SAT2D
BIOLOGICAL BASIS OF
BEHAVIOR II
Unit : I - V
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Phases of neurodevelopment
Postnatal development in human infants
Neuroplasticity in adults
Disorder of the neuro development
Autism
Williams syndrome
Unit 1 : Syllabus
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Neural development – an ongoing process; the
nervous system is plastic
A complex process
Experience plays a key role
Dire consequences when something goes
wrong
https://www.youtube.com/watch?v=Cu4lQYbOz
zY
Neurodevelopment
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Ovum + sperm = zygote
Developing neurons accomplish these things in
five phases
Induction of the neural plate
Neural proliferation
Migration and aggregation
Axon growth and synapse formation
Neuron death and synapse rearrangement
Phases of development
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A patch of tissue on the dorsal surface of the
embryo becomes the neural plate
Development induced by chemical signals from the
mesoderm (the “organizer”)
Visible three weeks after conception
Three layers of embryonic cells
Ectoderm (outermost)
Mesoderm (middle)
Endoderm (innermost)
Induction of neural plate
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FIGURE 9.1 How the neural plate
develops into the neural tube during
the third and fourth weeks of human
embryological development. (Adapted
from Cowan, 1979.)
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Neural proliferation:
Neural plate folds to form the neural groove, which then fuses to form the neural tube
Inside will be the cerebral ventricles and neural tube
Neural tube cells proliferate in species-specific ways: three swellings at the anterior end in humans will become the forebrain, midbrain, and hindbrain
Proliferation is chemically guided by the organizer areas – the roof plate and the floor plate
Migration: Once cells have been created through cell division in the
ventricular zone of the neural tube, they migrate
Migrating cells are immature, lacking axons and dendrites
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After migration, cells align themselves with others cells and form
structures
Cell-adhesion molecules (CAMs)
Aid both migration and aggregation
Axon growth and synapse formation
Once migration is complete and structures have formed
(aggregation), axons and dendrites begin to grow
Growth cone – at the growing tip of each extension, extends and
retracts filo podia as if finding its way
Aggregation
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Formation of new synapses
Depends on the presence of glial cells –especially astrocytes
High levels of cholesterol are needed –supplied by astrocytes
Neuron death and synapse rearrangement
50% more neurons than are needed are produced – death is normal
Neurons die due to failure to compete for chemicals provided by targets
Synapse formation
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Neurons that fail to establish correct connections are particularly likely to die
Space left after apoptosis is filled by sprouting axon terminals of surviving neurons
Ultimately leads to increased selectivity of transmission
FIGURE 9.8 The effect of neuron death and synapse rearrangement on the
selectivity of synaptic transmission. The synaptic contacts of each axon
become focused on a smaller number of cells
Synapse rearrangement
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1. Postnatal growth is a consequence of
Synaptogenesis
2. Myelination – sensory areas and then motor areas. Myelination of
prefrontal cortex continues into adolescence
Increased dendritic branches
3. Development of the prefrontal cortex
4. Effects of Experience on the Early Development,
Maintenance, and Reorganization of Neural Circuits
5. Competitive nature of experience and neurodevelopment
6. Experience fine tunes neurodevelopment
Postnatal development
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The mature brain changes and adapts
Neurogenesis (growth of new neurons) seen in
olfactory bulbs and hippocampus's of adult
mammals – adult neural stem cells created in the
ependymal layer lining in ventricles and adjacent
tissues
enriched environments and exercise can promote
neurogenesis
Neuroplasticity in adults
https://www.brainhq.com/media/news/brain-changing-adult-mind-through-power-plasticity
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3 core symptoms
1. Reduced ability to interpret emotions and intentions
2. Reduced capacity for social interaction
3. Preoccupation with a single subject or activity
Intensive behavioral therapy
Often considered a spectrum disorder
Autistic savants: intellectually handicapped individuals who
display specific cognitive or artistic abilities
Genetic basisSiblings of autistic have a 5%chance of being autistic
Several genes interacting with the environment.
Disorders of
Neurodevelopment: Autism
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1 in every 7,500 births
Mental retardation and an uneven pattern of abilities and
disabilities
Sociable, empathetic, and talkative – exhibit language skills,
music skills, and an enhanced ability to recognize faces
Profound impairments in spatial cognition
Usually have heart disorders associated with a mutation in a
gene on chromosome 7 – the gene (and others) is absent in
95% of those with Williams
Williams syndrome
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Evidence for a role of chromosome 7 (as in
autism)
General thinning of cortex at juncture of
occipital and parietal lobes, and at the
orbitofrontal cortex
“Elfin” appearance – short, small upturned
noses, oval ears, broad mouths
Williams syndrome continued
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Causes of brain damage
Neuroplastic responses to nervous system
damage
Treatment of nervous system damage
Amnesia and concussion
Amnesia of Korsakoff's syndrome
Alzheimer’s disease
Unit II – Syllabus
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Brain tumors
Cerebrovascular disorders
Closed-head injuries
Infections of the brain
Neurotoxins
Genetic factors
Causes of Brain Damage
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Epilepsy
Parkinson’s disease
Huntington’s disease
Multiple sclerosis
Alzheimer’s disease
http://study.com/academy/lesson/common-
neurological-disorders-list-and-descriptions.html
Neuropsychological
disorders
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Neuropsychological
disorders
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Neuropsychological disorders
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Neuropsychological disorders
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FIGURE 10.8 Cortical
electroencephalogram (EEG)
record from various locations on
the scalp during the beginning of a
complex partial seizure.
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FIGURE 10.11 Areas of sclerosis (see arrows) in the
white matter of a patient with MS.
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FIGURE 10.13 The typical distribution
of neurofibrillary tangles and amyloid
plaques in the brains of patients with
advanced Alzheimer’s disease. (Based
on Goedert, 1993, and Selkoe, 1991.)
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Degeneration – deterioration
Regeneration – regrowth of damaged neurons
Reorganization
Recovery
Neuroplastic Responses to
Nervous System Damage
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FIGURE 10.16 Three patterns of axonal
regeneration in mammalian peripheral
nerves.
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Reducing brain damage by blocking neurodegeneration
Promoting recovery by promoting regeneration
Promoting recovery by transplantation
Promoting recovery by rehabilitative training
Neuroplasticity and
Treatment of the Nervous
System Damage
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lRamachandran’s hypothesis: phantom limb caused by reorganization of the somato-sensory cortex following amputation
lAmputee feels a touch on his face and also on his phantom limb (due to their proximity on somatosensory cortex)
lAmputee with chronic phantom limb pain gets relief through visual feedback: view in mirror of his intact hand unclenching as seen in mirror box
Phantom Limbs:A
Neuroplastic Response
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FIGURE 10.23 The places on Tom’s
body where touches elicited
sensations in his phantom hand.
(Based on Ramachandran & Blakeslee,
1998.)
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Physiological and behavioral events of sleep
REM Sleeping and dreaming
Circadian sleep cycles
Effects of sleep deprivation
Four areas of brain involved in sleep
Circadian clock
Neural and molecular mechanisms
Psychopharmacology
Biopsychological theories of addiction
Intracranial stimulation
Pleasure centres of the brain
Unit III – Syllabus
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Electroencephalogram (EEG)
Reveals “brainwaves”
Electroculogram (EOG)
Records eye movements seen during
rapid eye
movement (REM) sleep
Electromyogram (EMG)
Detects loss of activity in neck
muscles during
some sleep stages
3 standard physiological measures of sleep
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FIGURE 14.2 The EEG of alert
wakefulness, the EEG that precedes
sleep onset, and the four stages
of sleep EEG. Each trace is about
10 seconds long.
Four stages of sleep
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80% of awakenings from REM yield reports of story-like dreams
External stimuli may be incorporated into dreams
Dreams run on real time
Everyone dreams
Penile erections are not a result of erotic dreams
Sleepwalking and talking are less likely to occur while dreaming
REM sleep and dreaming
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Recuperation theories
Sleep is needed to restore homeostasis
Wakefulness causes a deviation from homeostasis
Adaptation theories
Sleep is the result of an internal timing mechanism
Sleep evolved to protect us from the dangers of the night
https://www.theguardian.com/science/2013/oct1
7/sleep-cleans-our-brains-say-scientists
Why do we sleep and when do we?
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Recuperation theories predict:
Long periods of wakefulness will result in disturbances
Disturbances will get worse as deprivation continues
After deprivation, much of the missed sleep will be regained
Little effect of sleep deprivation:
Logical deduction, critical thinking
Physical strength and motor performance
Larger effect of sleep deprivation: executive function (prefrontal cortex)
Assimilating changing information
Updating plans and strategies
Innovative, lateral, insightful thinking
Reference memory
Effects of sleep deprivation
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Two consistent effects
Proceed more rapidly into REM as REM deprivation increases
REM rebound – more time spent in REM when deprivation is over
REM rebound suggests that REM sleep serves a special function
Purpose of REMProcessing of explicit memories?
Inconsistent findings
Antidepressant REM-blocking drugs do not interfere with memory
Default theory: it is difficult to remain in NREM sleep
Nycamp and others (1998) awoke sleepers in REM for 15 minutes. Result: no sleepiness or REM rebound the next day
REM-blocking drugs cause periods of wakefulness
REM sleep deprivation
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After sleep deprivation, most of lost stage 4 is regained and SWS is increased
Short sleepers get as much SWS as long sleepers
Naps without SWS do not decrease the night’s sleep
Gradual reductions in sleep time lead to decreases in stages 1 and 2
Little sleepiness produced with repeated REM awakenings, unlike SWS
Sleep deprivation increases sleep
efficacy
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Lesions do not reduce sleep time, but they abolish its circadian periodicity
Exhibits electrical, metabolic, and biochemical activity that can be entrained by the light-dark cycle
Transplant SCN, transplant sleep-wake cycle
Neural mechanism of entrainmentCutting the optic nerves before the optic chiasm eliminated the ability of the light-dark cycle to entrain circadian rhythms
However, cutting after the chiasm did not have this effect
Later the retinohypothalamic tracts were identified
Leave the optic chiasm and project to the adjacent suprachiasmatic nuclei
Mechanisms of entrainment of SCN cells to light-dark cycle
Rare retinal ganglion cells with no rods or cones
Circadian clock in the
suprachiasmatic nucleus
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Circadian rhythms – “about a day”
Virtually all physiological, biochemical, and
behavioral processes show some circadian
rhythmicity
Zeitgebers – environmental cues that entrain
circadian cycles
Circadian sleep cycle
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Several mammalian circadian genes have been identified
Some of these have also been identified in other species of other evolutionary ages
Expression of these genes follows a circadian pattern
Most of the gene expression appears to be entrained by activity of the SCN
Genetics of the circadian rhythm
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Two areas of the hypothalamus:
Posterior hypothalamus and the anterior hypothalamus were related to
excessive sleep or inability to sleep, respectively
Findings were in patients that had encephalitis lethargic
Two areas of the brainstem:
(“Isolated forebrain”) preparation – produced by severing cat brainstem
between the superior and inferior colliculi, resulting in continuous SWS
(“Isolated brain”) preparation – produced by transection caudal to the
colliculi, resulting in normal sleep cycle. Therefore, wakefulness
depends on the function of the reticular formation, or “reticular
activating system”
Four areas of the brain involved
in sleep
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Four areas of the brain involved in sleep
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Drugs that increase sleep (hypnotic drugs): benzodiazepines – Valium, Librium
Most commonly prescribed hypnotic drugs
Effective in the short term
Complications
Tolerance
Cessation leads to insomnia
Addiction
Use leads to next day drowsiness
Increase of stage 2 sleep while decrease of stage 4 and REM
Drugs that decrease sleep (antihypnotic drugs): stimulants and tricyclic antidepressants
Both increase activity of catecholamines
Act preferentially on REM – may totally suppress REM with little effect on total sleep time
Drugs that affect sleep
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Sleep disorders
Unit IV – Syllabus
Visual System
Audition
Somato sensation
Touch and pain
Chemical senses
Smell and taste
Touch and pain
Cortical Mechanisms
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The hierarchical organization of the sensory systems.
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The Ear
• Sound waves enter the auditory canal
of the ear and then cause the
tympanic membrane (the eardrum) to
vibrate.
• This sets in motion the bones of the
middle ear, the ossicles, which trigger
vibrations of the oval window.
• Sound wave > eardrum > ossicles
(hammer, anvil, stirrup) > oval window.
• Vibration of the oval window sets in
motion the fluid of the cochlea.
• The cochlea’s internal membrane, the
organ of Corti, is the auditory receptor
organ
Auditory System
Anatomy of the ear.
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Some of the pathways of the auditory system
that lead from one ear to the cortex.
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• There is evidence for interactions between the auditory and
visual systems
E.g. some posterior parietal neurons with both visual
and auditory receptive fields
• Interaction in primary sensory cortices indicate that sensory
system interaction is an early and integral part of sensory
processing
Auditory-Visual Interactions
https://www.smithsonianmag.com/arts-culture/how-do-our-brains-process-music-
32150302/
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• Lesions of auditory cortex in rats results in few permanent
hearing deficits
• Lesions in monkeys and humans hinder sound localization and
pitch discrimination
• Deafness in humans
• Total deafness is rare, due to multiple pathways
• Two kinds: conductive deafness (damage to ossicles) and
nerve deafness (damage to cochlea)
• Partial cochlear damage results in loss of hearing at particular
frequencies
Effects of Damage to the Auditory
System
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• Somatosensory system is three
separate and interacting
systems:
• Exteroceptive – external stimuli
• Proprioceptive – body position
• Interoceptive – body conditions
(e.g., temperature and blood
pressure)
Somatosensory System:
Touch and Pain
Four cutaneous receptors
that occur in human skin
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Dorsal-column medial-
lemniscus system
Anterolateral system
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Cortical Areas of Somatosensation
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• Despite its unpleasantness, pain
is adaptive and needed
• No obvious cortical
representation of pain
• Descending pain control
• Gate control Theory
Perception of Pain
Basbaum and Fields’s (1978) model of the descending
analgesia circuit
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• Olfaction (smell)
- Detects airborne
chemicals
• Gustation (taste)
- Responds to chemicals in
the mouth
• Food acts on both systems to
produce flavor
Chemical Senses: Smell and Taste
The human olfactory system.
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.
Taste receptors, taste buds, and
papillae on the surface of the
tongue
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Anosmia – inability to smell
Most common cause is a
blow to the head that
damages olfactory nerves
Incomplete deficits seen
with a variety of disorders
Ageusia – inability to taste
Rare due to multiple
pathways carrying taste
information
Brain Damage and the Chemical Senses
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• Improves perception of what is attended to and interferes with that which is
not
• Internal cognitive processes (endogenous attention) and external events
(exogenous attention) focus attention
• Cocktail-party phenomenon – indicates that there is processing of
information not attended to
• Change blindness – no memory of that which is not attended to
We do not appear to remember parts of a scene that are not the focus
of our attention
• Simultanagnosia – a difficulty attending to more than one visual object at a
time. Typical cause: bilateral damage to the dorsal stream (involved with
localizing objects in space)
Selective Attention
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Different views
Control of movements
Disruption of movement by disorders of
Muscles
Spinal cord
Brain
Unit V – Syllabus
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Three Principles of Sensorimotor Function
• Hierarchical Organization
Association cortex at the highest level, muscles at the lowest
Parallel structure – signals flow between levels over multiple
paths
• Motor Output is Guided by Sensory Input
• Learning Changes the Nature and Locus of Sensorimotor Control
E.g. conscious to automatic
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A general model of the sensorimotor system
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• Posterior parietal association cortex
• Dorsolateral prefrontal association
cortex
• Each composed of several different
areas with different functions
• Some disagreement exists about
how to divide the areas up
Sensorimotor Association Cortex
The major cortical input and output
pathways of the posterior parietal
association cortex
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Damage to the Posterior Parietal Cortex
• Apraxia – disorder of voluntary movement – problem only
evident when instructed to perform an action – usually a
consequence of damage to the area on the left
• Contralateral neglect – unable to respond to stimuli
contralateral to the side of the lesion – usually seen with large
lesions on the right
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Identifying the Areas of Secondary Motor
Cortex
At least eight different areas:
• Three supplementary motor areas -
SMA and preSMA, and
supplementary eye field
• Two premotor areas
Dorsal and ventral
• Three cingulate motor areas
Four areas of secondary motor cortex and their output to the
primary motor cortex.
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Responses of a mirror neuron of a
monkey.
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• Precentral gyrus of the frontal lobe
• Major point of convergence of cortical sensorimotor signals
• Major point of departure of signals from cortex
Cerebellum and Basal Ganglia
• Interact with different levels of the sensorimotor hierarchy
• Coordinate and modulate
• May permit maintenance of visually guided responses despite
cortical damage
Primary Motor Cortex
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• Two dorsolateral
Corticospinal
Corticorubrospinal
• Two ventromedial
Corticospinal
Cortico-brainstem-spinal tract
• Both corticospinal tracts are direct
Descending Motor Pathways
Divisions of dorsolateral motor
pathway
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Divisions of ventromedial motor pathway
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• Motor circuits of the spinal cord show considerable
complexity
• Independent of signals from the brain
Sensorimotor Spinal Circuits
https://www.coursera.org/learn/medical-neuroscience/lecture/UuYqd/internal-
anatomy-of-the-spinal-cord-gray-and-white-matter
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• Motor units – a motor neuron plus muscle fibers;
all fibers contract when motor neuron fires
• Number of fibers per unit varies – fine control,
fewer fibers/neuron
• Muscle – muscle fibers bound together by a
tendon
• Motor pool – all motor neurons innervating the
fibers of a single muscle
• Fast muscle fibers – fatigue quickly
• Slow muscle fibers – capable of sustained
contraction due to vascularization
• Flexors – bend or flex a joint
• Extensors – straighten or extend
• Synergistic muscles – any two muscles whose
contraction produces the same movement
• Antagonistic muscles – any two muscles that
act in oppositionFunction of the intrafusal motor neurons.
Muscles
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• Stretch Reflex: monosynaptic, serves to maintain limb
stability. E.g. Patellar tendon reflex is monosynaptic
• Withdrawal Reflex is NOT monosynaptic
• Reciprocal Innervation – antagonistic muscles interact so that
movements are smooth – flexors are excited while extensors
are inhibited, etc.
• Recurrent Collateral Inhibition – feedback loop through
Renshaw cells that gives muscle fiber a rest after every
contraction
• Walking – a complex reflex in some animals
Reflexes
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• Perhaps all but the highest levels of the sensorimotor system have
patterns of activity programmed into them, and complex movements are
produced by activating these programs
• Cerebellum and basal ganglia then serve to coordinate the various
programs
• Central sensorimotor programs may be hierarchically organized and
capable of using sensory feedback without direct control at higher levels
Central Sensorimotor Programs
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• Programs for many species-specific behaviors established
without practice
Fentress (1973) – mice without forelimbs still make
coordinated grooming motions
• Practice can also generate and modify programs
• Response Chunking
Practice combines the central programs controlling
individual response
• Shifting Control to Lower Levels
Frees up higher levels to do more complex tasks
Permits greater speed