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Exploring Neuroscience > Unit 4 > Flashcards

Unit 4 Flashcards

1
Q

*Upper Motor Neurons

A
  • Neurons in the motor system that command lower motor neurons
  • Originate (cell bodies in) the brain
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2
Q

*Lower Motor Neurons

A
  • Directly command muscle contraction (innervate muscle)
  • Last neuron in pathway
  • Originate (cell bodies) in ventral horn of SC
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3
Q

*Skeletal Muscle

A
  • Controlled by somatic motor system (voluntary control)

- Striated

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4
Q

*Cardiac Muscle, Smooth Muscle

A
  • Controlled by autonomic motor system (involuntary control)
  • Controls peristalsis, blood pressure and flow
  • Cardiac= striated, smooth= not striated
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5
Q

*Anatomy

A

muscles–> muscle fiber/muscle cell–> myofibrils

  • Motor neurons innervate muscle cells
  • Muscle fibers contract and fire APs
  • Depolarization causes release of calcium filled vesicles–> induce contraction of sarcomeres
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6
Q

*Muscle Innveration steps/ How a lower motor neuron causes a mucle fiber/cell to contract

A
  1. Lower motor neurons release ACh
  2. ACh produces large EPSP in muscle fiber
  3. EPSP evokes muscle action potential
  4. Action potential triggers Ca2+ release
  5. Fiber contracts
  6. Ca2+ reuptake
  7. Fiber relaxes
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7
Q

*Alpha Motor Neurons

A
  • A type of lower motor neuron that innervates skeletal muscles directly
  • One AMN per muscle fiber, but can innervate multiple fibers
  • Smaller motor units= finer control
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8
Q

*Motor Unit

A

-Motor neuron and all the muscle fibers it innverates

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9
Q

*Motor Neuron Pool

A

-All the AMNs that innervate a single muscle

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10
Q

*Types of Motor Units

A
  1. Slow twitch (red muscle)

2. Fast twitch (white muscle)

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11
Q

Slow Twitch (Red Muscle)

A
  • Large number of mitochondria and enzymes (myoglobin)
  • Slow to contract and slow to fatigue
  • Can sustain contraction
  • Least force, longer time
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12
Q

*Fast Twitch (White Muscle)

A

-Fewer mitochondria
-Anaerobic metabolism
-Contract and fatigue rapidly
Types: fast fatiguable and fast-fatigue resistant

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13
Q

*Fast Fatiguable

A
  • Highest force

- Smallest ammount of time

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14
Q

*Fast-Fatigue resistant

A

-Medium force and time

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15
Q

*Control of contraction by Alpha Motor Neurons

A

-Reserve maximal contraction for when needed
Control force by:
1. Varying firing rate of motor neurons
2. Recruiting additional symergistic motor units
-Recruiting more motor units that contract in that area

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16
Q

*Muscle Spindles

A
  • Specialized skeletal muscle fibers contained in fiberous capsules ( stretch receptors, intrafusal fibers)
  • Parallel w/ muscle
  • Middle third= swollen, where group 1a sensory axons wrap around muscle fibers
  • **Proprioceptors= body awareness
  • **Detect changes in muscle length
  • Contractile fibers
  • *Shorten, but don’t contribute much force
  • *Innvervated by gamma motor neurons (LMNs)
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17
Q

Group 1a Sensory Neurons

A
  • Muscle spindle receptors
  • Thickest myelinated axons in body
  • Largest and fastest conductance
  • Enter SC via dorsal roots, branch and innervate interneurons and AMNs in ventral horn
  • One 1a axon synapses on every AMN in motor pool for same muscle it originated in
  • **Fire less frequently when contracted
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18
Q

*Stretch Reflex

A
  • Alpha motor neuron fires from 1a stimulation (extrafusal)
  • Gamma Motor neuron fires from 1a stimulation (intrafusal)
  • *Only in SC, not brain
  • When a muscle is pulled, it tends to pull back (myotatic reflex= muscle stretch)
  • **Protective
  • Sensory feedback loop from muscle
  • **As muscle is stretch, firing rate increases
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19
Q

*Gamma Motor Neurons

A
  • -Bulk of muscle mass= Extrafusal muscle fibers, innervated by alpha motor neurons
  • -Muscle spindles= intrafusal muscle fibers, innervated by gamma motor neurons
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20
Q

*Muscle movement

A
  • Muscles move joints by pulling
  • Flexors= bend/contract
  • Extensors= extend muscle
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21
Q

*Reciprocal Inhibition

A

-Contraction of one muscle set accompanied by relaxation (inhibition) of antagonist muscle

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22
Q

*3 types of input to Lower Motor Neurons

A
  1. information from UMNs originating in brain (voluntary movement)
  2. Sensory info from muscle spindles (muscle length)
  3. Interneurons from SC (generate spinal programs)
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23
Q

*Spinal Interneurons

A
  • Most input to AMNs mediated by spinal interneurons
  • *Excitatory use glutamate
  • *Inhibitory use glycine
  • Synaptic input to spinal interneurons
    1. Primary sensory axons
    2. Descending axons from brain
    3. Collaterals of LMN axons
    4. Other interneurons
  • Curcuits= responsible for executinf stereotyped and reflexive movements of body
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24
Q

*Flexor Withdrawal Reflex

A
  • Doesn’t require concious input
  • Complex reflex arc used to withdraw limb from aversive stimulus
  • Depends on how painful the stimulus is and where it occurs
  • Triggered by delta A axons that branch to neighboring spinal segments (nociceptors)
  • *Slower than strerch reflex bcuz delta A axons smaller than 1a axons
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25
Q

*Crossed-Extensor Reflex

A

-Flexor w/drawal reflex in lower extremity needs to be balanced on opposite side of body
-Activation of extensor muscle and inhibition of flexors on opposite sode
Breakdown:
1. On same side of painful stim: excite flexors, inhibit extensors
2. On opposite side: excite extensors and inhibit flexors

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26
Q

*Central Pattern generators

A
  • Neuron or neurons that generate rhythmic patterns of activity
  • Circuits of spinal interneurons
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27
Q

*SIMPLE Central Pattern Generator

A
  • Reciprocal inhibition btwn 2 sets of neurons–> rhythmic output
  • UMN–> excitation and inhibition–> extensory and flexor LMNs
  • As one is excited, simultaneouslt inhibits other so limb is only flexed or extended
  • Excitations of 2 are counterbalanced–> rhythmic pattern of flexing and extending
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28
Q

*Axons descending from brain (upper motor neurons

A
  1. Lateral pathways
    - Corticospinal tract
    - Rubrospinal tract
  2. Ventromedial Pathways
    - Tectospinal tract
    - Vestibulospinal tract
    - Pontine reticulospinal tract
    - Medullary reticulospinal tract
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29
Q

*Lateral Pathways

A

-Voluntsary movement and fine coordination of distal muscles

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30
Q

*Ventromedial Pathways

A
  • Originate in brainstem
  • Voluntary movement of proximal muscles and trunk
  • Involuntary movements
  • Maintaining body position/posture
  • Defensive reactions
  • Balance
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31
Q

*Corticospinal Tract

A
  • Originates in neocortex (brain)
  • Decussates in medulla (midline)
  • Largest and longest in CNS
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32
Q

*Rubrospinal Tract

A
  • Originates in red nucleus of midbrain (brainstem)
  • Decussates in Pons (midline)
  • Vestigal, can help with recovery after injury to corticospinal
  • Controls flexing of arms
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33
Q

*Vestibulospinal tracts

A
  • Head balance, head turning
  • Close connection w/ cochlea
  • Originate in medulla (brainstem)
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34
Q

*Tectospinal Tract

A
  • Orienting responses to sights and sounds

- Originates in colliculus in midbrain (Brainstem) and has close connection to retina

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35
Q

*Pontine Reticulospinal Tract

A
  • Starts in pons (brainstem)
  • Enhances antigravity muscles
  • Maintains standing by extensor muscles in legs
  • Different than the vestibulospinal tract
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36
Q

*Medullary Reticulospinal Tract

A
  • Starts in medulla (brainstem)
  • Liberates antigravity muscles from reflex control
  • Opposite from pontine tract
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37
Q

*Pyramidal Cells/ Betz Cells

A

-Drive numerous motor pools and different muscles
*Axons in corticospinal tract
Two sources of input to Betz cells”
1. Cortical areas (area 6 anterior, areas 3, 1, and 2 posterior)
2. Thalamus (which recieves basal ganglia and cerebellar connections)
**Envolvement occurs b4 exciting corticospinal tract

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38
Q

*Primary motor cortex/ M1

A
  • Brodmann Area 4/ precentral gyrus/ motor strip/M1
  • Anterior to central sulcus
  • Organization mirrors arrangement of primary somatosemsory cortex
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39
Q

*Wilder Penfield

A
  • Stimulated primary motor cortex
  • Causes contract of small group of muscles depending on where in the motor map u stimulate
  • Direction of movement is encoded by the net result of groups of neurons firing (pop coding)
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40
Q

*Somatosensory Association Cortex

A
  • A5

- Inputs from somatosensory cortex areas 3,1, and 2

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41
Q

*Posterior Parietal Cortex

A
  • A7

- Inputs from higher orfer visual cortical areas

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42
Q

*Prefrontal Cortex

A
  • Represents highest levels of motor control
  • Decisions made about actions and outcome
  • Planning
  • Abstract thought
  • Anticipating consequence of action
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43
Q

*Premotor Cortex “higher” motor area

A
  • A6, skilled movement
  • 2 parts w/ similar fxns, diff groups of muscles innervated
  • Preparing and initiating ,ove,ent plans
  • Highly connected to M1
    1. Lateral region-> premotor area (pma)–> responds to cues to move
    2. Medial region–> supplementary motor area (SMA)–? prepares sequences of voluntary movement and active 1-2 secs before movement
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44
Q

*Steps in preparation of movement

A
  1. Ready= parietal and frontal lobes
  2. Set- area 6; supplementary and premotor areas
  3. Go- area 4
    - Mentally rehearsing movements only activates A6
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45
Q

*Basal Ganglia/ Frontostriatal System

A
  • Selection and initiation of volitional movements
  • Recieves input from neurons in frontal cortex in the striatum
  • *Provides major input to area 6
  • *Forms 2 main loops
    1. Direct pathway
    2. Indirect pathway
  • *At rest, thalamus is tonically inhibited, for motor cortx to be excited, talamus must be disinhibited
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46
Q

*Parkinson’s Disease

A
  • Trouble initiating willed movements due to increased inhibition of thalamus by basal ganglia
  • Sypt: hypokinesia, bradykinesia, akinsesia, rigidity, tremors
  • Cellular basis: Loss of input to direct pathway
  • L-dopa treatment
  • Inability to propagate movement
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47
Q

*Huntington’s Disease

A
  • Symp: chorea, hyperkinesia, dyskinesias, dimentia, personality disorder
  • Loss of indirect pathway
  • Cortical degeneration responsible for dementia and personality changes
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48
Q

*Cerebellum

A
  • Fxn: sequencing of muscle contractions, monitoring and correcting both plans and actions
    1. Copy of motor plan
    2. Vestibular and Proprioceptive input
  • Lesions–> ataxia, dyssynergia, and dysmetria
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49
Q

What happens if upper motor neurons are damaged?

A

-We lose voluntary muscle control

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50
Q

Behavior

A
  • Basic fxn of life
  • Maintains homeostasis
  • Motivated behavior= result of brain’s response to internal and external cues
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51
Q

Somatic and Autonomic NS

A
  • SNS directs quick, specific behavior
  • ANS input sets stage for general behaviors
  • -Sympathetic= fight, flight
  • -Parasympathetic= rest, digest
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52
Q

Homeostasis

A
  • Physiological mechanism respond to changes to maintain regulated set range
  • Changes identified through sensory systems
  • Ex: rxn to cold
  • -Physiological= constricted blood vessels, goose bumps
  • -Behavioral= shivering, seeking warmth (due to physiological)
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53
Q

Cycle of Homeostasis

A

-Imbalance–> change detected by receptor–> input via afferent pathway sent to control center–> output sent via efferent pathway to effector–> response to change= imbalance corrected

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54
Q

Hypothalamus

A
  • Essential for maintaining homeostasis
  • Directly linked to pituitary gland (allows control/comm over periphery)
  • Specific cells responsive to particular stimuli (direct or indirect)
  • Produces wide variety of neuropeptides
  • –Projects to forebrain, brainstem
  • –Direct release into periphery via pituitary
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55
Q

Magnocellular neurons

A
  • Express oxytocin, vasopressin

- Release to periphery

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56
Q

Parvocellular neurons

A
  • Express CRH and other neuropeptides

- Produce effects in periphery

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57
Q

Neurohormones

A
  • Hormones produced in the brain
  • Can act at distant sites throughout the body
  • Actions start and last on a relatively longer time scale than neurotransmitters
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58
Q

Vasopressin and Fluid regulation

A

-Hypothalamus gets input from blood volume and salt concentration
Low blood volume –> Angiotensin II detected by SFO —> vasopressin cells in hypothalamus.
-SFO–> lateral hypothslamus (promotes drinking behavior)
One of the results: kidneys retain water

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59
Q

Leptin

A
  • Peptide
  • Secreted from fat cells, activate lepin receptors in arcuate nucleus of the hypothalamus
  • Decreased leptin stimulates feeding behavior
  • Secretion response: increased metabolism
  • ANS response: increase sympathetic activity and metabolism
  • Somatic/ behavior response: inhibit feeding behavior
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60
Q

Homeostasis of Body Weight

A
  • Short term regulation of feeding
  • Satiery signals: Gastric distension, CCK peptide from intestines, Insulin acts on hypothalamus
  • Orexigenic signals: ghrelin from stomach, orexin in lateral hypothalamus
61
Q

Optogenetic stim of lateral hypothalamus

A
  • Mice eat more food when projections in lateral hypothalamus are activated
  • Importance of connections btwn BNST and lateral hypo in feeding
62
Q

Anterior Pituitary

A
  • Gland w/ secretory cells
  • Hypothalamic-pituitary portal system= capillary bed that carries neurohormone in blood , leads to action in pituitary
  • Neurohormones act on hormone-secreting cells in Ant P to affect other hormone release in bloodstream
63
Q

HPA Axis

A
  • Regulates stress response
  • Hypothalamus –> produces CRH and released to anterior pituitary
  • Anterior Pituitary–> Produces ACTH, releases to periphery
  • Adrenal gland–> produces cortisol and releases to bloodstream
  • Negative feedback in hypothalamus turns off stress response
64
Q

Steroid Hormones

A
  • Derived from cholesterol
  • Ex: CORT, primary stress hormone
  • ACTH cleaved from POMC
65
Q

CORT

A
  • Serves to maintain homeostasis
  • Stessors produce imbalance
  • HPA axis is activated
  • CORT produces response by binding to glucocorticoid receptors
  • negative feedback–> HPA axis goes to baseline by CORT binding to receptors to turn off HPA activation
66
Q

Stress chart

A

Stress-> hypothalamus–CRH–> pituitary– ACTH–> Adrenals–CORT–> Blood

67
Q

CORT levels

A
  • Rise b4 waking up and peak shortly after (be alert)
  • Altered by many neuropsychiatric disorders, linked with symptoms of changes in sleep and appetitw
  • -Higher at baseline in depressed patients
68
Q

Stress levels and learning

A
  • Sometimes stress is helpful
  • Hippocampus- important in learning and memory, responds to cortisol from HPA axis
  • Acute stress aids in learning (esp emotional learning)
  • Chronic/ high stress impairs most learning and memoru
69
Q

Motivated Behavior

A
  • Action that has drive or goal behind it
  • -Homeostatic mechanism (ex: eating to maintain energy levels)
  • —-Drive reduction theory (eating to reduce hunger)
  • —-Hedonic sensation (pleasure or reward)
  • Cog goal-driven process= studying to get a degree
70
Q

Reward

A

-A feeling of pleasure in response to stimulus

71
Q

Reinforcer

A
  • A stimulus that makes a behavior more likely to occur again
  • *Presumably has reward properties
72
Q

Intracranial self-stimulation

A
  • Experiment by Olds and Milner
  • Rats would learn to press lever to recieve electrical stimulation in the brain
  • only in certain regions that would sustain behavior= medial forebrain bundle= reward pathway
73
Q

Mesocorticolimbic dopamine pathway

A
  • Essential for reward
  • VTA->PFC–> Nucleus Accumbens
  • Dopamine neurons in VTA fire in response to reward
  • W/ learned associations, neurons increase firing to cues that predict rewards
  • –Decresse firing when reward is absent
74
Q

Food reward and homeostatic drive

A
  • Interact to control feeding behavior
  • Nucleus accumbens releases dopamine, increases food intake (reward signal)
  • Serotonin release in hypothalamus increases w/ food- satiety signal
75
Q

Drugs and reward

A
  • Better at activating reward pathway that natural rewards
  • EX: cocaine acts directly on dopamine pathway by blocking dopamine transport/ reuptake–> more dopamine in synapse
  • Other drugs increase dopamine release
  • -Heroine acts on opiod receptors= stimulates DA neurons
  • -Nicotine acts on ACh receptors= stimulates DA neurons
76
Q

Drug use and Homeostatic set points

A
  • Cause imbalance in normal neural fxn, cells response to and maintain homeostasis
  • Repeated drug used–> new homeostatic set point/ allostasis–> Drug use becomes necessary to maintain homeostasis, w/o causes withdrawals
77
Q

Sex

A
  • Biological sex= male or female
  • Genetically determined
  • Hormonally controlled
78
Q

Gender

A
  • Categories on a spectrum
  • Socially/structurally determined
  • Placement= psychologically/personally determined
  • Elements of hormonal control, experience, and culture
  • Male or female in our culture, but other cultures differ
79
Q

Biological Sex Differences

A
  • SRY infleunces formation of gonads
  • –Gene for testis-determining factor (TDF)
  • Gonads influence:
    1. Internal sex organs
    2. External genitalia
    3. Brain regions
  • Organizational effects of gonadal hormones= irreversible
80
Q

Hormonal Control of biological sex: male

A

Male– testis determining factor–> primordial gonads develop into testes–> 1. defeminzation (mullerian system withers away), 2. androgens–> wolffian sistem develpes, 3. androgens–>Primordial external genetalia develop into penis and scrotum
2 and 3= masculinization

81
Q

Hormonal control of biological sex: female

A

Female–> primordial gonads develop into ovaries–> 1. Mullerian system develops, 2. wollfian system withers away, 3. primordial external genetalia develop

82
Q

Sex Hormones

A
  • Produced in gonads and de novo in brain
  • Synthesized from cholesterol
  • Aromatase is key enzyme in concersion btwn testosterone and estradiol
  • Structutre allows for passage through tissue/cell membranes
  • Receptors are present in brain and throughout body
  • -Estrogen receptors: ERa and ERB
  • -Androgen receptors : AR
83
Q

Sex Hormone Action in the Brain

A
  1. Fast/direct effects
    - -Modulating neurotransmitter receptors (GABAa recep.)
    - -Membrane receptors (GPCRs)-> influence synapt. transmission and downstream effects
  2. Prolonged/Indirect Effects
    - Intracellular/ nuclear steroid receptors
    - -Travel into nucleus
    - -Bind to hormone response elements throughoiut genome
    - -Affect gene transcription
    - -Long-lasting changes in cell
84
Q

Activational Effects

A
  • Effect of sex hormones–> secondary sex characteristics
  • May change, cycle, or be reversible
  • Recieving exogenous hormones can alter there characteristics
85
Q

Puberty

A
  • Health can determine when one enters puberty

- Leptin has role in influencing timing

86
Q

HPG axis

A
  • Hypothalamic-pituitary-gonadal axis
  • Hyp. released GnRH to anterior pituitary
  • Pituitary releases LH and FSH into circulation
  • Gonads produce sex steroid hormones which act throughout body and brain
  • Neg feedback from steroid hormones dampens HPG axis activity
87
Q

Sexual Behavior

A
  • Linked w/ hormonal cycles
  • Humans one of few animals that fuck outside of reproduction
  • Human females change sexual behavior w/ hormones
  • Rats only sexually receptive when fertile
88
Q

Spinal Mechanisms

A
  • Mechanoreceptors in sex organs are sufficient to induce engorgement and erection
  • Clit and glans penis= densly innervated w/ mechanoreceptors
  • Spinal reflex in sacral SC–> parasympathetic activation allowing blood flow to sex organs and production of lubricating fluid
  • Mechanosensory info–> activation of sympathetic axons in lumbar spinal cord–> orgasm
  • Lumbar spinothalamic cells project to intalaminar thalamus (sensation of orgasm)
89
Q

Testosterone

A
  • Supports sexual behavior in males

- Increases sexual behavior in females as well

90
Q

Oxytocin

A
  • Released at orgasm in both males and females
  • Also releases milk from lactiferous ducts
  • Important in pair bonding
91
Q

Monogamy

A
  • Genetic monogamy

- Social monogramy= 2 people choose to be together

92
Q

Non-monogamy

A
  • Polygyny= 1 male, many women
  • Polyandry= 1 female, many men
  • Promiscuity
93
Q

Mating Strategies

A

-High oxytocin and vasopressin receptors in VP and nucleus accumbens in monogamous species–> pair bonding

94
Q

Sexual Dimorphism of brain

A
  • Some brain areas are diff btwn males and females
  • Some behaviors diff btwn males and females
  • *Only average diffs
  • Ex: social/emotional behaviors better in women, better at verbal tasks, men good at spacial rotations
95
Q

Sexual orientation

A
  • BNST/ SDN size corresponds to gender identity

- Larger= male, female smaller unless testosterone added

96
Q

Cannon Bard Theory

A

Sensory stim–> stim percieved–>emotional experience (feeling)–> emotional expression (behavior, automatic response)

97
Q

James-Lang Theory

A

Sensory stim–> stim percieved–> emotional expression–> emotional experience

98
Q

Types of emotion

A
  • Emotional experience
  • Emotional expression
  • Unconcious emotion
99
Q

Limbic System

A
  • Papez curcuit= neocortex, fornix, cingulate cortex, anterior nuclei of thalamus, hypothalamus, hippocampus, amygdala
  • Bidirectional communication btwn cortex and hypothalamus, suppoeting interconnectedness btwn emo experience and emo expression
100
Q

Papez Circuit

A

Neocortex cingulate cortex –> hippocampus–fornix–> hypothalamus–> anterior nuclei of thalamus–> cingulate cortex

101
Q

Amygdala Projections

A
  • Afferent projections to amygdala come from cortex, hippocampus, hypothalamus, all sensory systems
  • Efferent projections from amygdala to hypothalamus, BNST– important in stress/coping response
102
Q

Learned Fear

A
  • Tone paired w/ mild shock leads to association–> response to tone
  • Amygdala plays critical role in emo learning
103
Q

Agression

A
  • Lesions in Amygdala decrease agressive behavior
  • Stim of subregions of hypothalamus–> diff attack behaviors
    1. Predatory agresssion (killing)
  • Lateral hypo
    2. Affective aggression (agg against same sex)
  • Medial hypo
    3. Selective agression (agg against opp sex)
  • Vasopressin, Ant. hypothalamus
104
Q

Empathy

A

-The ability to understand and share the feelings of another
*Cognitive empathy – understanding of another’s feelings
*Behavioral empathy – acting for the benefit of another
Prosocial behavior
-Requires observing, recognizing, understanding, and responding to another’s emotion

105
Q

Perception of emotion in somatosenmsory cortex

A
  • Activated in response to emo faces

- Unconciously imagine yourself making same face

106
Q

Perception of emotion premotor area

A
  • Mirror neurons activated in response to facial movements of others
  • Help w/ empathetic understanding
107
Q

Perception of emo, prefrontal cortex

A

-Meaning and tone of speech, interpreted to identify emotions

108
Q

Neuropsychiatric disorders and emotions

A
  • Show disruption in emotional face recognition
  • Valence= important (can’t identify neg emotions)
  • Dysregulated signaling in amygdala, PFC, and tempora; and parietal refions
109
Q

What brain pathways are activated by looking at someone responding to aversive stimulus?

A
  • Visual processing pathways
  • Face recogniton region
  • Emotion-related region
  • Pain-processing pathways
110
Q

Animals and empathy

A

-Rats free other rats from restraints, shared their chocolate (learned behavior)

111
Q

Language

A
  • system by which sounds, symbols, and gestures are used for communication
  • A system for representing and communicating information
  • Uses words combined according to grammatical rules
  • Expressed through gestures, writing, and speech
112
Q

Speech

A

-An audible form of communication built on the sounds humans produce

113
Q

HUMAN Language

A
  • Complex, flexible, powerful system for communication
  • Creative use of words according to rules
    • Ex: friend as noun and verb
114
Q

ANIMAL Language

A
  • Controversial whether their communication is “language”

- Do not meet definition of human language: complex, flexible, rules

115
Q

Language as a Process

A
  • Aspect of Language
  • Comes into brain through visual and auditory systems
  • Motor system: produces speech, writing
  • Brain processing btwn sensory and motor systems essential for language
116
Q

Mechanisms of Language in infants

A

-Recognize word sounds very early
-Statistical learning—combinations of sounds
-Syllable emphasis
“Motherese”
—–Adults talk to infants—speech slower, exaggerated, vowel sounds clearly articulated
***Activation of left temporal lobe

117
Q

Phonemes

A

-Fundamental Sounds of Language

118
Q

How do we study neuroscience of language?

A
  • Only specific aspects of language (i.e. vocalization or song learning) can be assessed in animal models
  • Post-mortem tissue samples have limitations in connections to specific behaviors
  • Study of aphasias has been key, with knowledge of damage, or post-mortem analysis
  • Study of stimulation during brain surgery
  • fMRI
  • Genetic associations with language dysfunctions
119
Q

FOXP2 Gene

A
  • First identified in a family with verbal dyspraxia (inability to produce speech)
  • —-FOXP2 gene mutation – gene codes for transcription factor, induces many genes’ transcription
  • —-Affects development of motor cortex, cerebellum, and striatum
  • —-Deficits in muscular control of lower face
  • —-Also signs of broader grammatical and cognitive deficits
120
Q

Aphasia

A
  • Partial or complete loss of language abilities
  • Often without cognitive impairment, or impact on speech production muscles
  • Supports the idea that there is an independent language-associated brain region
  • Case studies–> speech production regulated by frontal cortex
121
Q

Language Processing and Brain

A
  • Left side of brain
  • Sometimes right side or bidirectional in left-handed people
  • *fMRI activation in response to grammatical error
122
Q

Broca’s Aphasia

A
  • Damage in motor association cortex of frontal lobe
  • Speech is nonfluent, agrammatical
  • —Difficulty speaking but can understand heard/read language – good comprehension
  • —Paraphasic errors (adding syllables)
  • —Pauses to search for words (anomia), repeats “overlearned” things, difficulty repeating words
123
Q

Wernicke’s Aphasia

A
  • Posterior temporal lobe damage
  • Fluent speech but poor comprehension
  • —-Strange mixture of clarity and gibberish
  • —-Correct sounds, incorrect sequence
  • —-Speech patterns mirrored in playing music, writing
  • Area specialized for storing memories of sounds that make up words
124
Q

Neural Circuitry of Speech Production

A
  1. Visual or Auditory cortex
  2. Wernicke’s area (comprehension)
  3. Broca’s area (planning sound production)
  4. Motor cortex (produce language)
125
Q

Wernicke-Geshwind Model

A
  1. Reptition of Spoke word–> Input via auditory cortex OR Repeating aloud a written word–> Input via Striate cortex (transformation in angular gyrus)?
  2. Meaningful words parsed via Wernicke’s area
  3. Arcuate Fasciculus passes word signals to Broca’s area
  4. Motor cortex controls speech articulation
126
Q

Arcuate Fasciculus

A
  • Axon bundle
  • Connects Wernicke and Broca areas
  • If severed, no ability to repeat words
127
Q

Limitations of Wernicke-Geschwind Model

A
  1. Overestimates significance and specificity of cortical brain regions
  2. Assumes transformation of other types of language to speech is necessary
  3. Does not account for the role of subcortical brain regions
128
Q

Parallel Processing in Language

A
  • Simultaneous handling and responses to language
  • 1st Dorsal pathway
  • 2nd Dorsal Pathway
  • Ventral pathway
129
Q

1st Dorsal Pathway

A
  • the superior temporal gyrus (Wernicke’s and auditory areas) connects with premotor cortex
  • involved in speech production and repeating words
130
Q

2nd Dorsal Pathway

A
  • Second dorsal pathway: superior temporal gyrus connected with Broca’s area
  • involved in processing complex syntactic (sentence) structure
  • analysis of words arranged according to a grammar system
131
Q

Ventral Stream

A

-Takes the sounds of speech and extracts their meaning

132
Q

Connectivity Aphasia

A
  • Disconnection lesion of arcuate fasciculus and parietal cortex
  • Good comprehension, speech fluent, but difficulty repeating words
  • Symptoms: repetition substitutes/omits words, paraphasic errors, cannot repeat function or nonsense words, polysyllabic words (similar to Broca’s)
133
Q

Global Aphasia

A
  • Lesion in frontal or temporal lobes
  • Poor comprehension, little speech, difficulty repeating words
  • Common after stroke
134
Q

Aphasia in Bilinguals

A

-Language affected is usually language most fluent in or first language

135
Q

Sign Language Aphasia

A
  • Broca’s or Wernicke’s aphasia have similar effects in verbal and sign language
  • Can be produced by lesions
  • Verbal and sign effected together–> indicates overlapping regions
136
Q

Assymetrical Processing of language

A
  • Left frontal lobe controls language/speech
  • Left latural fissure longer and less steep than right
  • left part of wernicke’s area larger than right
  • Fxnl: 90% humans right handed
  • Size of insula best predicotr of laterality of language
137
Q

Left Hemisphere Controls and Limitations

A
  • Language
  • Right visual field
  • Unable to describe anything to left of visual fixation point
138
Q

Right Hemisphere Controls and Limitations

A
  • Left visual field, difficulty verbalizing
  • If image in left visual field w/ object in left hand, unable to describe
  • Read and understand numbers, letters, short words, but no verbal response
  • Able to write
  • Drawing, ouzzles, sound nuances
139
Q

Split Brain Study

A
  • Severed axons of corpus callosum–> hemispheres cannot communicate
  • If item or word in left visual field–> right hemisphere–> cannot verbalize what they are seeing
  • If item or word in right visual field–> left hemisphere__. can verbalize word or object
140
Q

PET Scan of Auditory Stimuli

A
  • Right= music-related (tone of voice/ affecruve prosody)

- Left= language-related (linguistic prosody)

141
Q

Effects of Brain stimuliation of Langauge

A
  1. Vocalizations
  2. Speech arrest
  3. Speech dificulties similar to aphasia
142
Q

Stim of Motor Cortex and Language

A
  • Immediate speech arrest

- Non-speech vocalization

143
Q

Stimulation of Left broca’s area

A
  • Speech Arrest from strong stimulation
  • Speech hesitation from weak stim.
  • Anomia
144
Q

Stimualtion of Posterior Parietal Lobe near Sylvian fissue and in temporal lobe (left)

A
  • Word confusion

- Speech arrest

145
Q

fMRI activation during word generation

A
  • Wernicke’s area
  • Motor Cortex
  • Broca’s area
146
Q

fMRI activation when story read aloud

A
  • Wernicke’s area

- Auditory cortex

147
Q

fMRI activation when mentally/silently repeating sentences heard

A
  • Broca’s area

- Wernicke’s area

148
Q

Direct Pathway of Frontostriatal System

A
  • Inhibts inhibitors

- Disinhibits thalamus, thalamus excites cortex, cotrex sends motor plan

149
Q

Indirect Pathway of Frontostriatal System

A
  • Excites inhibitors

- Strengthens inhibition on the thalamus., thalamus does not excite cortex, motor plan not sent

Exploring Neuroscience (6 decks)

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