sat2d biological basis of behavior ii unit : i - v · sat2d- biological basis of behavior ii 2 ......

SAT2D

BIOLOGICAL BASIS OF

BEHAVIOR II

Unit : I - V

TM

SAT2D- BIOLOGICAL BASIS OF BEHAVIOR II 2

Phases of neurodevelopment

Postnatal development in human infants

Neuroplasticity in adults

Disorder of the neuro development

Autism

Williams syndrome

Unit 1 : Syllabus

TM


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

https://www.youtube.com/watch?v=Cu4lQYbOzzY



TM


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

TM


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

TM


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.)

TM


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

TM


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

TM


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

TM


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

TM


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

TM


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















TM


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

TM


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

TM


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

TM


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

TM


Brain tumors

Cerebrovascular disorders

Closed-head injuries

Infections of the brain

Neurotoxins

Genetic factors

Causes of Brain Damage

TM


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

http://study.com/academy/lesson/common-neurological-disorders-list-and-descriptions.html














TM


Neuropsychological

disorders

TM


Neuropsychological disorders

TM


FIGURE 10.8 Cortical

electroencephalogram (EEG)

record from various locations on

the scalp during the beginning of a

complex partial seizure.

TM


FIGURE 10.11 Areas of sclerosis (see arrows) in the

white matter of a patient with MS.

TM


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.)

TM


Degeneration – deterioration

Regeneration – regrowth of damaged neurons

Reorganization

Recovery

Neuroplastic Responses to

Nervous System Damage

TM


FIGURE 10.16 Three patterns of axonal

regeneration in mammalian peripheral

nerves.

TM


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

TM


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

TM


FIGURE 10.23 The places on Tom’s

body where touches elicited

sensations in his phantom hand.

(Based on Ramachandran & Blakeslee,

1998.)

TM


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

TM


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

TM


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

TM


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

TM


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?

https://www.theguardian.com/science/2013/oct17/sleep-cleans-our-brains-say-scientists













TM


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

TM


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

TM


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

TM


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

TM


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

TM


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

TM


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

TM


Four areas of the brain involved in sleep

TM


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

TM


Sleep disorders

Unit IV – Syllabus

Visual System

Audition

Somato sensation

Touch and pain

Chemical senses

Smell and taste

Touch and pain

Cortical Mechanisms

TM


TM


The hierarchical organization of the sensory systems.

TM


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.

TM


Some of the pathways of the auditory system

that lead from one ear to the cortex.

TM


• 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/

https://www.smithsonianmag.com/arts-culture/how-do-our-brains-process-music-32150302/
















TM


• 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

TM


• 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

TM


Dorsal-column medial-

lemniscus system

Anterolateral system

TM


Cortical Areas of Somatosensation

TM


• 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

TM


• 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.

TM


.

Taste receptors, taste buds, and

papillae on the surface of the

tongue

TM


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

TM


• 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

TM


Different views

Control of movements

Disruption of movement by disorders of

Muscles

Spinal cord

Brain

Unit V – Syllabus

TM


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

TM


A general model of the sensorimotor system

TM


• 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

TM


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

TM


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.

TM


Responses of a mirror neuron of a

monkey.

TM


• 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

TM


• Two dorsolateral

Corticospinal

Corticorubrospinal

• Two ventromedial

Corticospinal

Cortico-brainstem-spinal tract

• Both corticospinal tracts are direct

Descending Motor Pathways

Divisions of dorsolateral motor

pathway

TM


Divisions of ventromedial motor pathway

TM


• 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

https://www.coursera.org/learn/medical-neuroscience/lecture/UuYqd/internal-anatomy-of-the-spinal-cord-gray-and-white-matter






















TM


• 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

TM


• 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

TM


• 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

TM


• 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

sat2d biological basis of behavior ii unit : i - v · sat2d- biological basis of behavior ii 2 ......

Documents