) associated with LTP

A

LTP is often initiated on the POSTSYNAPTIC side (with more neurotransmitter receptors) but retrograde signaling of nitric oxide (NO) can drive presynaptic modifications (e.g., more vesicles of neurotransmitters).

279
Q

What is long-term depression (LTD)?

A

Long-term decrease in the strength of the connection between two neurons (i.e., decreased synaptic strength).

Persistent low-frequency stimulation of the inputs to a quiet neuron often causes LTD.

LTD is often initiated on the POSTSYNAPTIC side (with less neurotransmitter receptors) but retrograde endocannabinoid signaling can drive presynaptic modifications (e.g., less calcium-influx per action potential).

280
Q

Similarities in LTP and LTD

A

LTP and LTD are a function of the number of times the synapse was activated as well as whether the postsynaptic neuron fired at those precise times.

281
Q

What is an NMDA receptor?

A

Coincidence detector
Plays a large role in learning and memory
They are located in almost every glutamatergic synapse in the brain

282
Q

how does an NMDA work?

A

Ionotropic glutamate receptor that has a large ion pore.

When the NMDA receptor binds glutamate and opens, magnesium ions (Mg2+) try to pass through its pore, but they get stuck in it and block all current flow. [Only occurs when the membrane potential is below threshold (< -40mV), such as when the cell is at rest.]

If the membrane is depolarized (i.e., more positive than -40 mV) because of other synaptic inputs, then Mg2+ ions will not try to enter though the NMDA receptor, and thus they won’t clog the pore.

Na+ and Ca2+ ions will enter a cell through NMDA receptors, but only when these receptors are bound to glutamate and Mg2+ is not clogging the pore.

283
Q

What is an AMPA receptor

A

The glutamate receptor that mediates most excitatory fast synaptic currents in the brain. It is ionotropic and opens upon glutamate binding. It lets in sodium ions which cause EPSPs (excitatory postsynaptic potentials) that depolarizes neurons.

Most glutamate synapses in the brain have AMPA and NMDA receptors

284
Q

What is an NMDA receptor (short def of what it does)

A

Ionotropic glutamate receptor that only passes current upon glutamate binding when the membrane potential is slightly depolarized. If glutamate binds when the cell is hyperpolarized, the pore will get blocked by Mg2+.

Open, unblocked NMDA receptors allow sodium and calcium ions through

285
Q

WHat is CaMKII

A

Type II calcium-calmodulin kinase

It is an enzyme that is activated by calcium influx through NMDA receptors. It plays a role in the intracellular signaling cascade that establishes long-term potentiation, by increasing the number of postsynaptic AMPA receptors (in excitatory glutamatergic synapses).

286
Q

What is Associative long-term potentiation

A

The increase in synaptic strength that occurs in weak synapses when they are active right around the time when stronger inputs caused the postsynaptic neuron to spike

287
Q

What is Hebb’s Rule?

A

Hypothesis that the cellular basis of learning involves the strengthening of synaptic connections that are active when the postsynaptic neuron fires an action potential.

This is known as: Fire together, wire together…more strongly than before.

The synaptic connection DOES have to initially exist.

288
Q
A

Intro to Behavioural Neuroscience McGill (PSYC 211 - 2023 Fall) (3 decks)

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