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Flashcards in Limbic System Deck (38)
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1
Q

% of people treated for mood disorders?

A

50%

2
Q

Five functions of Limbic system:

A
  1. mood
  2. emotion
  3. feelings
  4. motivation
  5. critical for memory
3
Q

4 limbic system pathways:

A
  1. hippocampus –> fornix –> mammilary bodies OR septal nuclei
  2. mammilary bodies –> mammilothalamic tract –> anterior nucleus of the Thalamus
  3. Amygdala –> stria terminalis –> septal nucleus
  4. midbrain via hypothalamus –> medial forebrain bundle –> forebrain
4
Q

NE is produced where?

A

Locus ceruleus (pons)

5
Q

seretonin 5HT is produced where?

A

Raphe nuclei (Ra, midbrain, pons)

6
Q

NE and 5HT role in Limbic system?

A

arousal

sleep cycle

7
Q

Mesolimbic system produces what NT?

A

dopamine

8
Q

dopaminergic neurons have cells bodies where? and project where?

A

ventral tegmental area (VTA)

project to:

nucleus accumbens

medial prefrontal cortex

amygdala

septal nuclei

9
Q

Two substances that block DA reuptake?

A

cocaine

amphetamine

10
Q

Two possible ways to decrease drug seeking behavior:

A

lesion in VTA or nucleus accumbens

DA receptor blockers

11
Q

natural rewards associated with dopamine:

A

sex

food

12
Q

two areas affected in Alzheimers associated with decreased Ach:

A

nucleus basalis

septal nucleus

13
Q

Region of Limbic system involved in fear conditioning:

A

amygdala

14
Q

impaired goal directed behavior

lack of emotion in decision making

poor social judgement

poor emotional control

…these are sx of injury to?

A

Prefrontal lobe

prefrontal lobe syndrome

15
Q

Prefrontal lobe region involved with working memory and executive function?

A

Dorsolateral

16
Q

Prefrontal lobe region sending INHIBITORY projections to amygdala?

A

Orbital frontal cortex

Amygdala usually stimulates hypothalamus

17
Q

What happens in BL hippocampal lobectomy?

A
anterograde amnesia (no new memories)
   -facts and experiences (semantic and episodic)

***can still learn motor skills (implicit memory)

18
Q

Disease involving amygdala disfunction with sx of:

  • impaired recognition of facial expressions (emotions)
  • inability to judge “like” emotions (fear vs anger, surprise vs happiness)
A

Urbach-Wiethe disease

19
Q
  1. flashbacks
  2. avoidance of situations that parralel initial trauma
  3. hyperarousal (increased anxiety)

Triad of sx for:

A

Post Traumatic Stress Disorder

20
Q

Etiology of PTSD?

A

INCREASED amygdala activity

DECREASED prefrontal cortex inhibition of amygdala–“take the brakes off”

21
Q

Fragmentation of mood, thought, and movement are sx of:

Ex: delusions, hallucinations, social withdrawal

A

Schizophrenia

22
Q

Neurochemical basis for Schitzophrenia:

A

Increased DA activity

23
Q

Anti-psychotic that blocks DA receptors:

Side effects?

A

haloperidol

motor dysfunction (Parkisonian-like)

24
Q

Atypical anti-psychotic that blocks DA receptors, 5HT receptors and glutamate reuptake

A

clozapine

25
Q

What does PCP do?

A

blocks NMDA glut receptors

Tx: increase Glut receptor activity

26
Q

Lethargy, anhedonia, and loss of sleep are sx of:

A

depression

27
Q

what is the “monoamine hypothesis” for depression?

A

decrease in NE and/or 5HT receptor activity

28
Q

Three tx’s for depression:

A
  1. MAO inhibitors
  2. tricyclics (Imiprine)
  3. SSRIs (Fluoxitine AKA Prozac)
29
Q

MOA for MAO inhibitors?

A

Blocks degredation of NE or 5HT in presynaptic neuron

30
Q

MOA for tricyclics?

A

blocks reuptake of NE and 5HT

31
Q

MOA for SSRIs (Fluoxitine/Prozac)?

A

blocks reuptake of 5HT

32
Q
  • no new memories
  • disorientation in space and time
  • confabulation

….this is the triad of sx for:

A

Karsakoff’s Syndrome

33
Q

Causes of Karsakoff’s?

A

Chronic EtOH

Vit B1 (thiamin) deficiency

34
Q

Area damaged in Karsakoff’s?

A

mammilary bodies

35
Q
  • Oral tendencies
  • changes in emotion (neutral affect due to amygdala damage)
  • hypersexuallity (increase in # and variety of sexual activities due to damage to pathways to hypothalamus)
  • visual agnosia

…these are sx of which disease?

A

Kluver-Bucy Syndrome

Temporal lobe damage

36
Q

Etiology of Alheimer’s disease:

A
  • loss of cholinergic input to hippocampus (nucleus basillis)
  • loss of neurons to multiple brain areas
  • presence of neurofibrillary tangle (NFTs: phosphorylated TAU proteins) and B-amyloid plaques
37
Q

Drug used to treat Alzheimer’s that blocks acetylcholinesterase?

A

Donepezil (Aricept)

38
Q

Progressive neurodegenerative disease caused by repeated head trauma?

A

Chronic Traumatic Encephalopathy (CTE)