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Neuro Med > Exam 6: Limbic System I > Flashcards

Exam 6: Limbic System I Flashcards

1
Q

What does the limbic system control?

A

mood, emotion, feelings, motivation; critical for memory

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2
Q

Where does the hippocampus project to? Via what?

A

Mammillary body, septal nuclei; fornix

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3
Q

Where do the mammillary bodies project to? Via what tract?

A

Anterior thalamic nucleus; mamillothalamic tract

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4
Q

Where does the amygdala project to? via what?

A

septal nucleus; stria terminalis

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5
Q

Where does the midbrain (via hypothalamus) project to? Via what bundle?

A

Forebrain; medial forebrain bundle

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6
Q

What neurotransmitter does the locus ceruleus release?

A

Norepinephrine

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7
Q

Where is the locus ceruleus located?

A

pons

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8
Q

What neurotransmitter does the raphe nuclei release?

A

serotonin

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9
Q

Where is the raphe nuclei?

A

midbrain and pons

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10
Q

What is the locus ceruleus and rephe nucleus responsible for in a humn?

A

arousal and sleep/wake cycles

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11
Q

What neurotransmitter is involved in the mesolimbic system?

A

dopamine

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12
Q

Where does the ventral tegmental area (VTA) project to? (4 different areas)

A

Nucleus accumbens, medial prefrontal cortex, amygdala, septal nuclei

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13
Q

What is the action of cocaine and amphetamines?

A

blocks DA uptake

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14
Q

Where does a lesion in the brain decrease drug-seeking behavior? How does it work?

A

VTA and Nucleus accumbens; decreases amount of dopamine in the brain that acts as a reward

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15
Q

What neurotransmitter does the nucleus basalis and septal nucleus release?

A

Acetylcholine

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16
Q

What role does the amygdala have in the limbic system?

A

fear conditioning

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17
Q

What do lesions in the amydala lead to?

A

prevents fear conditioning

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18
Q

what do lesions in the prefrontal lobe lead to?

A

Impairment in goal directed behavior, lack of emotion in decision-making (Lack of risk aversion), Poor social judgement (antisocial behavior), poor emotional control (increased impulsivity)

19
Q

What areas are involved with the symptoms of a lesion to the prefrontal lobe?

A

Dorsolateral PFC and Orbital frontal cortex

20
Q

What do lesions of the hippocampus lead to?

A

anterograde amnesia, temporally graded retrograde amnesia, explicit or declarative memory (semantic and episodic)

21
Q

T/F: motor skills are not lost in a lesion to the hippocampus

A

True

22
Q

What are symptoms of Urbach-Wiethe disease?

A

impaired recognition of emotion in facial expressions, memory loss especially of information with emotional content

23
Q

What are the symptoms of PTSD?

A

re-experiencing phenomena in the form of flashbacks, avoidance of situations that parallel initial trauma, hyperarousal/hypervigilence

24
Q

What is the etiology of PTSD?

A

increased amygdala activity, decreased medial prefrontal cortex activity (which usually plays a role in inhibiting amygdala)

25
Q

What are the positive/negative symptoms of schizophrenia?

A

Positive: delusions, hallucinations. negative: Social withdrawal

26
Q

What symptoms of schizophrenia are the target of treatment?

A

Positive symptoms: delusions and hallucination

27
Q

What are the two main hypotheses of schizophrenia?

A

Dopamine and glutamate hypotheses

28
Q

Explain the dopamine hypothesis of schizophrenia?

A

Increase in dopamine receptor activity

29
Q

What are the treatments for the dopamine hypothesis of schizophrenia?

A

haloperidol, clozapine

30
Q

What is the mechanism of action and side effects of haloperidol?

A

Blocks dopamine receptors; causes motor dysfunction (Parkinsonian like)

31
Q

What are the mechanisms of action of clozapine?

A

Block DA-receptors, block 5HT receptors, block glutamate reuptake

32
Q

Explain the glutamate hypothesis of schizophrenia? What was the idea that people though of?

A

Decrease in glutamate in synapse ; PCP blocks NMDA glutamate receptor

33
Q

What are symptoms of depression?

A

lethargy, annedonia, loss of sleep

34
Q

What is the hypothesis behind the cuase of depression?

A

monoamine hypothesis (depression due to decrease in NE and 5HT activity

35
Q

What is the monoamine hypothesis?

A

depression due to decrease in NE and/or decrease in 5HT activity

36
Q

What are the three main treatments for anti-depression? what are their actions?

A

monoamine oxidase inhibition, tricyclics (imipramine) (block reuptake of 5HT and NE, SSRI (fluoxetine) (Block reuptake of 5HT)

37
Q

What are the symptoms of Korsakoff’s syndrome?

A

Disorder of immediate memory, disorientation, confabulation

38
Q

What are the causes of Korsakoff’s syndrome?

A

chronic alcoholism, vitamin deficiency

39
Q

What is the brain etiology of Korsakoff’s syndrome?

A

damage to mamillary bodies or to mamilothalamic tract

40
Q

What are symptoms of Kluver-Bucy syndrome?

A

Oral tendencies, changes in emotions, hypersexuality, visual agnosias

41
Q

What are symptoms of alzheimer’s disease?

A

Loss of memory, mood disorder (anxiety/depression), loss of motor function, complete loss of cognitive function

42
Q

what is the etiology of Alzheimer’s disease?

A

loss of cholinergic input to hippocampus (nucleus basalis), loss of neurons in multiple brain areas, present of neurofibrillary tangles and Beta-amyloid plaques

43
Q

What are the symptoms of chronic traumatic encephalopathy

A

Cognition: anterograde amnesia, dysfunction in goal-directed behaviors. Mood: depression, apathy. Behavior: decreased impulse control, increased aggressiveness

44
Q

What is the etiology of chronic traumatic encephalopathy

A

generalized brain atrophy including prefrontal cortex, temporal lobes (amygdala, hippocampus), and parietal lobes

Neuro Med (39 decks)

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