Essay quesitons: Chapter 17 &18 Flashcards Preview

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Flashcards in Essay quesitons: Chapter 17 &18 Deck (9)
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1

Describe the James-Lange Theory.

What were three of its weaknesses that resulted in the development of the Cannon-Bard theory. 

Describe how the Cannon-Bard Theory circumvented these weaknesses.

 

The James-Lange theory-1st physio theory of emotion suggest that there is a stimulus, then the perception/interpretation of the stimulus, afterwards a specific pattern of autonomic arousal emotion is experienced the issues with the

Perception of bear--> Physiological reactions --> Feeling of fear

Weaknesses to the James-Lange Theory

 1) Similar bodily changes occur regardless of the emotion that is experienced,

2) The internal organs that provide feedback to the brain are not very sensitive

3) Changes that occur in the internal organs happen too slowly to account for emotional experiences and 

  Canon-Bard’s theory attempted to fix this matter by making emotional experience and emotional expression parallel processes. That has no direct causal relation.
 

2

 Describe the neuroanatomical substrates of, and the 6 symptoms of the Kluver-Bucy Syndrome

Neuroanatomical substrates - Bilateral anterior temporal lobectomy- removal of Inferior temporal cortex and Amygdala

Symptoms of Kuver-Bucy Syndrome: 

1. Loss of fear (and tameness in monkeys)
2. Indiscriminate dietary behavior
3. Increased autoerotic, homosexual and heterosexual activity
4. Hypermetamorphosis – tendency to attend to every visual stimulus
5. Tendency to examine all objects visually (or by mouth in monkeys)
6. Visual agnosias

3

 What are the muscles that appear to be largely involved in voluntary and involuntary smiles? 

What evidences suggests that voluntary and involuntary facial expressions are controlled by different brain regions, and what are those regions? 

Describe the facial feedback hypothesis and the results from Rutledge and Hupka (1985) that support it.

 

                                   Muscles

i. Involuntary - Orbicularis oculi (eye)
ii. Voluntary - Zygomaticus major (mouth/cheek)

                                Brain regions

i. Involuntary – Motor Cortex
ii. Voluntary – Basal Ganglia


                         Facial Feedback Hypothesis

i. Facial expressions influence emotional experiences
ii. Facial expressions trigger muscle and brain interpretation making you begin to feel that emotion
iii. Rutledge and Hupka  - viewed a series of slides while making either a happy or angry face, those that were making a happy face felt more happy while viewing the slides and those that were making angry faces appeared to feel more angry.

4

Explain the basic paradigm used to study fear conditioning in rats. 

What have we learned about the brain regions involved in this form of conditioning?

 Describe the basis of PTSD in this context and the brain regions involved for the PTSD fear response.

 

 Fear conditioning is the establishment of fear to a situation that would other wise be seen as neutrl stimulus.

In rats....   
There is a tone and then a shock this is repeated over and over until the animal has learned.    Once they hear that tone again they will react fearful or defensive like freezing, increase heartrate, increase blood pressure.

 Hippocampus plays a key role in memory for spatial location
1. Bilateral hippocampal lesions block the subsequent development of a fear response to the context without blocking the development of a dear response to the explicit conditional stimulus

 Amygdala Complex and Fear Conditioning
i. Lateral nucleus of the amygdala is critically involved in the acquisition, storage, and expression of conditioned fear
ii. Both the prefrontal cortex and the hippocampus project to the lateral nucleus of the amygdala

c. PTSD
i. Persistent failure to extinguish conditioned fear
ii. Recurrent and sometimes intrusive flashbacks
iii. Medial prefrontal cortex
1. In general – individuals with PTSD have a decrease in activity in medial prefrontal cortex
2. Infralimbic cortex – responsible for inhibiting amygdala resulting in normal extinction (extinction of conditioned fear)
iv. Evidence suggests abnormalities in mPFC of PTSD patients

5

Explain the basic characteristics/components of cell-mediated and antibody-mediated immunity.

 

 Cell-mediated

  1.  Directed by T cells
  2. Macrophage ingests a foreign microorganism
  3. The macrophage then displays the microorganism’s antigens on the surface of its cell membrane, and this display attracts T cellsiv. Millions of
  4. different receptors for T cells, only a limited amount of the T cells to bind to it
  5.  Once binded, multiplication of the bound T cell, creating more T cells with the specific receptor necessary to destroy all invaders that contain the target antigens and all body cells that have been infected by the invaders

 Antibody-mediated

  1. Directed by B cells
  2. B cell binds to a foreign antigen for which it contains an appropriate receptor
  3. This causes the B cell to multiply and to synthesize a lethal form of its receptor molecules, antibodies, which are released into the intracellular fluid, where they bind to the foreign antigens and destroy or deactivate the microorganisms that possess them
  4. Memory B cells have a long life and accelerate antibody-mediated immunity if there is a subsequent infection by the same microorganism

 

6

 Describe 3 positive and 3 negative symptoms of schizophrenia, using the appropriate terminology. 

What are 3 different neurological abnormalities associated with schizophrenia?


 

 Positive – presence of things not normally there

  •  Delusions
  • Hallucinations
  • Disorganized speech
  • Grossly disorganized or catatonic behavior

 Negative – absence of things normally there

  •  Reduced expression of emotion
  • Poverty of speech (absence of normal speech)
  • Difficulty in initiating goal-directed behaviors
  • Memory impairment

Neurological Abnormalitie CNS changes in schizophrenia
1. Enlarged ventricles

  • . Reduction in gray matter
  • Shrunken cerebellar vermis
  •  Thickened corpus callosum
  • Defects in myelin sheaths in cerebral cortex
  • Abnormal clusters of neurons
  • Hypofrontality – decreased activity in prefrontal cortex (negative symptoms)

2. Hippocampal disorganization

  •  Degree of disorganization is positively correlated with severity of schizophrenia
  • Similar disorganization in parahippocampal cortex, entorhinal cortex, and cingulate gyrus
  •  Developmental? – different wiring in the brain

3.  Glutamate hypothesis of schizophrenia

  • PCP induces positive and negative symptoms of schizophrenia
  • Both positive and negative effects
  • Affects glutamate, not dopamine, specifically the NMDA receptors

 

7


Explain the regulation of the HPA axis by the amygdala and hippocampus as a biological basis for anxiety disorders. 

What are anxiolytic medications? 

How do alcohol and benzodiazepines work?

 

       Regulation of HPA by amygdala and hippocampus
 Amygdala involvement

  •  Sensory input to basolateral nucleus
  • Relayed to central nucleus
  • Related to bed nucleus of the stria terminalis
  • Activation of HPA axis

Hippocampus involvement.

  • Glucocorticoid receptors monitor cortisol releases from adrenal glands
  •  Activation of glucocorticoid receptors reduces HPA axis activity
  • Anxiolytic medications

Anxiolytis Medication: 

SSRIS

  • May be particularly good for OCD
  • Delayed effects

Benzodiazepines

  •  GABA agonists facilitate GABA-induced inhibition
  • Patients with panic disorder show reduced benzodiazepine binding sites in PET images of frontal lobes

Alcohol and Benzodiazepines

  • Alcohol and benzodiapines have GABA receptors so both are inhibitory.  Have same effect and do same thing.

8

Compare and contrast the characteristics of Type I bipolar disorder, Type II bipolar disorder, and cyclothymia.  Describe the neuroanatomical abnormalities believed to be associated with affective disorders.

 

 Type 1 bipolar disorder

  •  Mania with or without major depression
  • 1% of the population with equal occurrence in men and women

Type 2 bipolar disorder

  •  Hypomania and major depression
  • Mild mania without disruptions in judgments or performance
  • .6% of the population

Cyclothymia

  •  Hypomania with minor depression

Neuroanatomical abnormalities

  • Depression is associated with underactivity at serotonergic and noradrenergic synapses
  • Metabolic rate of subgenual anterior cingulate cortex in mania/depression
  • Proposed disruption of circuit between subgenual ACC, dorsal ACC, and amygdala

 

9

 Explain the Monoamine hypothesis and the Diathesis-stress hypothesis of affective disorders, providing evidence to support each.


 

 Monoamine hypothesis

  •  Reserpine-induced depression
  • Decreases central catecholamines and serotonin
  • Interferes with loading of nt into synaptic vesicles

Monoamine oxidase inhibitors (MAOIs)

  •  Elevate mood
  • Inhibit enzymes which destroys catecholamines and serotonin

Imipramine

  •  Inhibits reuptake of serotonin and norepinephrine
  • Hypothesis proposes that depression results from a deficit in one of the diffuse modulatory systems, but not a direct effect

 Diathesis-stress hypothesis

  • If you are genetically  perdisposed to depression, when you are faced with stressors in your life will atomatically become depressed.