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PoliSci 281 - Midterm > Biopsych - Midterm 3 > Flashcards

Biopsych - Midterm 3 Flashcards

1
Q

Physical definition of sound

A
  • sound is pressure changes in the air or other medium
  • Receptors in the auditory system transduce vibratory energy (vibration of molecules in a medium)
  • Sound is percieved
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2
Q

Perceptual definition of sound

A

sound is the experience we have when we hear

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3
Q

Amplitude

A

Size of waveform pressure variations

Determines perceived loudness

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4
Q

Frequency

A
  • Number of waveform repetitions per second
  • Determines perceived pitch, measured in cycles/sec
  • Cycles per second. 1 cycle/sec = 1 Hertz (Hz)
  • Audible spectrum: 20 to 20,000 Hz.
  • Spectrum varies for species (e.g., extends higher for dogs, bats), age
  • Frequency of stimulus is associated with pitch perception (in vision, frequency of stimulus is associated with color perception)
  • Pure tones don’t exist
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5
Q

Complexity

A

Combination of component frequencies that make up all natural sounds

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6
Q

Intensity

A
  • amount of energy in stimulus: loud or faint sounds.
  • We can hear a broad range of intensities:
    - from very faint sounds (rustling of leaves) to very loud ones: jet engine.
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7
Q

Velocity

A
  • depends on the medium in which waves travel.
  • In air, sound travels at 750 miles/h (1250 Km/h) (sound barrier),
  • Velocity is greater in denser media (wood, metal)
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8
Q

Outer Ear

A

Auditory canal and tympanic membrane (eardrum)

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9
Q

Middle Ear

A

-3 ossicles: hammer (malleus), anvil (incus), stirrup (stapes). —function: interface between air in outer ear and liquid in inner ear.

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10
Q

Inner ear

A

Oval and round windows.

  • Cochlea, contains the Organ of Corti (Fig. 7.5)
  • Organ of Corti: Tectorial membrane, Hair cells (receptors) Basilar membrane
  • Stirrup pushes oval window in, forcing round window out, creating liquid wave inside cochlea.
  • Wave in cochlea induces vibrations in basilar membrane
  • Hair cells on basilar membrane collide with tectorial membrane.
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11
Q

Function of Auditory system

A
  • Perception of objects and events through the sounds that they make.
  • What? (Recognition, identification)
  • Where? (location)
  • Auditory structures are arrayed according to frequency
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12
Q

Fourier Analysis

A

Mathematical procedure for breaking down complex waves into their component sine waves.

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13
Q

Decibel (dB)-

-Denominator

A

-Logarithmic unit used to express the ratio between two values of a physical quantity: dB=20(logP1/P0)
Denominator:
-Lowest threshold of hearing (reference unit)
-Simplifies calculations & representation of very large and small numbers

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14
Q

Cochlea

A
  • Vibrations of cochlear fluid are ultimately dissipated by the round window, an elastic member in the cochlea wall.
  • Cochlea is extremely sensitive
  • Humans can hear differences in pure tones that differ in frequency by only .2%
  • Has a internal membrane running up to its tip called organ of coti
  • Major principle of cochlear coding is that different frequencies produce maximal stimulation of hair cells at different points along the basilar membrane. w/ higher membranes producing greater activation at the tip of the basilar membrane.
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15
Q

How sound waves travel

A

Waves go from outer ear-> auditory canal & cause the tympanic membrane (ear drum) to vibrate–> vibration to 3 ossicles–>triggers vibrations in oval window–> transfers vibration to fluid in cochlea

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16
Q

Measuring Perceived Pitch with Pure Tone Frequencies

A

Traditionally used in studies of frequency spectrum of auditory system
Frequency of the sound will determine the pitch you perceive
Human spectrum:
20 - 20,000 Hz
But pure tones do not exist in natural world!

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17
Q

Transduction

A

Hairs in hair cells are bent, which opens ion channels on hair cells.
Receptor potential in hair cell is created, and transmitter is released.
Receptor potential produces action potentials in ganglion cells (spiral ganglion, in the cochlea) whose axons form the auditory nerve (8th pair).

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18
Q

Recognition of sound (what?)

A
  • Anterior Auditory Pathway involves identifying sounds
  • Basilar membrane analyses the component frequencies of sound.
  • The basilar membrane is tonotopically organized:
  • Different regions of membrane vibrate with different frequencies (as a keyboard).
  • Base (near windows) is thick and stiff and vibrates with HIGH frequencies.
  • Apex (end of membrane) is thin and flexible and vibrates with LOW frequencies.
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19
Q

Auditory pathway

A

-Spiral ganglion cells project to the cochlear nucleus, in the medulla (myelencephalon), from here to other nuclei, but eventually to the thalamus (medial geniculate nucleus),
and from here to the auditory cortex temporal lobe, FIG.7.7).
-Neurons in primary auditory cortex respond to pure tones, but neurons in seconary auditory cortex require more complex sounds. For instance, in monkeys, neurons in secondary auditory cortex respond better to monkey calls.
-Primary auditory cortex are organized in functional columns: all the neurons encountered during a vertical micro electrode penetration of primary auditory cortex tend to respond optimally to sounds in the same frequency range.
- This pathway is tonotopically organized, like cochlea, areas of primary and secondary auditory cortex organize on basis of frequency.

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20
Q

Sound Localization (where?):

A
  • Posterior Auditory pathway is involved in locating sounds
  • requires two ears.
  • Auditory system can analyze differences in the intensity and in the time of sound arrival between the the two ears.
  • Comparison of time of arrival occurs in the Medial Superior Olives, in the medulla
  • Comparison of intensity of sound between the two ears is done in the Lateral Superior Olives.
  • The Medial and Lateral Superior Olives are in the medulla (myelencephalon/hindbrain)
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21
Q

Bilateral Lesion

A

Following this there complete loss of hearing b/c their is shock delivered to the lesion, but sound comes back in a few weeks.

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22
Q

Unilateral Auditory Cortex Lesion

A

Disrupts ability to localize sounds in space contralateral but not ipsilateral to the lesion.

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23
Q

Deafness

A

Complete deafness is rare. Two kinds
1. Nerve deafness, or inner ear deafness: damage to cochlea or hair cells, or nerve
Bilateral lesions of the primary auditory cortex in laboratory mammals produce no permament deficit in their ability to detect sounds. However, cortical lesions can disrupt the ability to localize brief sounds, and to recognize complex sounds.
2. Conductive deafness, or middle ear deafness. Patients hear their voices.
Titnitus: ringing of ears

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24
Q

Zygote

A

Single cell formed by amalgamation of an ovum and a sperm. It divides into 2 daughter cells, which further divide until a mature organism is produced.

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25
Q

Embryos three layers

A

ectoderm, mesoderm and endoderm

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26
Q

Induction of neural plate

A
  • A small patch of entodermal tissue on the dorsal surface of the developing embryo.
  • 3 weeks after conception, tissue that is destined to develop into the human nervous system becomes neural plate.
  • Cells of the neural plate are referred to as embryonic stem cells (neural and glial stem cells): Stem cells must have-
    - They have unlimited capacity for self-renewal
    - They have the ability to develop into different types of mature cells.
  • The neural plate leads to the formation of the neural tube, from where forebrain, midbrain and hindbrain develop (by 40 days after conception).
  • The inside of the neural tube will eventually become the cerebral ventricles and spinal canal.
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27
Q

Totipotent

A
  • Ability to develop into any type of cell in the body if transplanted to appropriate site
  • earliest embryo cells are totipotent
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28
Q

Multipotent

A

Can develop into most mature nervous system cells, but not other kinds
-cells of neuron plate = embryonic stem cells

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29
Q

Proliferation:

A

-cells lining the ventricles divide and form neurons and glial cells.

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30
Q

Neural Proliferation

A

One lips of neural groove fuse to make neural tube, cells of the tube begin to proliferate

  • doesn’t occur simultaneously or equally in tube
  • Most cell divisions occur in ventricular zone
  • Cells in different parts of neural tube proliferate in particular sequence that is responsible for the pattern of swelling & folding that gives brain the characteristic shape.
  • Controlled by chem signals from 2 organizers in neural tube
    1. floor plate: runs along midline of anterior surface of tube
    2. Roof plate: runs along midline of dorsal surface of tube
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31
Q

Migration:

A
  • Movement of cells from ventricular zone to final destination.
  • During this the cells are in immature form lacking axon and dendrites that characterize mature neurons.
  • 2 major factors: time and location
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32
Q

Radial migration

A

-From the ventricular zone to the surface of the neural tube

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33
Q

Tangential migration

A
  • Parallel to the wall of the neural tube

- Most cells engage in both migrations

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34
Q

Somal translocation migration

A

-Method by which developing cells migrate

caterpillar-like movement

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35
Q

Glia-mediated migration

A

Method by which developing cells migrate
-when neural proliferation is done, walls of the neural tube are thickening, a temporary network of glial cells called radical glial cells appear in developing neural tubes

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36
Q

Inside out pattern

A

Cortex develops “inside out”. This means that newborn cells migrate from ventricular zone to form cortical layer 6 first, and then 5, 4, 3 and 2 (layer one does not have neurons).

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37
Q

Neural crest

A
  • Located dorsal to the neural tube
  • Neural crest cells develop into the neurons and glial cells of the PNS.
  • Chemicals guide migrating neurons by attracting or repelling them.
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38
Q

Aggregation

A
  • Cells accumulate in certain areas forming nuclei (singular: nucleus)
  • one developing cells have migrated them must align themselves with other developing neurons that have migrated to the same area to form the structure of the Nervous system.
  • Migration and aggregation are both mediated by cell-adhesion molecules that are located on surfaces of neurons and other cells.
  • Cell adhesion molecules recognize molecule and stick to them.
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39
Q

Differentiation

A

Neurons take their adult morphology

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40
Q

Myelination

A

In humans, starts in spinal cord and progresses toward forebrain.

41
Q

Axon Growth

A

Once neurons migrate to their appropriate positions and aggregate into neural structures axon and dendrites grow from them
-At each growing tip on an axon or dendrite is a amoebae like structure called growth cone, extends and refracts cytoplasmic extensions called filopodia, as if searching for the correct path.

42
Q

Blueprint hypothesis

A

This hypothesis proposes that there are preformed pathways and tunnels.
Pioneer growth cones, guidepost cells. : First to travel the paths
Fasciculation: when developing axons grow along paths established by preceding axons.
Role of cell-adhesion molecules (NCAMs)
Evidence against blueprint hypothesis:
Cells with altered locations (transplants) still find targets

43
Q

Chemoaffinity hypothesis

A

-connections are highly specific.
-Sperry’s eye-rotation experiments (1943).
-After cutting optic nerves and rotating eyes 180 deg, the axons of retinal ganglion cells regenerated back to original target regions in the optic tectum (mesencephalon).
Frogs whose eyes had been rotated, but without cutting the optic nerves, responded in the same way.
How specific are the connections?
If half of the retina was distroyed, remaining axons project in an orderly way on the entire tectum .
If half of the tectum was destroyed, all of retinal axons accomodated in the remaining tectum and formed appropriate map (Fig. 9.6, bottom panel).
These observations support the Chemical Gradient Hypothesis:

44
Q

Fine-tuning of connections by spontaneous and experience-evoked neural activity

A

Neural activity can lead to a strengthening of some synapses and a weakening of others.
The Hebb postulate: Neurons that fire together wire together.
Role of glutamate receptors. Respond to glutamate.
NMDA receptors, are glutamate receptors that are also stimulated by N-methyl-D-aspartate (NMDA)
Detect correlated activity between presynaptic and postsynaptic cells.
non-NMDA receptors. are glutamate receptors that do not respond to NMDA
Role of spontaneous and evoked activity

    Critical or sensitive periods in development.
45
Q

Why does the CNS produce more neurons that it needs?

A

To compensate for failure of some axons to find target.

To compensate for target variability in size

46
Q

Neuron Death

A

During normal development, many neurons die. It is believed that they fail to compete successfully for life-preserving chemicals.
Among these chemicals are the neurotrophins or trophic factors, such as Nerve growth factor (NGF), and brain derived neurotrophic factor (BDNF).
Lack of trophic factors triggers Apoptosis, or active, programmed cell death (different from Necrosis, or passive cell death)

47
Q

Apoptosis

A
  • Active cell death
  • Safer than necrosis
  • DNA and other internal structures are cleared apart and packaged in membrane before the cell breaks apart
  • Membrane contains molecules that attract scavenger microglia and other molecules that prevent inflammation
  • removes neurons in safe way.
  • if genetic programs for apoptopic cell death are blocked it could lead to cancer
48
Q

Necrosis

A

break apart and spill content into extracellular fluid and could cause harmful inflammation.

49
Q

Synapse Rearrangement

A
  • Synapses that are “wrong” are likely to disappear
  • when neurons die the space they leave vacant on postsynaptic membranes is filled by sprouting axon terminals of surviving neurons
  • increases selectivity on transmission.
50
Q

The vulnerable developing brain

A
  • Many factors can go wrong during development
  • More than 200 genetic mutations associated with mental retardation
  • The developing brain is more vulnerable than the mature brain to the effects of malnutrition, toxic chemical and infections.
  • For instance, impaired function of the thyroid gland (endocrine gland) in infancy produces mental retardation that can be permanent. In the adult, thyroid impairment produces lethargy and other symptoms, but not mental retardation.
  • Epilepsy
51
Q

Rett Syndrome

A

Anomaly of brain development with mental retardation affecting mainly girls older than 1-2 years.
Associated with lack of dendritic development, perhaps due to deficit of neurotrophic factors

52
Q

fetal alcohol syndrome

A

(mental retardation, motor problems, hyperactivity, decreased alertness, heart defects and facial abnormalities. Dendrites tend to be short, with few branches.

53
Q

Learning

A

changes in the nervous system that are induced by experiences

54
Q

Memory

A

focuses on how these changes are maintained over time, and expressed (recalled).
-Learning and memory are both impossible w/o each other

55
Q

Amnesia

A

condition characterized by the incapacity to remember

56
Q

Bilateral medial temporal lobectomy

A

removal of the medial portion of the temporal lobe in both sides of the brain

57
Q

Lobectomy

A

removal of a cerebral lobe

58
Q

What HM had removed

A

The tissue removed on both sides included the hippocampus, amygdala and adjacent cortex (rhinal cortex).

59
Q

What kind of Amnesia did HM have

A
  • He had some degree of retrograde amnesia (backward-acting); could remember past but not 2 yrs prior to surgery.
  • severe antrograde (forward-acting) amnesia
    • Short-term memory was within normal range
    • But he could not form new long-term memories.
    • He could not consolidate new memories (process of transferring short-term memories into long-term memories
60
Q

Testing anterograde amnesia with objective tests:

A

Digit span + 1 test. HM could remember about 6 digits; normal can remember about 15.
Block-tapping memory-span test. HM could follow 5 blocks, within the normal range.
However, HM’ s memory for sensorimotor tasks was preserved:
Mirror drawing test (Fig. 11.2), and Rotary-pursuit test (Fig. 11.3). HM could improve by training, although he could not remember that he had practiced.
He also improved in some non-sensorimotor tasks, such as the Incomplete-picture test (Fig. 11.4), but could not recall previously performing the task.
He also learned a Pavlovian conditioning task. Eyeblink response: pairing sound with air puff on the eye.

61
Q

Major Scientific Contribution of HM’s Case

A
  • Medial temporal lobe plays big role in memory
  • Diff regions are more important for some kinds of memory but not others
  • the surgery abolished HM’s ability to form certain kinds of long term memories w/o disrupting his performance on tests
  • Evidence there is different kinds of memory: Remote (memory for distant past experience), long term and short term
  • Consolidating episodic memories depends on medial temporal lobe
62
Q

2 categories for Long term Memory- 2 parallel systems

A

One is explicit and one is implict

63
Q

Explicit Memories

A
  • (declarative) Long term memories that are conscious and thing you can demonstrate by telling others.
  • Semantic memories (IMPAIRED HM) are explicit memories for general facts or information, for example, what one would learn in school, language, grammar and facts.
  • Episodic memories are explicit memories for events and experiences in one’s life (seeing a particular movie).
64
Q

Implicit Memories

A

Procedural or non-declarative: Things that you know that you can show by doing, memories that are expressed by improved test performance, but without conscious awareness.

  • Skill learning
  • Priming (incomplete picture test, word priming test)
  • Conditioning
65
Q

Why are there two parallel memory systems?

A
  • The conscious (explicit) system may have evolved to confer flexibility: ability to use implicit learning in different ways or contexts.
    • Studies showed that although amnesic patients were able to learn an implicit task, they could not use this knowledge in a different context.
  • The implicit system was more simple, it evolved first
66
Q

Cerebral Ischemia

A

Interruption of blood supply to their brains, ofter suffer from medial temporal lobe amnesia

67
Q

Amnesia of Korsakoff’s Syndrome

A
  • Disorder of memory because of large consumption of alcohol
  • Thiamine deficiency
  • Lesion to medial diencephalon & diffuse damage to several other brain structures; neocortex, hippocampus & cerebellum
  • severe anterograde amnesia for explicit episodic memories but progresses into severe retrograde
68
Q

Alzehimers

A
  • Major cause of amnesia
  • progressive disorder
  • terminal
  • implicit memory for verbal and perceptual memory is deficient, but implicit memory for sensorimotor learning is not
  • acetycholine reduced –> degeneration of basal forebrain
69
Q

Posttraumatic amnesia

A
  • Amnesia resulting from nonpenetrating blows to the head that cause concussion (temporary disturbance of consciousness) or coma (loss of consciousness).
  • Permanent amnesia for events that occurred during the subsequent period of confusion
  • there is a period of confusion during which the patients have short-term memory and appear reasonably lucid, but they fail to consolidate these memories into long-term memories
70
Q

Gradients of Retrograde Amnesia and Memory Consolidation

A

-The fact that concussions disrupt recent memories suggests that the storage of older memories is protected by a process of consolidation.

71
Q

memory consolidation

A
  • The translation of short-term memories into long-term memories
  • From a malleable and vulnerable state to a more stable and permanent one
72
Q

How do symptoms of coma or concussion provide evidence for memory consolidation?

A

(1) Failure to convert STM into LTM shortly after regaining consciousness
(2) Permanent retrograde amnesia for events immediately before incident
(3) Older memories are spared

73
Q

engram

A

A change in the brain that represents a memory

74
Q

Hypotheses of memory consolidation

A

(1) Donald Hebb
Reverberating short-term circuits maintain memory until it’s consolidated into LTM
-Before becoming LTM they are susceptible to disruption of neural activity, such as that caused by ECS.

75
Q

electroconvulsive shocks (ECS)

A

-Consolidation has been studied with electroconvulsive shocks (ECS) to test the hypothesis that disrupting neural activity with the shocks would erase those memories that had not yet consolidated.
-The idea is that the length of the period of retrograde amnesia would correlate with the time needed for memory consolidation.
-Results from one experiment in rats suggested that consolidation took less than one hour (Fig. 11.7).
Electric shocks applied later than one hour after the training did not erase what the rats had learned (the location of a water spout).
However, experiments in humans that were treated with ECS for depression suggested that shocks could erase memories up to 3 years old (Fig. 11.8).
Thus, consolidation may be an ongoing process, which makes Hebb’s hypothesis unlikely.

76
Q

Reconsolidation

A

-Recent studies suggest that each time a memory is retrieved from long-term storage, it is again stored in short-term memory, being therefore susceptible to post traumatic amnesia.
OR
The act of making a memory liable/vulnerable once again, when such memory is being retrieved from long-term storage

77
Q

Standard Consolidation Theory

A

Memories are temporarily stored in hippocampus until they can be transferred to a stable cortical storage system

78
Q

Multiple- trace theory

A

Proposed that the hippocampus and other structures store memories for as ling as they exist, not just the period of time before consolidation.

79
Q

Monkey- Delayed nonmatching-to-sample test

A

-Food under object, screened lowered for a while, and the monkey should know to pick the other object b/c it should have food underneath it.
-Monkeys with medial lateral cortex amnesia arent good at this test if the screen is down too long. Same results w/ humans
-One problem with monkeys is that lesions aimed at hippocampus also lesioned the rhinal cortex (cortex adjacent to the hippocampus)
Therefore, researchers could not be sure whether memory deficits in monkeys were due to lesion of the hippocampus or rhinal cortex.

80
Q

The Delayed Nonmatching-to-Sample Test for Rats

A

However, the rat model presented the advantage that lesions could be restricted to the hippocampus (Fig. 11.12).
The version of the delayed nonmatching-to-sample task in rats is the Mumby box (Fig. 11.13). This box has 3 compartments.
In one compartment, the rat is exposed to the sample object concealing the food.
In the middle compartment, the rat is made to wait through the delay.
In the third compartment, the rat was presented with the sample object that had to be rejected in favor of the new one that now conceals the food.
Rats performed as well as monkeys with delays up to one minute.

81
Q

Neuroanatomical Basis of the Object-Recognition Deficits Resulting from Medial Temporal Lobectomy (Rodent)

A

The rodent model revealed that the hippocampus and amygdala were not involved in deficits of object-recognition memory tested with delayed nonmatching-to-sample tasks.
Instead, these experiments found that the rhinal cortex was important for object recognition memory
** Experiments conclude hippocampus plays big role in object-recongnition

82
Q

Hippocampal Lesions Disrupt Spatial Memory

A
  • The hippocampus does play a key role in memory for spatial location
  • Damage of the hippocampus result in severe deficits in spatial memory tested in mazes like the Morris water maze and the radial arm maze tests.
  • In the radial arm maze, each day rats quickly learn the position of the arms with food (reference memory for the general principles and skills needed in the task) and refrain to visit an arm more than once during the day (working memory: ability to maintain relevant memories while a task is being performed). Both reference and working memories are deficient after lesion of the hippocampus.
83
Q

Hippocampal Place Cells

A

Hippocampal Place Cells
When rats familiarize themselves with the environment, many cells in the hippocampus acquire a place field, that is, they fire when the rats is in a particular place in the environment.
-Represent cognitive component of enviroment, if cells fire a certain way, rat will behave in a certain way

84
Q

Food Cache Birds Study

A

Species of birds that remember where they store seeds have larger hippocampuses than birds that do not store seeds, supporting the idea that hippocampus is important for spatial memory in many, if not all, species.

  • in humans there is activation of hippocampal during performance of navigation tasks
  • taxi drivers have bigger hippocampi
85
Q

Cognitive Map Hypothesis

A
  • Theory of hippocampal function
  • -hippocampus contains a cognitive map of allocentric space that serves as spatial context useful for acquiring and recalling memory of any episode
  • -The hippocampus may use sensory input to form an allocentric map of the environment (space represented by the relation between external landmarks).
86
Q

Configural Association Theory

A
  • -Theory of hippocampal function
  • Hippocampus is critical for learning the significance of combinations of stimuli (e.g., you will be learning about biopsychology in this room, not any other topic
  • -The hippocampus may be important for recognizing spatial arrangements of objects (such as furniture, pictures, etc, in a familiar room).
87
Q

Where are memories stored?

A

-Some of these structures, such as the mediodorsal nucleus of the thalamus, and the basal forebrain appear to be damaged in patients suffering Korsakoff syndrome (often due to alcoholism) and Alzheimer syndrome.
-In general, memories are stored in areas that contribute to the acquisition of the memories
Inferotemporal cortex: object recognition

Hipoocampus: spatial location

Amygdala: plays a role in memory for the emotional significance of experiences. Rats with amigdala lesion fail to associate shocks with fear.

Cerebellum: implicit sensorymotor tasks
(eye blink response)
Prefrontal cortex: temporal order of events, as in cooking

Striatum (basal ganglia): habit formation

88
Q

SYNAPTIC MECHANISMS OF LEARNING AND MEMORY Two main approaches:

A
  • One approach studies the neural bases of learning in a sea snail (marine mollusk), called Aplysia (sea slug)
  • The other approach focuses on a phenomenon that it is thought to be related to learning in brains like ours. The phenomenon is called long-term potentiation (LTP). We will concentrate on this approach
  • –Hebb: changes in synaptic efficiency are the basis of long term memory
89
Q

Long Term Potentiation

A

LTP as a model for learning
LTP in mammalian brains is the most widely studied neuroplastic phenomenon
LTP: Enduring facilitation of synaptic transmission that occurs following activation of a synapse by intense high-frequency (100/sec) stimulation (for 1-4 secs) of the presynaptic neuron.
-It is long-lasting: hours or weeks.

90
Q

Properties that implicate LTP in learning and memory

A

1) LTP shows cooperativity (spatial effect): Nearly simultaneous stimulation of two or more axons produces LTP, whereas stimulation of just one is less effective.
If there are several inpus to a cell, only those that cooperate become facilitated, the others may actually weaken.
2) LTP shows associativity: Pairing a weak input with a strong input enhances later responses to the weak input.
3) LTP is the kind of synaptic facilitation that Hebb postulated in 1949 as the basis of learning and memory:

91
Q

Hebb’s postulate for learning

A

The synaptic efficacy between A and B will increase when A fires B consistently.
In order to account for associative learning and memory, synaptic facilitation must result from an interaction of simultaneous presynaptic and postsynaptic activity.
In fact, LTP does not occur if the postsynaptic cell does not fire (only the presynaptic).
Or when the postsynaptic cell fires alone.
It is the co-occurrence that matters.

92
Q

LTP: Role of NMDA Receptors

A

Receptors for Glutamate can be NMDA receptors, or non-NMDA receptors
The hebbian nature of LTP results from the properties of the NMDA receptor (Figs. 11.20 - 11.21).

NMDA receptors are normally blocked by Magnesium ions (Mg++) at resting membrane potentials (-70 mV)

          - -In order to repel the magnesium, it is necessary to depolarize the cell by activating non-NMDA receptors (e.g., AMPA receptors). - Glutamate can now open NMDA receptors, which let Na+ and Ca++ in. - Entry of Ca++ in postsynaptic cell induces cellular changes

NMDA receptors do not respond unless glutamate binds to the receptor and the neuron is already partially depolarized (which repels Mg++)

Ca2+ does not flow into cell unless both conditions are met. Ca2+ influx may activate protein kinases that induce changes necessary for LTP
Temporarily activate genes and produce certain proteins.
Proteins alter dendrites and potentiates synapse.
NMDA receptors are necessary for inducing LTP, but not for maintaining it.

93
Q

Signal from postsynaptic to presynaptic cell:

A

Changes in the postsynaptic cell may be transmitted to the presynaptic cell by the soluble gas Nitric Oxide (NO) (blocking the synthesis of NO blocks LTP), although other factors may also play a role.

94
Q

Maintenance and Expression of LTP

A

LTP begins in the postsynaptic neuron, which provides feed-back signals to the presynaptic neuron through soluble gases such as Nitric Oxide (NO)
Pre- and postsynaptic changes:
Insertion of glutamate receptors in postsynaptic membrane
Increase of of glutamate release in presynaptic neuron
NMDA receptors are needed for inducing LTP, but not for maintaining it

95
Q

LTP as a Neural Mechanism of Learning and Memory

A

Elicited by high frequency electrical stimulation of presynaptic neuron; mimics normal neural activity
LTP effects are greatest in brain areas involved in learning and memory
Learning can produce LTP-like changes
Blocking LTP interferes with learning
Mice with abnormal NMDA receptors did not have LTP and could not learn a spatial task

96
Q

LTP and behavior

A

-LTP can occur during training in vivo.
-Blocking LTP interferes with learning.
mice with a mutation of a gene controlling NMDA receptors did not have LTP and could not learn a spatial task
-astrocytes effect ltp

97
Q

Infantil Amnesia

A

remember nothing about our infancy

98
Q

Nootropic

A

smart drug that are supposed to help memory. They are not actually helpful.

PoliSci 281 - Midterm (3 decks)

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