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BCS 110 > Exam 4: Mental Functions > Flashcards

Exam 4: Mental Functions Flashcards

1
Q

Executive functions

A

Management (regulation, control) of basic cognitive processes including attention, working memory, and task flexibility

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2
Q

Personality

A

Individual differences among people in behavior patterns, cognition, and emotion

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3
Q

Morality

A

Differentiation of intentions, decisions, and behaviors between those that are good or right and those that are bad or wrong

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4
Q

What lobes carry out executive functions and express personality and morality?

A

Pre frontal lobes (“silent lobes”)

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5
Q

3 ways to define prefrontal cortex

A
  1. Non-motor area
  2. Granular frontal cortex (layer 4 present)
  3. Projection zone of DM nucleus of thalamus (gates info to and from prefrontal)
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6
Q

What does the executive system do? (4)

A
  1. Forms goals and objectives
  2. Devises plans of actions
  3. Selects cognitive skills needed, coordinates and applies skills
  4. Evaluates our actions as success or failure
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7
Q

What area of the brain forms the plan of action?

A

DLPFC

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8
Q

What part of the brain is the attention controller?

A

PPC

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9
Q

What part of the brain signals a need for adjustment

A

Dorsal anterior cingulate cortex

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10
Q

What does the Wisconsin Card Sorting Test test?

A

DLPFC- ability to switch gears

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11
Q

What does the Stroop Test test?

A

dACC- signals need for adjustment

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12
Q

Where is short-term memory (or working memory) and long-term plans processed?

A

In prefrontal cortex- DLPFC & VLPFC

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13
Q

What areas of the brain are involved in intelligence?

A
  • DLPFC
  • Parietal lobe
  • Anterior cingular cortex
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14
Q

Big 5 personality traits

A
  1. Openness
  2. Extroversion
  3. Conscientiousness
  4. Agreeableness
  5. Neuroticism
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15
Q

Extraversion associated brain region

A

Medial orbito-frontal cortex

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16
Q

Conscientiousness associated brain region

A

Middle frontal gyrus

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17
Q

Neuroticism associated brain regions

A
  • DMPFC
  • Cingulate gyrus/caudate
  • Medial temporal lobe
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18
Q

Agreeableness associated brain regions

A
  • Superior temporal sulcus

- Posterior cingulate cortex

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19
Q

Brain area for implicit moral issues

A

Left temporopatietal junction (TPJ)

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20
Q

Brain area for explicit making of moral right and wrong judgments

A

VMPFC

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21
Q

Frontal lobe syndromes- Dorsolateral (3)

A
  1. Perseverative behavior
  2. Field-dependent behavior
  3. Mental rigidity
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22
Q

Frontal lobe syndromes- Orbitofrontal

A
  • opposite of DL syndrome
  • behaviorally and emotionally disinhibited
  • oscillating between euphoria and rage
  • poor to no impulse control
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23
Q

Intracranial self-stimulation (ISS)

A

Brief bursts of weak electrical stimulation to pleasure centers, involved in mesotelencephalic dopamine system

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24
Q

What two midbrain areas of neurons is the mesotelencephalic dopamine system in?

A
  1. Substantial nigra

2. Ventral tegmentum

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25
Q

Nigrostriatal pathway

A

Substantia nigra neurons project to dorsal striatum (degenerate in Parkinson’s)

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26
Q

Mesocorticolimbic pathway

A

Ventral tegmental area neurons project to cortical and limbic sites, including nucleus accumbens

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27
Q

What type of pleasure is the mesocorticolimbic pathway involved in?

A

Anticipatory (NOT actual)

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28
Q

Inputs to ventral tegmentum (3)

A
  1. Glutamatergic excitatory input (PFC & LH)
  2. GABAergic inhibitory input (VTA interneurons and NAc)
  3. Dopaminergic input (from VTA to PFC and NAc)
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29
Q

What 2 structures does the nucleus accumbens excite?

A
  1. PFC (via the ventral palladium)

2. DM nucleus of thalamus

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30
Q

Role of NAc

A

Anticipatory reward pathway, natural reinforcers (ex: food)= increased dopamine

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31
Q

How do psychoactive drugs work?

A

Cross BBB and alter the way nerve cells send, receive, and process info=affects behavior, overstimulate reward circuit

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32
Q

Tolerance (2)

A
  1. Given dose has less effect
  2. Need larger dose to produce same effect
    - Shift in dose-response curve to right, can be metabolic or functional
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33
Q

Tobacco effect on reward circuit

A

Nicotine binds to acetylcholine receptors on dopaminergic neurons in the VTA. Channels opened, sodium flows in and depolarizes cell–> increased release of dopamine in NAc.

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34
Q

Alcohol effect on reward circuit

A

Ethanol reduces the activity of voltage-dependent
potassium channels in VTA neurons. As a result, the relative refractory period of VTA dopaminergic neurons is reduced, allowing them to fire more often. High
rates in VTA neurons–> increased release of dopamine in NAc.

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35
Q

Marijuana effect on brain circuit

A

THC binds to CB1 (anadamide) receptors on GABAergic inputs in the VTA, reducing calcium influx and thus transmitter release. VTA dopaminergic neurons can thus fire more often–> increased release of dopamine in NAc.

36
Q

Amphetamine effect on reward circuit

A

Competes with dopamine for “re”uptake in the NAc.
Once inside the terminal button, it causes reuptake transporters to reverse their mode of operation. The net effect is to increase the level of dopamine in the NAc.

37
Q

Cocaine effect on reward circuit

A

Cocaine acts as a serotonin-norepinephrine-dopamine
reuptake inhibitor [known as a triple reuptake inhibitor (TRI)]. Cocaine prevents dopamine reuptake in the NAc,
thus high levels of dopamine persist.

38
Q

Opiate effect on reward circuit

A

Opiates bind to endogenous opiate receptors on VTA
GABAergic neurons, enhancing potassium efflux and thus reducing transmitter release. VTA dopamine neurons are disinhibited–> increased release of dopamine in NAc

39
Q

6 basic human emotions

A
  1. Anger
  2. Happiness
  3. Surprise
  4. Disgust
  5. Sadness
  6. Fear
40
Q

James-Lang Theory (1884)

A

Stimulus triggers autonomic and somatic responses which triggers emotion (“I am trembling; therefore, I am scared”)

41
Q

Cannon-Bard Theory (1915)

A

Stimulus triggers both autonomic and somatic responses and emotion (physiological responses & emotion are independent)

42
Q

Modern view of emotions

A

All factors influence one another

43
Q

Limbic system and emotions (3)

A
  1. Cingulate gyrus
  2. Amygdala
  3. Hypothalamus
44
Q

Anterior Cingulate Cortex (ACC)

A
  • Dorsal: DLPFC & PPC

- Ventral: Amygdala & Hypothalamus

45
Q

What are lesions of the ACC associated with?

A

Fear, irritability, and depression

46
Q

3 nuclei groups of amygdada

A
  1. Corticomedial- receive olfactory input
  2. Basolateral-receive non-olfactory input
  3. Central nucleus-major output
47
Q

Lesions to what structures block fear conditioning to simple tones?

A

MGB and amygdala

48
Q

What circuits does the amygdala activate? (2)

A
  1. Behavioral circuits in periaqueductal gray

2. Sympathetic circuits in hypothalamus

49
Q

Hypothalamus and aggression (2)

A
  1. Posterior hypothalamus-elicits aggression

2. Medial prefrontal cortex-inhibits/directs response

50
Q

What side of the brain does production and processing of facial expressions happen?

A

Right hemisphere

51
Q

Cytokines

A

Small proteins produced by immune cells that combat infections and communicate with the brain (particularly the hypothalamus) to elicit appropriate behaviors

52
Q

5 major psychiatric disorders

A
  1. Schizophrenia
  2. ADHD
  3. Affective disorders
  4. Anxiety disorders
  5. Tourette’s syndrome
53
Q

SZ NT effect

A

Excess dopamine –> symptoms of SZ

54
Q

Non-dopamine theories of SZ

A
  • Neuroleptics don’t alleviate symptoms for weeks, only work for some people, only reduce positive symptoms
  • Hallucinogens mimic positive symptoms (agonists of SE)
  • Anesthetics mimic negative symptoms (agonists of glutamate)
55
Q

Too much serotonin creates…

A

Positive symptoms

56
Q

Too much glutamate creates…

A

Negative symptoms

57
Q

Brain area problem in SZ

A

Enlarged ventricles and fissues, reduced brain volume

58
Q

ADHD NT effect

A

Deficient Dopamine and NE

59
Q

Brain area problem in ADHD

A

Slow developing prefrontal cortex (and PPC)

60
Q

Brain area problem in affective disorders

A
  • Reduction in overall brain size (VA Cingulate Cortex)
  • Abnormal:
    1. Amygdala (causes emotion)
    2. Hippocampus (symptoms of emotional problems)
    3. Medial prefrontal cortex (watches emotional state)
61
Q

Affective disorder NT effects

A

Low monoamines- serotonin and NE

62
Q

Neuroplastic theory of affective disorders

A

Depression is caused by reduction in synthesis of neurotrophins in cortical areas and a decrease in adult neurogenesis in hippocampus

63
Q

5 major anxiety disorders

A
  1. Generalized
  2. Phobic
  3. Panic
  4. OCD
  5. PTSD
64
Q

Neurobiology of stress and anxiety

A
  • Amygdala assesses emotional significance

- HPA cortex circuit releases cortisol (excited by amygdala and inhibited by hippocampus)

65
Q

Anxiety disorder NT effects

A

Low serotonin (b/c of comorbidity of depression)

66
Q

Brain problems in anxiety disorder

A

Too much activity in prefrontal cortex and fewer benzodiazepine binding sites, smaller hippocampus (in depression)

67
Q

Tourette Syndrome NT effect

A

Abnormality in basal ganglia-thalamus-cortex feedback circuit

68
Q

Tourette Syndrome NT effect

A

Abnormality in basal ganglia-thalamus-cortex feedback circuit, too much dopamine- effectiveness of D2 blockers

69
Q

6 major causes of brain injury

A
  1. Tumors
  2. Vascular disorders (stroke)
  3. Closed-head injuries
  4. Infections
  5. Neurotoxins
  6. Genetic factors
70
Q

2 major types of stroke

A
  1. Cerebral hemorrhage-caused by aneurysm

2. Cerebral ischemia-disruption of blood supply (usually L cerebral artery)

71
Q

Infarct

A

Area of dead tissue

72
Q

Penumbra

A

Area of dysfunctional tissue surrounding infarct

73
Q

Glutamate theory os Ischemia

A

Glutamate storm= excess glutamate leaves damaged neurons in its wake, little initial damage but substantial neuron loss detected later

74
Q

Contusions

A

Injuries that involve damage to the cerebral circulatory system, causes internal bleeding and a hematoma (bruise), can be coup or countrecoup

75
Q

Concussion

A

No contusion but a disturbance of consciousness

76
Q

CSF and closed-head injuries

A

Run along outside of blood vessels enclosed by end feet from astrocytes, washes brain and carries waste out

77
Q

2 common types of brain infections

A
  1. Bacterial infections-lead to abscesses (ex: syphilis), can inflame meninges
  2. Viral infections- attack neural tissue (rabies) or have no specific affinity for it (mumps and herpes)
78
Q

Neurotoxins

A

Can produce toxic psychosis, some can be endogenous (ex: excessive glutamate, antibodies in autoimmune disorder)

79
Q

Genetic accident

A

Causes neuropsychological disorders, Down syndrome- extra chromosome 21

80
Q

4 neuroplastic responses to brain damage

A
  1. Degeneration
  2. Regeneration
  3. Reorganization
  4. Recovery of function
81
Q

Neuroplasticity degeneration

A
  1. Axotomy (cutting axon)
  2. Anterograde degeneration (degen. of distal segment)
  3. Retrograde (degen. of proximal segment)
  4. Transneuronal degeneration (degen. spreads from damaged neurons to neurons linked by synapses)
82
Q

Neuroplasticity regeneration

A

Regrowth of damaged neurons, better in lower order vertebrates (accurate axonal growth lost in maturity), nonexistent in CNS of adult mammals (oligodendrocytes prevent growth in CNS)

83
Q

Neuroplasticity reorganization

A

Reorganization of primary sensory and motor systems observed in lab animals following damage to peripheral nerves and cortical areas (compensating)

84
Q

2 mechanisms to account for neural reorganzation

A
  1. Strengthening of existing connections through release of inhibition (quick remapping)
  2. Est. of new connections (magnitude of effect is large)
85
Q

Neuroplasticity recovery of function: 3 main ways to reduce cognitive dysfunction

A
  1. Block neurodegeneration
  2. Promote recovery
  3. Rehabilitative training

BCS 110 (4 decks)

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