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NEUR-210 > Exam 3: Lectures 18-25 > Flashcards

Exam 3: Lectures 18-25 Flashcards

1
Q

Cerebellar connections

A

Inputs and outputs from and to the spinal cord, sensorimotor cortex, and association cortices

Connects ipsilaterally to body and contralaterally to cerebral cortex

Connected to the brain via superior, inferior, and middle cerebellar peduncles

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2
Q

How does the cerebellum control movement?

A

Movement and posture, coordination and accuracy of movement, accurately timed sequences of muscle contractions required for rapid, skilled movements

Supervised motor learning driven by feedback

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3
Q

Cerebellar motor syndrome symptoms

A

Ataxia: discoordination (with timing)
Dysmetria: incoordination (overshoot and undershoot)
Dysarthria: slow, scanning speech

Staggering, wide-based gait, clumsiness, loss of calibration and “autopilot”

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4
Q

How does the cerebellum learn?

A

Modification of reflexes: e.g., vestibulo-ocular reflex
Conditioned learning: Pavlovian
Procedural learning: performance enhanced based on practice and cues at a subconscious level

Learning capacity comes from long-term changes in synaptic strength

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5
Q

How do Purkinje cells contribute to learning?

A

Repeating, geometric cellular structure of cortex and neurons has huge computational capabilities

Huge degree of branching enables cell to receive large amounts of info and integrate to a single output

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6
Q

How does the cerebellum learn motor skills differently from the cerebral cortex and the basal ganglia?

A

Cerbellum: input –> processing –> output in relation to target –> error or success –> feedback to processing level

Cerebral cortex: input –> processing –> output

Basal ganglia: input –> processing –> output –> reward or punishment –> feedback to processing

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7
Q

What are the three functional divisions of the cerebellum?

A

Vestibular, spinal, cerebral

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8
Q

Vestibular

A

Contains the flocculus (balance, eye/head coordination) and the vestibular nuclei (sends info to spinal cord)

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9
Q

Spinal

A

Contains…

Vermis: gait and posture
Intermediate zone: limb control
Interposed nuclei: send info to motor and premotor cortices
Fastigial nuclei: send info to spinal cord

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10
Q

Cerebral

A

Contains…

Left cerebellar hemisphere: coordination and non-verbal cognition
Right cerebellar hemisphere: coordination and verbal cognition
Dentate nuclei: sends to motor, premotor, and association cortices

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11
Q

Cerebellar cognitive affective syndrome

A

Affects executive, language, and spatial cognition

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12
Q

Posterior fossa syndrome

A

Mutism, dysarthria, ataxia, hypotonia, emotional lability, and personality changes

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13
Q

Cerebellar malformations

A

In the vermis: affective and social challenges
In the hemispheres: executive, spatial, and language challenges

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14
Q

Hypothalamus

A

Controls sleep, thirst, hunger, sex drive (four F’s)

Maintains homeostasis through negative feedback loops

Drives based on physiological signals, needs, and reward values

Controls the autonomic nervous system (lateral = sympathetic; medial = parasympathetic)

Links with the endocrine system via the pituitary gland

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15
Q

Chemical control of sleep

A

Fall in glycogen causes the release of adenosine; high levels of extracellular adenosine inhibits neural activity (sleepy). During sleep, neurons rest and astrocytes renew glycogen (awake)

Adenosine receptors are found in the ventrolateral preoptic region of the hypothalamus

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16
Q

How does caffeine work?

A

Acts as an antagonist on adenosine receptors; inhibits adenosine binding and temporarily increases alertness

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17
Q

Neural control of sleep

A

Alertness and wakefulness are modulated by firing neurotransmitter systems (acetylcholine, norepinephrine, 5-HT, histamine, and orexin)

Regulated by the ventrolateral preoptic region which inhibits these systems

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18
Q

Circadian rhythms

A

Sleep cycle dictated by Earth’s rotation and the day-night cycle

Regulated in the suprachiasmatic nucleus (SCN) where neurons show a 24-hour clock of rhythmic activity and negative feedback; talks to pineal gland to secrete/inhibit melatonin

Synthesized/synchronized by the retino-hypothalamic tract

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19
Q

Five important hypothalamic lobes/nuclei

A

Feeding and sex:
- lateral hypothalamus
- arcuate nucleus
- ventromedial hypothalamus

Sleep regulation:
- preoptic area
- suprachiasmatic nucleus

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20
Q

Lateral hypothalamus

A

Orexinergic neurons for arousal, feeding, and reward

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21
Q

Arcuate nucleus

A

Energy balance, receptors for hunger and satiety, reproduction, and growth hormone release

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22
Q

Ventromedial hypothalamus

A

Energy balance, glucose metabolism, sex-specific social behaviors, and female mating activity

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23
Q

Preoptic area

A

Sleep, osmoregulation, temperature regulation

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24
Q

Suprachiasmatic nucleus

A

Sleep and circadian rhythm

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25
Q

Thirst signals

A

Increase in solute concentration, decrease in body fluids, and volumetric receptors in the kidneys and heart

Processing in the supraoptic nucleus of the hypothalamus, stimulating the pituitary to release antidiuretic hormone for water retention

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26
Q

Explain the role of osmoreceptors

A

Osmoreceptors sit outside the blood-brain barrier in the third ventricle and alter their firing rate based on receptor size (they shrink and expand)

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27
Q

Hunger signals in the body

A

The stomach produces ghrelin, which is a potent stimulator of food intake and thoughts about food (receptors in arcuate nucleus)

Glucoprivation (fall in glucose levels) and lipoprivation (fall in ability to metabolize fatty acids) project signals to the brain via the vagus nerve and stimulate eating

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28
Q

Satiety signals in the body

A

Gastric distention

Peptide YY secreted by GI tract in proportionally increasing amounts to number of calories ingested

Insulin (released from pancreas in response to elevated glucose) and leptin (released from adipose tissue in the long term)

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29
Q

Ob gene

A

Found in mice and very rarely in humans

Causes animal to have low metabolism; animal overeats, is obese, and often has diabetes in adulthood

Cannot produce leptin from adipose tissue

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30
Q

How do hypothalamic lesions impact food intake?

A

Lesion in lateral hypothalamus: impacts hunger centers; patient doesn’t feel the need to eat

Lesion in ventromedial hypothalamus: impacts satiety centers; patient overeats

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31
Q

Hunger signals in the brain

A

Ghrelin receptors in the arcuate nucleus –> release of NPY and AGRP excite the lateral hypothalamus –> releases melanin-concentrating hormone (LCH) and orexin –> stimulate hunger and decrease metabolic rate to preserve energy

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32
Q

Satiety signals in the brain

A

Leptin receptors in the arcuate nucleus –> inhibits release of NPY and AGRP –> reduction in MCH and orexin release –> reduction in eating behavior and increase in energy expenditure

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33
Q

How does the hypothalamus regulate sex drives?

A

Hypothalamus controls the release of hormones from the pituitary gland (this is the HPA-axis)

Hypothalamus contains some sexually dimorphic regions

Gonadotropin-releasing hormones (such as follicle-stimulating hormone or luteinizing hormone) stimulate production and release of hormones by anterior pituitary gland

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34
Q

Neural control of sexual behavior in males

A

Medial preoptic area is larger –> responsible for sexual behavior

Mating causes production of Fos protein

Enhanced by testosterone

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35
Q

Neural control of sexual behavior in females

A

Primarily in the ventromedial nucleus –> responsible for sexual behavior

Mating causes production of Fos protein

Enhanced by estradiol and progesterone

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36
Q

Neural activity during mating

A

Posterior pituitary gland releases oxytocin (specifically in monogamous relationships), produced by supraoptic and paraventricular nuclei

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37
Q

Neural basis of parental behavior

A

Maternal behavior mediated in the medial preoptic area –> activity increases after giving birth or with childcare even if subject is not a mother

Projects to the ventral tegmental area and the nucleus accumbens

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38
Q

Ventrolateral preoptic area

A

Sleep and arousal

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39
Q

Supraoptic nucleus

A

Thirst

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40
Q

Medial preoptic area

A

Male mating activity; male and female parenting behavior

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41
Q

Components of emotion

A
  1. Behavior and actions
  2. Physiological changes
  3. Cognitive appraisal
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42
Q

Explain valence and arousal

A

Valence: which motivational system is activated (positive or negative)

Arousal: intensity of activation (low to high)

Emotions are placed within the axes (looks like a Y shape)

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43
Q

Peripheral emotional responses

A

Behavioral: muscle movements

Autonomic: facilitates behavior (sympathetic/parasympathetic)

Hormonal: adrenal medulla produces epinephrine and norepinephrine (cortisol) which reinforce fight or flight

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44
Q

Emotion in the brain

A

Peripheral –> hypothalamus
Central –> cingulate and prefrontal cortices
Both –> amygdala coordinates peripheral response and conscious experience

45
Q

HPA-axis

A

Hypothalamus sends corticotropin-releasing hormone to the anterior pituitary which sends adrenocorticotropic hormone to the adrenal cortex which releases cortisol, epinephrine, and norepinephrine

Cortisol, epinephrine, and norepinephrine exert a negative feedback loop on the hypothalamus and the anterior pituitary

46
Q

Emotional regions of the hypothalamus

A

Limbic system (mammillo-thalamic tract to cingulate cortex)

Ventromedial nucleus (parasympathetic; damage causes high excitability and aggression)

Ventrolateral nucleus (sympathetic; damage causes placidity)

47
Q

Limbic system

A

Regulates drives, motivation, and emotion

Cingulate cortex, amygdala, parahippocampal areas, entorhinal cortex, hippocampus, and septal nuclei

48
Q

Papez Circuit

A

Links the prefrontal and cingulate cortices with limbic system, amygdala, and hypothalamus

Thinking/feeling stream: cingulate –> hippocampus –> amygdala

Body response stream: hypothalamus –> body –> thalamus

49
Q

Anterior cingulate cortex

A

Limbic drive in the Papez circuit; dictates what to attend to and what to ignore

Involved in motor control, pain perception, social interactions, and attention

Monitors current state and incoming info with potential affective/motivational consequences

50
Q

Amygdala

A

Fear-processing and emotional conditioning

Long-term memory consolidation

51
Q

Kluver Bucy amygdala removal

A

Patient showed lack of fear and tendency to approach objects that should elicit fear response

52
Q

S.M.

A

Bilateral amygdala damage (Urback-Wiethe disease)

Did not experience fear at all; could not identify fearful expressions or draw pictures of “fear”

53
Q

Amygdala communication

A

Input from cortex, ventromedial prefrontal cortex, thalamus, and hippocampus

Output to hypothalamus, midbrain, pons, and medulla

54
Q

Central nucleus of amygdala

A

Automatic activation by loud unexpected noises, approach of animals, heights, species-specific sounds and odors, and classically conditioned learned responses

55
Q

Amygdala fear “feeling”

A

Stimulation of the ANS causes a physiological response that stimulates the amygdala to “feel” fear

56
Q

Amygdala fear learning

A

Observational learning, vicarious learning, and instruction

57
Q

Amygdala emotional memory

A

Bilateral degeneration leads to no increase in memory of part of story accompanied by gruesome photos –> means that amygdala encodes stronger memory when related to strong emotions

58
Q

Amygdala face processing

A

Receives info from ventral stream via inferior temporal cortex and projects back to the V1 and higher areas

59
Q

Cognitive component of feeling

A

Ventromedial prefrontal regions connect with emotional processing areas in the amygdala

Dorsolateral prefrontal regions connect with non-emotional sensory and motor areas in the basal ganglia and parietal cortex

60
Q

Ventromedial prefrontal cortex

A

Includes medial orbitofrontal cortex

Input from: thalamus, temporal cortex, ventral tegmental area, olfactory system, and amygdala

Output to: cingulate cortex, hippocampus, temporal cortex, lateral hypothalamus, amygdala, and other PFC areas

Performs complex analyses of social situations, including inhibiting emotional responses and using emotion to guide behavior (damage means patients can only hypothetically understand how to respond to an emotional situation)

61
Q

Neural basis of emotional recognition

A

Amygdala can recognize particular facial expressions, especially fear

Superior temporal sulcus perceives direction of gaze

Insula and basal ganglia recognize facial expressions of disgust

62
Q

Core structures of emotional processing

A

Amygdala: physiological response

Nucleus accumbens: reward pathway

Hypothalamus: physiological response and release of hormones from pituitary

Orbitofrontal cortex and ventromedial prefrontal cortex: cognitive appraisal of emotional response and regulation of emotional state

Anterior cingulate cortex

63
Q

Extended regions of emotional processing

A

Anterior insula: feelings of disgust

Primary somatosensory cortex

Superior temporal sulcus: processing direction of eye gaze

Anterior temporal lobe

64
Q

Forms of learning

A

Perceptual, stimulus-reponse, motor, and relationalH

65
Q

Hebbian learning

A

Cells that fire together, wire together

66
Q

Cortical regions and emotion

A

Prefrontal cortex and cingulate cortex mediate the conscious experience of emotion as a feeling

67
Q

Sub-cortical regions and emotions

A

Amygdala and hypothalamus mediate sensation of emotion and autonomic response

68
Q

How do long-term changes indicate learning?

A

On the cellular level, learning only occurs with repetitive, long-lasting, and persistent changes to the networks of the brain

Molecular level occurs within and between individual neurons or groups of neurons

Systems level occurs in the connectivity and functionality of larger systems

69
Q

Changes in synaptic strength

A

Long-term potentiation (LTP) or long-term depression (LTD) underly learning

70
Q

Specific mechanism of learning

A

If pathway 1 is active, that synapse will be strengthened and there will be no change to pathway 2; entirely activity-dependent strengthening

71
Q

Associative mechanism of learning

A

If both pathways 1 and 2 are active, then both synapses will strengthen regardless of the strength or weakness of individual stimuli

72
Q

Long-term potentiation

A

Strengthening of synapses that takes place in the hippocampus

Activity in presynaptic neuron and depolarization of postsynaptic neuron necessary –> NMDA receptor unblocked –> glutamate binds and opens Ca++ channel –> Ca++ activates cascade which brings AMPA receptors to membrane –> aynapse is strengthened and more efficient

Also presynaptic increase in glutamate release via NO retrograde signals

73
Q

Long-term depression

A

Weakening of synapse that takes place in the cerebellum

74
Q

NMDA

A

Glutamate receptor found in hippocampus that gates Ca++ channels

Ca++ channels are blocked by Mg++ until postsynaptic neuron is depolarized

This is why both depolarization and NT presence are necessary

75
Q

AMPA

A

Glutamate receptor found in hippocampus that gates Na+ channels

Synapse strengthens due to insertion of more AMPA receptors

76
Q

Different types of memory

A

Sensory, short-term, working, and long-term

77
Q

Sensory memory

A

Brief; about 0.3 seconds
Unattended information is lost

78
Q

Short-term memory

A

Remains for seconds unless rehearsed

79
Q

Long-term memory

A

Relatively permanent and can be retrieved into short-term memory

Can be explicit or implicit

80
Q

Working memory

A

Actively using and manipulating information from the short-term

Prefrontal cortex and basal ganglia

Consider visuospatial sketchpad and phonological loop schematic

81
Q

Explicit long-term memory

A

Conscious memory; can be episodic or semantic

Medial temporal lobe and diencephalon

82
Q

Implicit long-term memory

A

Unconscious memory; can be procedural, priming, perpetual, or classical

83
Q

Episodic memory

A

Memory for specific events

84
Q

Semantic memory

A

General knowledge not tied to any time or place

85
Q

Procedural memory

A

Knowing how to do a skill

Basal ganglia

86
Q

Priming

A

Changes in perception and belief caused by previous experience

Neocortex

87
Q

Perceptual learning

A

Recalibration of perceptual systems as a result of experience

Reflex pathways and sensory association cortices; stimulus-dependent circuits such as FFA and PPA

Recognizing stimuli (faces, sounds, smells, voices, etc.)

88
Q

Classical conditioning

A

Learning about associations among stimuli

Amygdala and cerebellum

89
Q

Operant conditioning

A

Response based on outcome (reinforcement or punishment)

Supported by connections between sensory association and motor areas via cortico-cortical connections, hippocampus, basal ganglia, and thalamus

90
Q

How is the basal ganglia helpful to learning?

A

Positioned to link sensory and motor info via input to the striatum from the cortex

NMDA receptors help movements to become habitual

91
Q

How is the reward system reinforced?

A

Dopaminergic system starting in ventral tegmental area in the midbrain and extending to the amygdala, hippocampus, and nucleus accumbens

92
Q

Nucleus accumbens

A

In the basal forebrain; projects to the basal ganglia

Releases dopamine due to stimulation of VTA by administration of artificial stimulants or natural stimuli such as food, water, and sex

93
Q

Consolidation of short-term to long-term memory

A

Hippocampus processes info from sensory and motor cortices, basal ganglia, and amygdala –> modifies memory via projections back to areas that link together and preserve relationship

94
Q

Anterograde amnesia

A

Loss of ability to lay down new memories; can carry conversations in short-term memory but cannot convert to long-term

Caused by temporal lobe and hippocampal damage

H.M. and Clive Wearing

95
Q

Language lateralization

A

Left-hemisphere dominant for almost all right-handed people and the majority of left-handed people

96
Q

Broca’s aphasia

A

Impairment in speech planning and production, results in sparse, halting speech, misarticulated, and grammatical

Nonfluent

Impairment in phonological motor programs (Lichtheim model)

Lesion in Broca’s (inferior frontal gyrus)

97
Q

Wernicke’s aphasia

A

Speech comprehension deficit resulting in unintelligible, yet fluent speech

Fluent aphasia; speech includes frequent errors, paraphasias, and inability to repeat

Impairment to word sound lexicon (Lichtheim model)

98
Q

Dorsal language pathway`

A

Sound-to-motor

99
Q

Ventral language pathway

A

Sound-to-meaning

100
Q

How are different aphasias evaluated?

A

Fluency: flow of speech (nonfluency caused by damage to Broca’s)

Content: words and ideas expressed; anomia and empty speech

101
Q

Anomia

A

Word-finding failures, pauses, and word errors

Can be evaluated by a naming test

102
Q

Conduction aphasia

A

Disrupts connection between word sound lexicon and phonological motor programs (Lichtheim model)

Can understand and produce speech with mostly good content, but cannot repeat (poor verbal working memory)

Phonemic paraphasias (pike instead of pipe) and successive approximation

103
Q

General principles of development

A
  1. Development follows predictable patterns with typical variations
  2. Change over time (maturation and learning)
  3. Nature and nurture
  4. Sensitive and critical periods
  5. Plasticity (insult and learning)
104
Q

Prenatal development

A

Neurulation, cell proliferation, and myelination

105
Q

Developmental milestones

A

Gross motor, fine motor, language, cognitive, and social

106
Q

Gray matter changes over time

A

Brain volume and gray matter peak around 9-14 years old

107
Q

White matter changes over time

A

White matter continues to increase into adulthood, mostly linearly

108
Q

Critical period

A

Begins and ends abruptly and results in permanent changes to brain structure and function

For example, early visual deprivation caused complete lack of visual ability

109
Q

Sensitive period

A

Impact of experience is not consistent throughout life; the brain’s sensitivity to experience changes depending on developmental stage

NEUR-210 (3 decks)

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