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Exam 1 Flashcards

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1
Q

Define Biological Psychiatry

A

Understand metnal disorder in terms of biological function. Everything psych is bio, BUT lifestyle/environment alters biology

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2
Q

What does DSM tell us? What does it not?
What tries to fix this problem?

A

Tells symptoms of disorders.

Doesn’t tell you APPROACHES. Also HETEROGENEITY: disorder can look different in different people.

RDoC

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3
Q

To diagnose depression, you need / sumptoms including at least 1 of depressed mood and loss of interest/pleasure

A

5/9

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4
Q

3 causes of mental illness throughout time

A
  1. Supernatural
  2. Somatogenic (bio)
  3. Psychogenic
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5
Q

Who declared mental disorders disorders of the brain?

A

Wilhelm Griesinger (1817-1868)

German neurologist/psychiatrist

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6
Q

In first half 20th century, was emphasis more on bio?

A

No, psych with Freud

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7
Q

What brought back bio interest in 2nd half 20th century?

A

genetics development. Schizoprenia had genetic component.

Thorazine (Chlorpromazine) marketed in 1954

NEUROCHEMICAL INBALANCE became big explanatory model thanks to drug development

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8
Q

When did 1st edition of DSM come out?

A

1952

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9
Q

What did the gov declare 90’s to enhance public awareness of brain research?

What journal founded in 1997?

A

Decade of the brain

Molecular psychiatry

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10
Q

New findings: effects of psychiatric drugs not primarily exerted via NT in synaptic cleft, BUT

A

Up and down regulation of receptors, effects on intracellular cascades

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11
Q

DSM 5 on may 18th 2013, but what was Thomas Insel’s problem 3 weeks earlier?

A

Lacks validity

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12
Q

```

If DSM doesn’t have validity, then what is it good for?

A

Clinical utility

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13
Q

DSM 5 (2013) to DSM-5-TR (2022)

A

Updated sections. New diagnosis of prolonged grief disorder, 70 modified crieria set, intro and use of manual guides, considers racism/discrimination, New ICD-10_CM codes to monitor suicidal behavior and suicidal self-injury, updated old codes 50 coding updates for substance intoxication and withdrawal and other disorders

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14
Q

People only diagnosed with disorder IF

A

Harm to other or self and significant impariment

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15
Q

When was homosexuality taken out of the DSM

A

DSM 3

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16
Q

The DSM-5, more than other versions, tries to what?

A

Incorporate research findings in classifications

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17
Q

Why is DSM 4 anxiety split into 4 categories?

A

Data from neuroscience, imaging, and genetic studies suggests differences in heritability, risk, course, and treatment.

Fear based (phobias)
OCD
trauma (PTSD)
dissociative disorders

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18
Q

What is RDoC?

A

Research framework for investigating mental health disorders.

Integration of many levels of information.

Dimensional apporach involving multiple analysis levels

Framework to study mechanisms that cut across traditional diagnostic categories

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19
Q

What is required for RDoC to pass for group in internal NIHM workshop?

A
  1. Persuasive evidence for validity
  2. Evidence for neural circuit or system that implements the psychological function described

Implicit: linkable to psychiatric clinical phenomenon

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20
Q

Similarities and differences of RDoC and HiTOP

A

Similarities: both move away from diagnostic categories. Both work-in-progress approaches.

Differences: how they define dimensions, content and units of analysis, current gaps and limitations.

RDoC reserach framework
HiTop is a dimensional classification system (general p factor)

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21
Q

Who made the RDoC? Why?

A

NIMH

Neuroscience has not made major breakthroughs towards prevention and treatment. NO satisfacotry theory of pathophysiology, biology doesn’t map onto DSM

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22
Q

Why use the RDoC? How has neuroscience failed?

A
  1. Heterogeneity (more than 1 way for a symptom)
  2. measuring biology on different levels is very expensive
  3. Comorbidity
  4. Only enroll subjects based on diagnosis
  5. to understand mental health and illness adopt dimensional conceptualization
  6. DSM diagnosis aren’t great constructs to begin with
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23
Q

Why is PTSD not an anxiety disorder in DSM5?

A

fear/anxiety not central to PTSD

Fear- alarm to present/imminent danger real or perceived

Flashbacks specific to PTSD, low base-rate symptom

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24
Q

What symptoms does PTSD share with depression?

A

Anhedonia, difficulty sleeping, irritaiblity, difficulty concentrating

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25
Q

Give an example of an experiment using two units of analysis
from the RDoC Matrix (make sure to answer the following
questions in your response): What is your construct of
interest? Who would you recruit into your study? How would
you measure those two units?

A

Cognitive systems: Congitive control or attention

Populations: ADHD, Autism, NT

Genes, fMRI for circuits, behavior, you can do attention or cognitive control task

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26
Q

DSM good for clinical use, increase reliability since DSM 3, good for legal and social systems, clinical phenotypes, but why is it bad for research?

A
  1. Emphasis on reliability over validity
  2. Heterogeneity of disorders
  3. Extensive co-morbidity (Discrete disorders no symptom overlap)
  4. Antedates current knowledge of brain and behavior
  5. Difficult to relate diagnoses to genes, particular circuits, or basic behavioral mechanisms
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27
Q

Domains of RDoC

A
  1. Negative Valence Systems
  2. Positive Valence Systems
  3. Cognitive Control Systems
  4. Systems for Social Processes
  5. Arousal/Modulatory Systems
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28
Q

Units of Analysis on the RDoC

A

Genes, molecules, cells, circuits, physiology, behavior, self-report paradigms

GMCCP B S-R P

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29
Q

Negative Valence Systems Constructs

A
  1. Acute threat (fear)
  2. Potential threat (anxiety)
  3. Sustained threat
  4. Loss
  5. Frustrative nonreward
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30
Q

Positive Valence Systems Constructs

A
  1. Approach motivation
  2. Initial responsiveness to reward
  3. Sustained responsiveness to reward
  4. Reward learning
  5. Habit
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31
Q

Cognitive Systems Constructs

A
  1. Attention
  2. Perception
  3. Working Memory
  4. Declarative Memory
  5. Language Behavior
  6. Congitive (effortful) control
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32
Q

Systems for Social Processes constructs

A
  1. Affiliation/attachment
  2. Social Communication
  3. Perception/Understanding of self
  4. Perception/Understanding of others
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33
Q

Arousal/Modulatory Systems constructs

A
  1. Arousal
  2. Biological Rhythms
  3. Sleep-wake
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34
Q

RDoC Limits

A

units called behavior and self-report, but at present these units do not intend to include the majority of signs, symptoms, and behaviors requiring clinical attention

many self-report, behavioral, and task exemplars included in the RDoC matrix have inadequate or unclear psychometric properties and were
not developed to operationalize RDoC constructs

limited application in clinical practice

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35
Q

HiTop Limits

A

but do not take into account their underlying underpinnings.

Doesn’t include autism or ID

Includes understudied somatoform disorder

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36
Q

Anhedonia

A

No response to reward

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37
Q

Complexity of nervous system means there are different ways that

A

neurotransmission can occur

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38
Q

Does RDoC take the 1:1 neuron approach?

A

No, compels us to understand molecules and
channels within and between two neurons; to assembly of
neurons in circuits; to neural networks; emergent behavior

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39
Q

Motor cell will take ____ or more incoming fibers

A

10,000

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40
Q

Chemical synapse transmission

A

Presynaptic release chemical (NT) pick up by postsynaptic cell

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41
Q

Electrical Synaptic Transmission

A

Gap Junctions

Not synpase, connected with each other.
Direct signal going. Sodium ion, signal that creates AP.
Ions back and forth across neurons

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42
Q

Excitatory Synaptic Transmission

A

Sodium more likely to release AP

Depolarizing next cell, making it less negative

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43
Q

Inhibitory Synaptic Transmission

A

Less likely to fire AP

Make next cell more negative

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44
Q

Slow Synaptic Transmission

A

Metabotropic (postsynaptic cell goes through a lot to open ion channels, time scale difference) Slow.

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45
Q

Fast Synaptic Transmission

A

Ionotropic (NT bind, communication is quick, ions in)

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46
Q

Modulatory influences mean that it’s not 1:1. Give 1 example.

A

Dopamine might make it less likely to fire

Make it more negative

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47
Q

Nervous system is not linear

A

Circular.

Posynaptic cell also influences presynaptic cell. All connected one big system.

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48
Q

What illustrates complexity of synaptic transmission?

A
  1. Chemical vs. Electrical
  2. Excitatory vs. inhibitory
  3. slow vs. fast
  4. modulation
  5. Nervous system not linear
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49
Q

Synaptic basics

A

Calcium through voltage gated ion channels

Vesicles fuse and release NT

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50
Q

What concepts reflect complexity and non-linearity?

A
  1. Multiple receptor subtypes
  2. Autoreceptors
  3. Multiple receptors from numerous inputs converge on 1 target and may interact
  4. Erosion of Dale’s Law
  5. Neuromodulation of synpases and networks
  6. INFORMATION PROCESSING BY BRAIN OCCURS ON DIFFERENT TEMPORAL AND SPATIAL
    SCALES
    7.Feedback loops in the circuit
  7. divergence—cells branch extensively to supply many target cells
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51
Q

How do autoreceptors increase complexity?

A

Presynaptic cell releases NT, auto receptor puts it back in cell. Auto receptors on PREsynaptic cell. Regulate how much NT released. Can bring NT back. Monitoring system.

SSRIs use autoreceptors. Block autoreceptors so serotonin can’t come back. Stays in synapse for longer period of time.

Mental health meds focus on auto receptors.

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52
Q

What 3 principles underlie Erosion of Dales Law?

A
  1. NEURONS CAN RELEASE MULTIPLE NEUROTRANSMITTERS (gaba and glutamate)
  2. COHABITATION; CO-RELEASE INFORMATION PRCESSING AND EXPRESSION OF BEHAVIORS IN THE BRAIN IS DISTRIBUTED ACROSS NEURAL NETWORKS (inhibitory and excitatory)
  3. SPAN DISTANT SUBCORTICAL-CORTICAL REGIONS
53
Q

Only metabotrophic receptors

A

Dopamine, Histamine, Norepinephrine

54
Q

Only Ionotrophic

A

Glycine

55
Q

Give an example of the concept that MULTIPLE RECEPTORS FROM NUMEROUS INPUTS CONVERGE INTO
TARGET AND RECEPTORS MAY INTERACT

A
  1. POST-SYNAPTIC SIGNALS CAN BE AFFECTED BY NUMBER OF NT RELEASE OR SENSITIVITY OF RECEPTORS
  2. RANGE OF POST-SYNAPTIC SIGNALS IS A COMPLEX EXPRESSION OF THESE INPUTS
  3. For instance, habituation of gill reflex is mediated by less glutamate release at presynaptic cell
56
Q

Erosion of Dale’s Law

A
  1. NEURONS CAN RELEASE MULTIPLE NEUROTRANSMITTERS

2.COHABITATION & CO-RELEASE: DIFFERENTIAL RELEASE AS A FUNCTION OF AGE, DRUGS, ETC (CO-RELEASE IS PROCESS BY WHICH 2 OR MORE NT ARE RELEASED BY A SINGLE NEURON IN RESPONSE TO AN AP)

  1. FIRING RATE OF AFFERENTS CARRYING MULTIPLE SIGNALS
57
Q

What provides the brain with COMPLEXITY (DEGREES OF FREEDOM) TO MEDIATE COMPLEXITY OF BEHAVIORAL OUTPUT?

A

Neuromodulation of synapses and networks

58
Q

Broad concept of neuromodulation

A

variety of substances (small molecule transmitters, biogenic amines, neuropeptides and others) can be released in modes other than classical fast synaptic transmission (such as metabotrophic)

this produces adaptability in behavior

59
Q

Direct effects of neuromodulation

A
  1. Presynaptic modulators target the probability of vesicular release by modifying presynaptic Ca2+ influx, size of the reserve pool, proteins in the active zone
  2. Postsynaptically, NT receptor expression and properties can be modulated to change postsynaptic responses independent of NT release.
  3. Modulation of NT release can occur through LOCAL FEEDBACK that alters the level of release through retrograde messengers or autoreceptors
  4. Neuromodulator release itself can be subject to modulation (nitric oxide (NO) can modify glutamate or serotonin, known as metamodulation)
60
Q

Indirect effects of neuromodulation

A

Indirect = change excitability of neuron

  1. Presynaptic modulation that leads to change in AP shape (e.g., can make it longer)
  2. Postsynaptic modulation increases voltage-gated inward currents to enhance excitatory postsynaptic potentials (EPSPs)

(pre AP Shape and post EPSPs through increase voltage gated inward current)

61
Q

Consequence of the complexity of nervous system?

A

complexity of the nervous system makes it difficult to understand and thus treat mental health disorder because it’s harder to study these circuits and how they relate to behavior. It’s distributed and not localized.

62
Q

Three findings that have increased degrees of freedom?

A
  1. Multiple receptor subtypes for each NT
  2. Autoreceptors: presynaptic cell, regulate amount NT release. Not a direct relationship, effects post synpatic cell
  3. Neurons can release mutliple NT (cohabitation- you have multiple NT cohabiting same neuron)
63
Q

Receptors that regulate the pre-synaptic release of NT are

A

autoreceptors

64
Q

What disorders were moved to their own chapter in the DSM-5 because they didn’t fit the old stuff?

A

PTSD and OCD

65
Q

What is volume NT introduced in 1980s and why did it get noticed?

A

In some places too many receptors, too few terminals for NT

Strange because active substances must be getting to receptors without release from adjacent terminal

Solution: NT can diffuse to extracellular space and activate receptors from long distances

NTs can be released from dendrites, soma, and axon segments

66
Q

4 types of volume transmission

A
  1. plain old exocytosis (fuse to membrane, release to synapse) (some NT float away)
  2. Extrasynaptic exocytosis: ouside of synapse. NT released onto different segment
  3. Diffusion through PM
  4. Adjaent neuomodulator and glial cell: glutamate release, activtaes ionotrophic Ca2+, NO release
67
Q

Volume vs. Wired Tranmission

A

Volume: nonjunctional complex, transmission privacy limited to specificty of NT/selectivity of receptor, one source NT release affects many targets, LONG TRANMISSION DELAY, widespread general effects, effected by agonist drugs, low energy demands

Wired: junctional, transmission privacy presence of tranmission channel for NT at synpase, 1:1 transmission, MINIMAL TRANMISSION DELAY, discrete and essential infomrmation to targets, durgs don’t work, higher space and energy costs

68
Q

WHY IT IS IMPORTANT TO APPRECIATE THE
COMPLEXITY OF THE NERVOUS SYSTEM IN MENTAL HEALTH?

A
  1. Understanding of how brain actually works
  2. lack of complex understanding means treament failure
    - Individual differences in neuronal signaling could cause treament to perform differently in any individual
    - 1/3 depressed patients don’t respond to any antidepressant
69
Q

DESCRIBE SOME FEATURES OF THE NERVOUS SYSTEM THAT DEMONSTRATE THE COMPLEXITY AND NON-LINEARITY OF THE NERVOUS SYSTEM

A
  1. Multiple receptor substypes for single NT
  2. Volume transmission
  3. Receptor interaction/cohabitation
  4. Metabotropic receptors (Slow release)
  5. Co-release different NT (Erosion Dale’s Law)
  6. Distributed Networks
  7. Autoreceptors (presynaptic regulate NT release puts NT beack in cell. Monitoring system)

Electrical = gap junctions
Chemical = NT

70
Q

What are the primary neuromodulatory systems?

A

Norepinephrine, Dopamine, Serotonin, Acetylcholine, other peptides

Typically act on metabotropic receptors; slower
response than fast acting; however, there are
instances of ionotropic modulation

71
Q

Neuromodultion produces ________________________ of behaviors

A

adaptability

72
Q

nitric oxide (NO) can modify
glutamate or serotonin, known as….

A

Metamodulation

This is a direct effect of neuromodulation. Basically, neuormodulation itself can be neuromodulated

73
Q

Not the WAYS neuromodulation happens, but what 2 big things does it change? (The main ones)

A
  1. Synaptic strength and dynamics
  2. Neuronal excitability (availability of voltage-gated ion channels)
74
Q

What does Yuste think is partly to blame for our lack of ability to explain behavioral/cognitive states and psychopathology?

A

The neuron doctrine

75
Q

Unlike the neuron doctrine, what do neural network models assume?

A
  1. Neural circuit function arises from activation of groups (Ensembles) of neurons
  2. Ensembles generate emergent functional states that can’t indentified by studying one neurons at a time

can’t understand mental health from perspective of singal neuron. Identify how individual circuits work and interact with each other over the entire brain to produce psychopathology for a given person

76
Q

According to Yuste, what are some pieces of evidence for distributed circuits?

A
  1. most neural circuits have connectivity matrix of multiple inputs and outputs
  2. Most excitatory connections are weak (seems as though each neuron is trying to integrate as many excitatory inputs as possible without saturation). In contrast, inhibitory neurons are linked by gap junctions as unit
  3. Dendritic spines: important to maximize different axons/dendrites a cell can connect to. Important for integrating different inputs

Evidence when looking at DMN: areas of the brain fire together correspond to behavior state, but across the brain

77
Q

Single neurons do not mediate beheavior. Rather behaviors rely on the function of….

A

Distributed networks

78
Q

What is the ability of active substances to travel through extracellular space (non-synaptic) to activate receptors?

A

Volume Transmission

79
Q

What allows for complex behaviors?

A

Distributed networks

Alterations in networks involved in mental health disorders

80
Q

Neural networks model assumes emergent properties. What is this?

A

when you have something distributed across networks and everything works together at different timescales and in different spatial locations, behavior emerges that you might not be able to predict just from individual parts.

Example: DMN vs. task positive network. Might assume opposite state, but fire them together, might not be able to predict behavior.

81
Q

How does memory for our experience happen?

A

Changing STRENGTH of synpatic connections

82
Q

What refers to the strengthening or weakening of synaptic connections in response to increased or decreased neuronal activation?

A

Synaptic plasticity

83
Q

Synaptic plasticity differences in time scales

A

Short term: milliseconds to minutes

Long term: hours, days, years

84
Q

Impairments in synaptic plasticity thought to
contribute to…

A

neuropsychiatric disorders

85
Q

What are the ways synaptic plasticity occurs?

What NT, Receptors, and ions are involved?

A
  1. Ions: Voltage-Gated Calcium Channels
  2. Pair pulse facilitation/depression
  3. LTP/LTD

NT: Glutamate
Receptors: NMDA, AMPA
Ions: Calcium, Sodium, Magnesium

86
Q

Ions: Voltage-Gated Calcium Channels
(Synaptic plasticity)

A

Inflex Ca2+ ions triggers AP by depolarization

AP opens voltage gated calcium channels

The channels get NT released

87
Q

Paired pulse facilitation/depression

(synaptic plasticity)

A

When two stimuli are delivered in a short interval, the second stimuli can be enhanced or depressed by the first

Depression: inactivation voltage dependent sodium or calcium channels or depletions of ready release vesicles

Facilitation (20-500ms): residual calcium from first AP or activation protein kinases. High probability of NT release, 2nd stimuli likely to depress and vis versa.

88
Q

In LTP, synaptic strenght increases due to

A

repeated activity

89
Q

In LTD, after long stimuli, what decreases?

A

Efficacy in neuron synapse

90
Q

Describe short term synpatic plasticity (depression)

(halloween candy thing)

A

Less likely for NT to be released and have EPSP.

Less likely NT outside synapse to stimuli next cell and have postsynaptic potential in cell.

AP comes down neuron. Calcium channels open, NT released into the synapse. Now second signal comes down (AP), BUT few NT now able to be release (less candy in Halloween bucket). Pretend there is a third, now even less NT available. Now postsynaptic cell probably not going to fire. Not enough NT to stimulate the postsynaptic cell. That is depression. Not enough NT left. Depletion. Depleting cell of NT, cell is depressed. That’s short term depression.

How much calcium is there to shut NT off, how much NT is there to stimulate cell? Paired pulse, not enough NT left, being depleted from pulse. Second pulse, not as much left to stimulate cell.

91
Q

Describe short term synpatic facilitation

(halloween candy thing)

A

First pulse goes down. NT is released. 2nd pulse comes at time when a bunch of calcium left in presynaptic cell. 2nd pulse adds more calcium. Addition of previous calcium with new calcium releases a bunch of NT. That is going to stimulate the postsynaptic cell to make it more likely to polarize. Mechanism by which facilitation happens is residual calcium. Calcium still there, then you add to it. Confusing because they are opposite processes.

92
Q

Why sometimes depression sometimes facilitation?

A

With residual calcium, even if you don’t have that much NT left, with so much calcium, release larger % of what is left.

Depression, a smaller percentage released because you don’t have as much calcium around. 10 NT round 1, 6/10 released, 60% in first AP. Now only 4 left. So for depression, now 2nd AP comes down, you only release maybe 2/remaining 4 or 1/remaining 4, don’t have that much calcium.

But facilitation, you have calcium and residual calcium and additional, so even only 4 left during 2nd round, calcium means you release larger %. End up with more NT released even though some depletion. These can also happen at the same cell.

**Depression of facilitation depends on probability of NT release, and recent behavior at particular cell. **Ex: Huge AP, depolarized cell and release a ton of NT, probability of release goes down, not a lot left to repackage. But smaller signal, 2nd pulse likely increase probability of release. More NT around release. Determines if depression of facilitation at that time. What % NT released depends on calcium at that time.

93
Q

Short term synaptic plasticity:
1. What does it adapt and change?
2. What is it triggered by?
3. Process?

A
  1. Short term adaptations to sensory inputs,
    transient changes in behavioral states, short
    lasting forms of memory
  2. Triggered by short bursts of activity causing
    transient accumulation of calcium in presynaptic
    nerve terminals
  3. Increase in calcium causes changes in probability of NT release by modifying exocytosis
94
Q

Paired pulse facilitiation

A

2 stimuli delivered within a short interval

Facilitation: residual calcium left over from first AP, residual has not yet been uptaken (first action potential releases 10%, second
releases 20%)

95
Q

Paired Pulse Depression

A

Synaptic depression **decreases the ability of
synapses to release NT vesicles **

2 stimuli delivered within a short interval

Depression: occurs from
1. inactivation of voltage dependent sodium or calcium channels or
2. transient depletion of pool of vesicles

First action potential releases 10%, 10 vesicles are
released, 90 left. If have second action potential, 10% of 90 (9) so fewer are released and the amplitude of EPSP is smaller (depletion).

96
Q

Facilitation vs. Depression depends on cell’s history of what two things?

A

Activation and timing

97
Q

Can the same synapse display facilitation or depression?

A

Yes

98
Q

High P vs. Low P

A

P = Probability NT release

High P = depression
Low P = Facilitation

99
Q

Example of facilitation:
1. initial signal
2. second signal
3. result

A

Small inital signal, larger second signal, residual Ca2+

100
Q

Example of depression:
1. initial signal
2. second signal
3. result

A

Large intial signla, small second signal, depletion of vesicles

101
Q

What is the process that strengthens synaptic connections with frequent activitation and underlies learning and memory by strenghting synaptic connections?

A

LTP

102
Q

What hippocampus important?

A

Memory
Subfields classic to study LTP/LTD

Large number of gluatmate receptors in Hippocmpuas

103
Q

What are glutamate’s receptors?

A

NMDA and AMPA

Ionotrophic

104
Q

Glutamate NMDA receptors

A

blocked by Magnesium

need glutamate binding AND depolarization to open

Magnesium needs + charge in cell to repell out

When open, Na+ and Ca2+ can enter

105
Q

Gluatmate AMPA receptor process

A

Glutamate taken up, lets in + ions
Let’s in sodium

106
Q

Describe the persistence of LTP

A

Depends on new protein synthesis and transcirption in nucleus of cell

Signaling of nucleus depends on protein kinases (PKA, CaMKIV, Erk-MAPK)

Active transcription factors that promote expression of genes for maintaining synaptic enrichment

ultimately: Structural remodeling

107
Q

What do we mean by structural remodeling in LTP?

A

growth of new dendritic
spines, enlargement of spines, splitting spines

Structural remodeling: postsynaptic cell. huge response, gene expression happens, growth factors grow more spines. Now even more ways to take NT in and have signal potentiated.

108
Q

Are there other ways to get learning, not just LTP and LTD?

A

Yes, example: HM and his procedural memories

109
Q

LTD mechanisms

A

Modest increase in postsynaptic Ca2+ in dendritic spines due to modest NMDAR –> activation of protein phosphatase

Eventually leads to reduction of AMPAR

Longer term maintenance of LTD is being studied, might be releated to dendrite shirnkage

110
Q

Fear in RDoC

A

Molecules: Glutamate, NMDAR
Cells: neurons
Circuits: Central Nucleus, LatAmygala
Behavior: Freezing
Paradigms: Fear conditioning

111
Q

Fear conditioning in the brain

A

Associative memory depends on amygdala for induction and maintenance

Thalamus (presynpatic) amygdala recieves inputs (postsynaptic)

Central nuleus important for fear expression

Emotional stimulus –> audiotry thalamus –> laternal nucleus of amygdala to accessory basal and basal to centeral, then to lateral hypothallamus for synpathetic activitaiton.

112
Q

In Fear Conditioning, LTP at sensory input to ________

Fear conditioning induces synpatic potentiaion between thalamic and amygadala inputs into increase what?

Where there are thalamic synapses on lateral amygdala neurons, what happens?

A
  1. Lateral amygdala
  2. Synpatic Strength
  3. Insertion of new AMPARs
113
Q

Explain the cellular hypothesis of fear conditioning

A

Happens in lateral amygdala neurons

Glutamate causes depoalrization and opening of NMDAR and AMPA via US (loud noise/shock)

CS (tone sound/animal): EPSP, not enough to open NMDA. Pair CS and US. NMDA removes the magnesium and tons of + ions come rolling in. Some go to the cell nucleus to insert new AMPA receptors, other calcium diffuses to adjacent spines.

Now the EPSP is very big and the NMDA receptor is open. Gluatamte only opened the AMPAs before, but now, more AMPA receptors, so it depolarizes the cell so much that it removes the magnesium so the NMDA recpetors open too.

114
Q

Why is animal research beneficial?

A

Controlled paradigms; examine circuits

  • Patient histories are unclear; circumstances surrounding events are unclear/insufficiently remembered/reported
  • Extent of brain damage is unknown
  • Generational effects are difficult to control
115
Q

Challenges of Animal Models

A

Mouse can’t speak and model stuff like hallunications or feelings of guilt

Animal model FOR a disorder not OF

Animal models cannot mirror full extent of a given neuropsychiatric disorder

116
Q

Construct Validity of an animal model

A

To what extent the animal model matches a human diesease?

Construct symptom should overlap in human and animal model (ex: anhedonia)

Similarity between biological dysfunction in human and animal model (ex: neural circuits of reward)

117
Q

Face Validity

A

Degree of phenomenological similarity between the model and the disorder to modeled

Often just refers to behavioral and congitive aspects of disease, not biological/circuitry

118
Q

Predictive (pharmacological) Validity

A

Signifies that a model responds to treatments
in a way that predicts the effects of those
treatments in humans

  • If SSRIs have a particular effect on depression in humans, should see that same effect in the animal model.
119
Q

Processes we can model reasonably well in animals?

A

Abnormal social behavior, motivation/reward, working memory, fear, executive functioning, anhedonia, homeostatic symptoms (sleep, appetite, weight, energy), psychomotor retardation/agitation.

120
Q

Processess that we cannot model well in animals?

A

Hallucinations, delusions, sadness, guilt, worthlessness, suicidality

121
Q

4 Animal model approaches (broadly)

A
  1. Genetics
  2. Pharmacological
  3. Enviornmental
  4. Electical simulation and lesions
122
Q

Name some genetic animal model methods and strengths and weakness

A

Selective breeding and random mutation and screening (S: phenotypes of interest; W: may produce phenocopy of human disorder)

Transgenic animal (KO, KIN, overexpression) (S: recpaituales genetic abnormallity, focus on gene of interest; W: variable penetrance of genetic abnormality in rodents, human relevance of phenotype may be difficult to establish)

Virally mediated gene delivery to brain (S: Spatial and temporal control over genetic change, focus on gene of interest; W: does not recapitulate genetic cause of human disorder)

123
Q

Describe the pharmacological animal model and it’s strengths and weaknesses

A

Administration of NT agonist or antagonist

S: temporal and some spatial (w/intracranial delivery) control; focus on NT system of interest

W: Lack of evidence that common mental disorders involve selective lesions of a single NT system

124
Q

Describe the Enviornmental animal model and it’s strengths and weaknesses

A

Chronic social stress (adult or during development), chronic physical stress

S: May recapitulate risk factors in humans, easy to administer

W: lack of specificity for a given human disorder, lack of construct validity for most human disorder

125
Q

Describe electrical stimulation and lesions animal model and its strengths and weaknesses

A
  1. Brain stimulation, including optogenetic approaches (S: spatial and temporal control over circuit function, may recapitulation some findings in humans with DBS. W: Limits in knowledge of circuit abnormalities in human disorder).
  2. Anatomical lesions (S: may produce behavioral abnormalities reminiscent of human disorders; W: lack of evidence for anatomical lesions as cause of human disorder).
126
Q

The process by which synaptic connections become stronger with frequent activiation is known as…

A

LTP

127
Q

The process by which fewer NT released due to 2 stimuli being delivered within a short interval is known as…

A

Paired Pulse Depression

128
Q

Name the animal behavioral paradigm thought to be most valid for depression?

A

Chronic social defeat stress

129
Q

Describe molecular basis of fear conditioning. How do CS and UCS impact neuronal signaling, brain circuits involved, and behavioral correlates.

A

Brain: Tone (CS) and foot shook (USC) sensory inputs to thalamus. inputs go through thalamus which then inputs to laternal nucleus of amydala. Then we go to the central medial nucleus of amygdala and then behavioral output. Fear conditioning produces potentiation between thalamic and amygdala inputs and increases the synaptic strength

Molecular: paired conditioned stimulus then depolarizaiton in lateral amygdala neuron. Na+ and Ca2+ go to postsynaptic cell and diffuse to another dendritic spine that mediates conditioni stimulus, which changes the strength of inputs and adjacent unconditione stimulus inputs are also highly polarized via diffusion of molecules. After conditioning, greater AMPA receptors on the conditioned stimulus which is thalamic input synapses on later amygdala neurons. Therefore the conditioned stumlus can have the same responses without the UCS.

Bio Psych :( (4 decks)

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