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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
Thirst signals
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
26
Explain the role of osmoreceptors
Osmoreceptors sit outside the blood-brain barrier in the third ventricle and alter their firing rate based on receptor size (they shrink and expand)
27
Hunger signals in the body
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
28
Satiety signals in the body
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)
29
Ob gene
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
30
How do hypothalamic lesions impact food intake?
Lesion in lateral hypothalamus: impacts hunger centers; patient doesn't feel the need to eat Lesion in ventromedial hypothalamus: impacts satiety centers; patient overeats
31
Hunger signals in the brain
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
32
Satiety signals in the brain
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
33
How does the hypothalamus regulate sex drives?
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
34
Neural control of sexual behavior in males
Medial preoptic area is larger --> responsible for sexual behavior Mating causes production of Fos protein Enhanced by testosterone
35
Neural control of sexual behavior in females
Primarily in the ventromedial nucleus --> responsible for sexual behavior Mating causes production of Fos protein Enhanced by estradiol and progesterone
36
Neural activity during mating
Posterior pituitary gland releases oxytocin (specifically in monogamous relationships), produced by supraoptic and paraventricular nuclei
37
Neural basis of parental behavior
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
38
Ventrolateral preoptic area
Sleep and arousal
39
Supraoptic nucleus
Thirst
40
Medial preoptic area
Male mating activity; male and female parenting behavior
41
Components of emotion
1. Behavior and actions 2. Physiological changes 3. Cognitive appraisal
42
Explain valence and arousal
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)
43
Peripheral emotional responses
Behavioral: muscle movements Autonomic: facilitates behavior (sympathetic/parasympathetic) Hormonal: adrenal medulla produces epinephrine and norepinephrine (cortisol) which reinforce fight or flight
44
Emotion in the brain
Peripheral --> hypothalamus Central --> cingulate and prefrontal cortices Both --> amygdala coordinates peripheral response and conscious experience
45
HPA-axis
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
Emotional regions of the hypothalamus
Limbic system (mammillo-thalamic tract to cingulate cortex) Ventromedial nucleus (parasympathetic; damage causes high excitability and aggression) Ventrolateral nucleus (sympathetic; damage causes placidity)
47
Limbic system
Regulates drives, motivation, and emotion Cingulate cortex, amygdala, parahippocampal areas, entorhinal cortex, hippocampus, and septal nuclei
48
Papez Circuit
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
Anterior cingulate cortex
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
Amygdala
Fear-processing and emotional conditioning Long-term memory consolidation
51
Kluver Bucy amygdala removal
Patient showed lack of fear and tendency to approach objects that should elicit fear response
52
S.M.
Bilateral amygdala damage (Urback-Wiethe disease) Did not experience fear at all; could not identify fearful expressions or draw pictures of "fear"
53
Amygdala communication
Input from cortex, ventromedial prefrontal cortex, thalamus, and hippocampus Output to hypothalamus, midbrain, pons, and medulla
54
Central nucleus of amygdala
Automatic activation by loud unexpected noises, approach of animals, heights, species-specific sounds and odors, and classically conditioned learned responses
55
Amygdala fear "feeling"
Stimulation of the ANS causes a physiological response that stimulates the amygdala to "feel" fear
56
Amygdala fear learning
Observational learning, vicarious learning, and instruction
57
Amygdala emotional memory
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
Amygdala face processing
Receives info from ventral stream via inferior temporal cortex and projects back to the V1 and higher areas
59
Cognitive component of feeling
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
Ventromedial prefrontal cortex
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
Neural basis of emotional recognition
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
Core structures of emotional processing
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
Extended regions of emotional processing
Anterior insula: feelings of disgust Primary somatosensory cortex Superior temporal sulcus: processing direction of eye gaze Anterior temporal lobe
64
Forms of learning
Perceptual, stimulus-reponse, motor, and relationalH
65
Hebbian learning
Cells that fire together, wire together
66
Cortical regions and emotion
Prefrontal cortex and cingulate cortex mediate the conscious experience of emotion as a feeling
67
Sub-cortical regions and emotions
Amygdala and hypothalamus mediate sensation of emotion and autonomic response
68
How do long-term changes indicate learning?
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
Changes in synaptic strength
Long-term potentiation (LTP) or long-term depression (LTD) underly learning
70
Specific mechanism of learning
If pathway 1 is active, that synapse will be strengthened and there will be no change to pathway 2; entirely activity-dependent strengthening
71
Associative mechanism of learning
If both pathways 1 and 2 are active, then both synapses will strengthen regardless of the strength or weakness of individual stimuli
72
Long-term potentiation
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
Long-term depression
Weakening of synapse that takes place in the cerebellum
74
NMDA
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
AMPA
Glutamate receptor found in hippocampus that gates Na+ channels Synapse strengthens due to insertion of more AMPA receptors
76
Different types of memory
Sensory, short-term, working, and long-term
77
Sensory memory
Brief; about 0.3 seconds Unattended information is lost
78
Short-term memory
Remains for seconds unless rehearsed
79
Long-term memory
Relatively permanent and can be retrieved into short-term memory Can be explicit or implicit
80
Working memory
Actively using and manipulating information from the short-term Prefrontal cortex and basal ganglia Consider visuospatial sketchpad and phonological loop schematic
81
Explicit long-term memory
Conscious memory; can be episodic or semantic Medial temporal lobe and diencephalon
82
Implicit long-term memory
Unconscious memory; can be procedural, priming, perpetual, or classical
83
Episodic memory
Memory for specific events
84
Semantic memory
General knowledge not tied to any time or place
85
Procedural memory
Knowing how to do a skill Basal ganglia
86
Priming
Changes in perception and belief caused by previous experience Neocortex
87
Perceptual learning
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
Classical conditioning
Learning about associations among stimuli Amygdala and cerebellum
89
Operant conditioning
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
How is the basal ganglia helpful to learning?
Positioned to link sensory and motor info via input to the striatum from the cortex NMDA receptors help movements to become habitual
91
How is the reward system reinforced?
Dopaminergic system starting in ventral tegmental area in the midbrain and extending to the amygdala, hippocampus, and nucleus accumbens
92
Nucleus accumbens
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
Consolidation of short-term to long-term memory
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
Anterograde amnesia
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
Language lateralization
Left-hemisphere dominant for almost all right-handed people and the majority of left-handed people
96
Broca's aphasia
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
Wernicke's aphasia
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
Dorsal language pathway`
Sound-to-motor
99
Ventral language pathway
Sound-to-meaning
100
How are different aphasias evaluated?
Fluency: flow of speech (nonfluency caused by damage to Broca's) Content: words and ideas expressed; anomia and empty speech
101
Anomia
Word-finding failures, pauses, and word errors Can be evaluated by a naming test
102
Conduction aphasia
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
General principles of development
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
Prenatal development
Neurulation, cell proliferation, and myelination
105
Developmental milestones
Gross motor, fine motor, language, cognitive, and social
106
Gray matter changes over time
Brain volume and gray matter peak around 9-14 years old
107
White matter changes over time
White matter continues to increase into adulthood, mostly linearly
108
Critical period
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
Sensitive period
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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