B&B Neuro Flashcards

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1
Q

Functions of the hypothalamus

A
  1. Homeostatic mechanisms controlling hunger, thirst, sexual desire, sleep-wake cycles, etc
  2. Endocrine control via the pituitary
  3. Autonomic control
  4. Limbic mechanisms
    mnemonic: HEAL
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2
Q

contains axons & terminals of neurons whose cell bodies are located in the hypothalamus (supraoptic and paraventricular nuclei are the hypothalamic nuclei that have termination here)
-secretion of oxytocin & vasopressin into circulation

A

posterior pituitary

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3
Q

region where hypothalamic neurons release regulating factors carried by portal vessels to the anterior pituitary
-these can either stimulate release of hormones or inhibit release of hormones from the glandular (anterior) pituitary

A

median eminence

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4
Q

4 major regions of hypothalamus

A
  1. preoptic area
  2. anterior (supraoptic) region
  3. middle (tuberal) region
  4. posterior (mammillary) region
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5
Q

contains lateral and medial preoptic nuclei

A

preoptic area

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6
Q
  • contains supraoptic & paraventricular nuclei (these contain oxytocin & vasopressin) which project to the posterior pituitary
  • contains suprachiasmic nucleus (SCN) or “master clock”
A

anterior (supraoptic) region of the hypothalamus

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7
Q

nuclei from which descending autonomic fibers originate

A

paraventricular nuclei

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8
Q

contains the arcuate nucleus, ventromedial nucleus and dorsomedial nucleus

A

middle (tuberal) region of the hypothalamus

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9
Q

projects to the median eminence to control anterior pituitary

A

arcuate nucleus

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10
Q

includes the medial mammillary nucleus, intermediate mammillary nucleus, lateral mammillary nucleus & posterior hypothalamic nucleus

A

posterior (mammillary) region of the hypothalamus

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11
Q

lesion to this area of the hypothalamus causes insomnia

A

anterior region

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12
Q

lesion to this area of the hypothalamus destroys histaminergic neurons in the TMN, as well as orexin-containing neurons, causing hypersomnia

A

posterior region

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13
Q

hormones of the anterior pituitary (6)

A
  1. ACTH
  2. Growth hormone
  3. prolactin
  4. thyroid-stimulating hormone
  5. luteinizing hormone
  6. follicle-stimulating hormone
    * note: release is controlled by the hypothalamus via hypophysial portal system
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14
Q

hormones of the posterior pituitary (2)

A
  1. oxytocin

2. vasopressin (ADH)

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15
Q

stimulates appetite and lesion to this area of hypothalamus causes weight loss
“tells when to eat”

A

lateral nucleus of hypothalamus

“lesion lateral loss”

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16
Q

inhibits appetite and lesion to this area of the hypothalamus causes weight gain
“tells when to stop eating”

A

medial hypothalamus

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17
Q

hormone that increases appetite

A

Ghrelin

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18
Q

regulates thirst

-activated by hypovolemia or elevated body temp

A

osmoreceptors of the anterior hypothalamus

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19
Q

Detects increased body temp and activates heat dissipating mechanisms
-lesion causes hyperthermia

A

anterior hypothalamus

“cool facade” or dog pANTs to cool off

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20
Q

conservation of heat

-lesion causes poikilothermia

A

posterior hypothalamus

“hot posterior”

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21
Q

feedback loop for cortisol

A

hypothalamus releases CRH which stimulates release of ACTH by the anterior pituitary. ACTH stimulates adrenals to produce cortisol. Cortisol inhibits release of CRH.
*chronic steroid administration can cause atrophy of adrenals and abrupt discontinuation of steroids can cause life-threatening deficiency of cortisol

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22
Q

Functions of the limbic system

A
  1. Homeostatic functions: autonomic & neuroendocrine
  2. Olfaction
  3. Memory
  4. Emotions and drives
    mnemonic: HOME
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23
Q

Major structures of the limbic system (9)

A
  1. Limbic cortex
  2. Hippocampal formation
  3. Amygdala
  4. Olfactory cortex
  5. Diencephalon
  6. basal ganglia
  7. basal forebrain
  8. septal nuclei
  9. brainstem
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24
Q

nuclear complex that lies in the anteromedial temporal lobe & controls emotions and drives

A

amygdala

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25
Q

contains cholinergic neurons that provide major cholinergic innervation for entire cerebral cortex

A

nucleus basalis (of Meynert)

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26
Q

contains cholinergic neurons that project to the hippocampal formation and play important role in memory function

A

medial septal nucleus

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27
Q

mediates changes in HR, peristalsis, gastric secretion, piloerection, sweating, & other changes seen in strong emotion

A

reciprocal connections between amygdala, hypothalamus & brainstem

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28
Q

nuclei of amygdala (3)

A
  1. corticomedial
  2. basolateral
  3. central
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29
Q

connects olfaction with hypothalamus relating appetite states

A

corticomedial nucleus of amygdala

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30
Q

involved in direct and indirect connections of amygdala to cortical areas, basal forebrain & olfactory areas

A

basolateral nucleus

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31
Q

involved in rational thinking (weighing consequences based on contingency and the triggers of emotional states)

A

amygdala
prefrontal cortex
striatal & thalamic connections

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32
Q
  • expression and comprehension of affective aspects of speech
  • negative emotions
  • perception of facial expressions
A

right hemisphere

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33
Q
  • positive emotions

- language

A

left hemisphere

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34
Q

contains medium spiny neurons that modulate in the influence of dopamine
-receives projections from the VTA

A

nucleus accumbens

*drugs of abuse prolong the action of dopamine in the nucleus accumbens or potentiate the activation of neurons of the VTA & nucleus accumbens

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35
Q

Functions of the association cortex (6)

A
  1. higher-order sensory processing
  2. motor planning
  3. language processing and production
  4. visual-spatial orientation
  5. determining socially appropriate human behavior
  6. abstract thought
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36
Q

Unimodal association cortices (4)

A
  1. somatosensory association cortex
  2. Visual association cortex
  3. Auditory association cortex
  4. Motor association cortex
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37
Q

Regions of the association cortex (4)

A
  1. dominant hemisphere
  2. nondominant hemisphere
  3. frontal lobes
  4. visual association cortex
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38
Q

skilled complex motor tasks for both limbs (praxis)

  • language
  • mathematical calculation
  • analytical skills of trained musicians & sequence
  • follow written directions
A

dominant hemisphere

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39
Q
  • nonverbal functions
  • complex visual-spatial skills
  • emotional significance to language (prosody) and events
  • mathematical estimation
  • music perception (complex music in trained musicians & musical ability in untrained)
  • attention to both sides of the body
  • big picture: “overall gestalt” -> finding one’s way
A

nondominant hemisphere

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40
Q
  • contralateral neglect syndrome with lesion
  • perceptual awareness (inferior lobe governs attention)
  • lesion causes one to get lost moving from one room to another in own home
A

parietal association cortex

41
Q
  • planning, control and execution of actions
  • personality
  • lesion causes:
  • impaired restraint
  • disordered thought
  • perseveration (repetition of behavior)
  • inability to plan appropriate action
A

frontal association cortex

42
Q

mismatch of verbal or cognitive symbols with sensory stimuli

difficulty naming

A

agnosia

43
Q

inability to recognize and identify faces

A

prosopagnosia

44
Q

recognition and identification of stimuli that are attended to, particularly complex stimuli

  • right lesion: agnosia for faces & objects
  • left lesion: difficulty with language-related material
A

temporal association cortex

45
Q

recognition of voluntary behavior

A

parietofrontal mirror system

46
Q

recognition of affective behavior

A

limbic mirror system

47
Q

roles of mirror neurons

A
  1. recognition and understanding of what others are doing, as well as why they are doing it
  2. intention of interaction
48
Q

empathetic activation of motor circuits provide a link between observed actions and observer’s store knowledge of the nature, motives and consequences of his own corresponding actions
*Note: in autism there is a lack of activation of the motor system when the child observes someone performing an action -> do not understand the intentions of others

A

Direct matching hypothesis

mirror neurons

49
Q

area that lies in the opercular and triangular portions of the inferior frontal gyrus in the dominant hemisphere & produces words and sentences

A

Broca’s area

50
Q

syntax and comprehension depend upon this area

A

frontal structures

51
Q

defect in language processing caused by dysfunction of the dominant hemisphere

  • affects both spoken and written language
  • note: most common cause is cerebral infarct
A

aphasia

52
Q

Caused by infarct of left middle cerebral artery (superior division)
-decreased fluency (phrase length

A

Broca’s aphasia “expressive aphasia”

53
Q

Caused by infarct of left MCA inferior division

  • impaired comprehension (cannot follow commands)
  • normal fluency to spontaneous speech but is empty, meaningless and full of paraphasic errors
  • neologisms
  • impaired naming
  • impaired repetition
  • reading and writing fluent but meaningless
  • contralateral visual field cut
  • apraxia
  • anosognosia
  • angry or paranoid behavior
A

Wernicke’s aphasia “receptive aphasia”

54
Q

unaware of deficit

Impaired awareness

A

anosognosia

55
Q

Caused by left MCA inferior & superior infarcts

  • weakness on right side of face and paralysis of right limbs
  • impaired fluency, comprehension & repetition
  • damage to anterior language region, basal ganglia & insula, and auditory cortex
A

Global aphasia

56
Q

normal fluency and comprehension but impaired repetition

  • paraphasic errors common
  • naming impaired
A

Conduction aphasia

57
Q

inability to carry out an action in response to verbal command, in absence of any comprehension deficit, motor weakness or incoordination

A

apraxia

58
Q

disturbance of speech articulatory apparatus without language disturbance

  • foreign accent syndrome
  • effortful, poorly articulated speech with normal written language
  • may be mute
A

aphemia

59
Q

causes of agraphia without aphasia

A

lesions of parietal lobe in language-dominant hemisphere

lesions of corpus callosum (disconnect between language and motor)

60
Q

cause of alexia without agraphia

A

lesion of dominant occipital cortex extending to corpus callosum, preventing processing of visual info from right hemifield
-can’t name colors

61
Q

cause of alexia with agraphia

A

lesion of the dominant inferior parietal lobule in the region of the angular gyrus

62
Q

synaptic terminals are strengthened by correlated activity during development and will be retained or sprout new branches
-weakened by uncorrelated activity

A

Hebb’s postulate

63
Q

the time when experience and neural activity that reflects that experience have maximal effect on the acquisition or skilled execution of a particular behavior
-once this time is over, the core features of the behavior are unaffected by subsequent experience

A

Critical Period

64
Q

cortical blindness

  • loss of acuity, diminished stereopsis & problems with fusion that arise from early deficiencies in visual experience
  • most often the result of strabismus
A

amblyopia

65
Q

crossed eyes

A

esotropia

66
Q

wall eyes

A

exotropia

67
Q

two eyes cannot be aligned

A

strabismus

68
Q

two regions of the brain that can generate adult stem cells

*Note: stem cells can differentiate to glial cells, neurons and additional stem cells

A
  1. olfactory bulb

2. hippocampus

69
Q

inability to establish new memories

*lesion to hippocampus can cause it

A

anterograde amnesia

70
Q

difficulty retrieving memories prior to neuropathology

*lesion to temporal lobe may cause this

A

retrograde amnesia

71
Q

element of LTP & memory storage that ensures only events of high significance are placed in memory

A

cooperativity

72
Q

element of LTP & memory storage: paired input of weak stimulus with strong stimulus is required to cause superpolarization to expel magnesium
(AMPA + NMDA)

A

associativity

73
Q

element of LTP & memory storage: if the synapse is not activated by a stimulus, the NMDA receptors lose response to glutamate

A

synapse specificity

74
Q

functions of sleep

A
  1. restoration of brain glycogen
  2. conservation of energy
  3. consolidation of synaptic connections producing memories
75
Q

histaminergic nuclei modulate the neurons of the raphe and locus ceruleus

A

Tuberomammillary nucleus (TMN)

lateral hypothalamus secretes orexin to activate the TMN & promote waking

76
Q

neurons in thalamus are synchronized with those in the cortex “disconnecting” the cortex from the outside world
-maximal during slow wave sleep

A

Bursting (oscillatory) state

*note these neurons are tonically active when awake

77
Q
  • chronic condition affecting mostly men
  • frequent REM sleep attacks during the day
  • cataplexy (temporary loss of muscle tone)
  • may be caused by orexin-2 receptor gene
A

narcolepsy

tx: modafinil, amphetamines, methylphenidate

78
Q

detection of synchronized activity of ensembles of pyramidal cortical neurons

A

field potentials (of EEG)

79
Q

phases of a seizure

A
  1. interictal period
  2. synchronized activity within seizure focus
  3. seizure spread
  4. secondary generalization
    (2-4 = ictal phase)
80
Q

Acute confusional state with hallucinations and agitation characterized by fluctuating behavior

A

delirium

81
Q

failure of recent memory and other intellectual functions, usually with insidious onset and gradual progression

A

dementia

82
Q

delayed dementia from head trauma

A

dementia pugilistica

83
Q

multi-infarct dementia characterized by step-wise decline in cognitive function

A

vascular dementia

84
Q
characterized by personality change and disinhibition
Variants include:
-primary progressive aphasia
-progressive nonfluent aphasia
-progressive apraxia
-semantic dementia
A

frontotemporal dementia (FTD)

85
Q

headache with elevated ICP with no mass lesion

most common in adolescent females

A

pseudotumor cerebri

86
Q

can be caused by subarachnoid hemorrhage or orthostatic headache or neoplasms

A

mass effect

87
Q

vaculitis that affects the temporal arteries and other vessels supplying the eye

A

temporal arteritis

88
Q

sudden burst of aggressive behavior (sham rage) is elicited by a lesion this region of the midbrain tegmentum; stimulation causes pleasant sensation

A

septum

89
Q

location of the primary auditory cortex

A

superior band of Sylvian fissure in the temporal lobe

Wernicke’s cortex is adjacent to this

90
Q

encoding, storage and retrieval of learned information

A

memory

91
Q

storage and retrieval of material that is available to consciousness
Ex: phone number, words to a song, past event

A

declarative memory

92
Q

procedural memory
The acquisition and storage of neural associations and motor skills that are unconscious and not dependent on medial temporal portions of the brain
Ex: knowing how to sing a song

A

nondeclarative memory

93
Q

ability to hold and manipulate information in the mind for seconds to minutes while it is used to achieve a particular goal
-closely related to attention

A

working memory = short-term memory

94
Q

What would a medial temporal lobe lesion cause?

A

Impaired retrograde episodic memory. It encodes and consolidates declarative memories.
Semantic memory would be spared.

95
Q

What would a lesion to the hippocampus cause?

A

profound anterograde amnesia for declarative memory

96
Q

major long-term repository for many aspects of declarative memory

A

cerebral cortex

97
Q

LTP sequence

A

Glutamate released from presynaptic neuron binds to NMDA and AMPA receptors. AMPA receptors open and generate action potential that expels the Mg2+ blocking the NMDA channel. NMDA channel is now permeable to calcium ions. Calcium ions trigger downstream signaling pathways that increase the response of the postsynaptic cell to glutamate & increase release of glutamate from the presynaptic neuron.

Note: Memantine for Alzheimer’s disease is a noncompetitive antagonist for the NMDA receptor. It sits on the Mg2+ site.

98
Q

causes relative paralysis during REM sleep

A

increased GABAergic neuron activity in the pontine reticular formation projecting to inhibitory neurons that synapse with the LMN in the spinal cord

99
Q

main functions of acetylcholine in the CNS

A

attention, memory & learning