reticular formation 

location

reticular formation 

part of the midbrain

contributes to cortical arousal

pontomesencephalon

how it works (3)

locus coeruleus 

GABA (5)

 inhibitory neurotransmitter

Inhibits thalamus and cortex

uessential for sleep

udecrease the temperature and metabolic rate

udecrease stimulation of neurons

acetylcholine

excitatory so increases cortical arousal 

The hypothalamus contains neurons that release “histamine”

effects?

Increases arousal 

Orexin

What does it do?

Where is it located?

Serotonin

what does it do?

location?

Interrupts REM sleep

Located at the Dorsal raphe and pons

uDuring REM sleep

activity increases in the ? and decreases in the ?

uemotional system

has to do with dreams because often our dreams are emotional

Paradoxical sleep

upons

uthe lateral geniculate of the hypothalamus

uthen the occipital cortex

[image]

Insomnia

causes (4)

dependant on?

Sleep apnea    

Sleep apnea results (5)

Sleep apnea causes (4)

1. genetics

2. hormones

3. old age

4. deterioration of the brain     mechanisms that control breathing and obesity

Continuous Positive Airway Pressure (CPAP) mask

Narcolepsy    

Narcolepsy    

Four main symptoms

 udreamlike experiences one has difficulty distinguishing from reality

Narcolepsy Causes (2)

Narcolepsy Treatment

Periodic limb movement disorder

(3)

REM behavior disorder

(5)

associated with damage to

movement during REM sleep

u acting out dreams

uelderly men, brain diseases, Parkinson’s

uassociated with damage to the pons

 uinhibits the spinal neurons that control large muscle movements

Night terrors (2)

Sleep talking (4)

original function of sleep (3)

Moderate sleep deprivation results in (6)

Caffeine increases arousal by 

adenosine

neuromodulator accumulates during wakefulness and increases drowsiness

u1/3

u1/5

uhighest percentage of REM

uinconclusive about functions of REM

Hypothesis (2)

uinconclusive about functions of REM

Hypothesis

Maurice (1998)

activation-synthesis hypothesis

(6)

clinico-anatomical hypothesis (3)

Dreaming    

Since primary visual and auditory areas of the cortex have lower activity... (2)

Dreaming    

Activity is high in? (2)

uthe inferior part of the parietal cortex

uimportant for visual-spatial perception

uactivity is also high in areas outside of V1

uaccounting for visual imagery of dreams

patients with damage in the inferior part of the parietal cortex

emotional responses

behavioral component

emotional responses

facilitate the behaviors

provide quick mobilization of energy for vigorous movement

emotional responses

Fear (2)

Fear 

Fear 

Fear 

Fear

Anger, Aggression, and Impulse Control  

uneural circuits in the brain stem

Anger, Aggression, and Impulse Control  

uactivity of serotonergic synapses inhibits aggression

Anger, Aggression, and Impulse Control  

udestruction of serotonergic axons in the forebrain facilitates aggressive attack, presumably by removing an inhibitory effect

Anger, Aggression, and Impulse Control

uEarly experiences development of aggressive behavior

uheredity also plays a significant role

userotonergic neurons play inhibitory role

udepressed rate of serotonin release (indicated by low levels of 5-HIAA in the CSF) are associated with aggression and other forms of antisocial behavior, including assault, arson, murder, and child beating

Anger, Aggression, and Impulse Control

uDamage = serious/debilitating impairments of behavioral control and decision-making

uappear to be a consequence of emotional dysregulation

Communication of Emotions

Many species communicate their emotions by

upostural changes, facial expressions, and nonverbal sounds (sighs, moans, and growls)

uThese expressions serve useful social functions

utell others how we feel and what we are likely to do 

Communication of Emotions 

uFacial Expression of Emotions: Innate Responses

uDarwin’s hypothesis

ufacial expression = innate, species-typical repertoire of movements of facial muscles

Communication of Emotions 

uFacial Expression of Emotions: Innate Responses 

Studies (3)

utribe in New Guinea and Westerners (1971)

uno differences between expressions of congenitally blind, noncongenitally blind, and sighted athletes

uEuropean English-speakers/natives of isolated Namibian villages, sounds sighs, groans, laughs, members of both cultures had no difficulty choosing the correct vocalizations of members of their culture and the other culture

Communication of Emotions 

uNeural Basis of Recognition of Emotions (3)

ufacial expression recognition generally automatic, rapid, accurate

u2008 study found observers quickly recognized brief expressions

uif given time to think about the expression, showed very little improvement

Communication of Emotions 

uLaterality of Emotional Recognition

uWe recognize other's feelings by vision and audition

uMany studies have found that right hemisphere plays a more important role in comprehension of emotion

Left = Language

Communication of Emotions 

uplays a role in emotional responses

uplays a role in emotional recognition

ulesions of the amygdala (the result of degenerative diseases or surgery for severe seizure disorders) impair people’s ability to recognize facial expressions of emotion, especially expressions of fear

Communication of Emotions

uRole of Imitation of Emotional Expressions: Mirror Neuron System

Study

u2000 study discovered possible link between somatosensation and emotional recognition

u108 patients with localized brain lesions

u patients’ ability to recognize and identify facial expressions of emotions

umost severe damage to this ability caused by damage to the somatosensory cortex of right hemisphere

usuggests that when we see a facial expression of an emotion, we unconsciously imagine ourselves making that expression

uoften, we do more than imagine making the expression; sometimes imitate what we see

Communication of Emotions

uRole of Imitation of Emotional Expressions: Mirror Neuron System

What is it?

umirror neurons important in control of movement

uactivated during particular behavior or when seeing another performing that behavior

upresumably, these neurons are involved in learning to imitate the actions of others

uability to empathize

Communication of Emotions

uRole of Imitation of Emotional Expressions: Mirror Neuron System

mirror neurons location? (2)

ulocated in ventral premotor cortex of the frontal lobe

ureceive input from superior temporal sulcus and posterior parietal cortex

uvolitional facial paresis

What is it?

Cause?

uDifficulty in moving the facial muscles voluntarily

ucaused by damage to the face region of the primary motor cortex or its subcortical connections.

Communication of Emotions 

roles of the right hemisphere (3) 

urecognizing emotions in the voice

urecognizing facial expressions of others

uespecially negative emotions

Lateralization

Knecht's study

ultrasonic procedure to measure changes in cerebral blood flow while people performed a verbal task, assessed the relationship between handedness and lateralization of speech mechanisms in people without any known brain damage.

?% of right handed people are left hemisphere dominant for speech

¡95%

¡70%

90%

Lateralization of speech refers to 

¡the sequential activities of stringing words together in the correct order, and recognizing such strings in other’s speech

Speech Disorders

Aphasia (3)

·Disturbance in speech cause brain damage

·Production

·Comprehension

·Left hemispheric damage

·not the result of

·Lack of motivation

·Sensory/motor deficit  (e.g paralysis)

Broca’s Area

What? where? 

§Speech Production

§part of frontal cortex, located just rostral to the base of the left primary motor cortex, that is necessary for normal speech production.

Broca’s aphasia

(4)

·Damage to inferior left frontal lobe

·Evidence for hemispheric lateralization

·Slow, laborious speech

·Difficulty with function words (a, the, in, about)

Broca’s Aphasia

    Three major difficulties

·Agrammatism– can’t speak 

·Anomia- cant recall 

·Difficulty with Articulation – speech errors

BROCA’S APHASIA

Three major difficulties

·can’t speak grammatically correct

§cant comprehend/properly employing grammatical devices, such as verb endings and word order.

BROCA’S APHASIA

Three major difficulties

Anomia

§impaired recall of words

§difficulty remembering appropriate words to describe.

BROCA’S APHASIA

Three major difficulties

Apraxia of Speech 

– speech errors

§Articulation difficulty

–problems with tongue, lips, and throat to produce proper sequence of sounds.

Wernicke’s Area    

Wernicke’s Aphasia

(damage to superior left temporal gyrus, Wernicke’s area)

(6)

·Word recognition disrupted

·Poor speech comprehension, evident in non-verbal tasks (“point to object…”)

·Cannot repeat statements made by others

·Fluent but meaningless speech

·Patients can use content words, correct grammar

·Patients are unaware of comprehension deficit

Recognition of spoken words

Pure word deafness

(3)

·disruption of inputs to Wernicke’s area

·inability to understand language, repeat words, and write from dictation

·spontaneous speaking, reading, and writing

·damage to posterior language area

·Can repeat but not comprehend statements

·Suggests distinction between speech recognition versus comprehension

ability to recognize words

ability to understand words

two types of brain injury can cause pure word deafness

Speaking, watching other's speak, thinking of speaking, and listening all activate brain regions involved in language 

¡posterior language area

Damage

analysis and recognition of words

ability to recognize words

understand OR produce meaningful speech of their own

arcuate fasciculus    

People with transcortical sensory aphasia can repeat what they hear

suggests a direct connection between Wernicke’s area and Broca’s area  

Conduction aphasia

(2) 

inability to repeat words

but ability to speak normally and comprehend speech 

Broca’s area with the inferior parietal cortex

Wernicke’s area with the inferior parietal cortex

conduction aphasi

spare the ability to repeat speech but would impair comprehension

Circumlocution    

Studies on Broca’s area and verbs

Prosody

(4)

Prosody

Disrupted by (3)

right hemisphere   

Stuttering (4)

•connections grow between areas of the brain?

–Led to the search for localized representations of memory

Ivan Pavlov

created what?

classical conditioning 

classical conditioning 

•two stimuli changes the response to one of them

–conditioned stimulus (CS) paired with unconditioned stimulus (US) results in unconditioned response (UR)

–after several pairings, response elicited by CS without US

–new response conditioned response (CR)

Operant Conditioning    

•responses followed by reinforcement or punishment that strengthens or weakens behavior

–reinforcers increase the probability that the response will occur again

–punishment decrease the probability that the response will occur again

Karl Lashley wanted to  prove Pavlov's hypothesis

–searched for physical representations of what had been learned.

–Believed that a knife cut should abolish the newly learned response

Findings of Lashley’s studies (2) 

•learning and memory not dependant on connections across the cortex

•learning not dependant on a single area of the cortex

Lashley proposed two key principles about the nervous system    

•Equipotentiality – all parts of the cortex contribute equally to learning

•Mass action – the cortex works as a whole, not as isolated units

Hebb (2) 

•early memory research

•differentiated between short-term memory and long-term memory

–STM limited capacity;

–STM fades quickly without rehearsal

–LTM can be retrieved by cue/hint; STM lost cannot be retrieved by cue

•Researchers propose information enters the ? where its consolidates into ?

• Later research figured what?

-STM

-LTM

-weakened distinction between STM and LTM

–Proposed by Baddeley & Hitch

alternative to short-term memory

–temporary storage of information to actively work on it for a period of time

Common test of working memory is 

•Research points to the ? for the storage of working memory information

•Brain may use elevated levels of ? to ?

-prefrontal cortex

-calcium

-increase the likelihood of later responses

•Changes in the prefrontal cortex 

•Declining activity of prefrontal cortex (elderly) associated with decreasing memory

•Increased activity is indicative of compensation for other regions in the brain

•Damage to areas of the hippocampus–results in amnesia

These areas are active during memory formation and retrieval

H.M. (5)

•famous case study

•hippocampus removed to prevent seizures

•After, great difficulty forming new long-term memories

•STM or working memory remained intact.

•Suggested hippocampus is vital for formation of new long-term memories

2 major types of amnesia

 •Anterograde amnesia –cant form new memory after brain damage

•Retrograde amnesia – the loss of memory prior to brain damage

Explicit memory

Implicit memory

–deliberate recall of information (memory)

– the influence of recent experience on behavior without realizing one is using memory

Episodic memory

Declarative memory

–ability to recall single events

–ability to state a  memory into words

Procedural memory    

–ability to develop motor skills (remembering or learning how to do things)

–declarative memory functioning (especially episodic)

–spatial memory

–configural learning and binding

Research on role of the hippocampus in episodic memory

damage impairs two types of tasks 

•Delayed matching

–subject sees an object and must later choose the object that matches

•Delayed nonmatching

– subject sees an object and must later choose the object that is different than the sample

Damage to the hippocampus also impairs spatial tasks such as    

•Radial mazes

–maze with arms and reinforcer at the end

•Morris water maze

–rat must swim through murky water to find rest platform just underneath the surface

Hippocampus may also be important for contextual learning

–remember detail & context of an event

–suggests hippocampus important in consolidation

–damage impairs recent learning more than older learning

–the more consolidated memory depends less  on hippocampus

Memory Consolidation mechanisms of consolidation?

influenced by?

what impairs memory?

•Reverberating circuits of neuronal activity were thought to be the mechanisms of consolidation

•Consolidation influenced by the passage of time and emotions

–Prolonged stress impairs memory

Memory Consolidation

–small to moderate amounts of cortisol activate the amygdala and hippocampus where they enhance storage and consolidation of recent experiences

Different brain damage results in different types of amnesia

Two common types of brain damage

–Korsakoff’s Syndrome

–Alzheimer’s

–caused by prolonged thiamine (vitamin B1) deficiency

–impedes the ability of the brain to metabolize glucose

–leads to a loss or shrinkage of neurons in the brain

–often due to chronic alcoholism

Korsakoff’s syndrome

symptoms (5)

• apathy
• confusion
• forgetting
• confabulation
• guesses to fill in memory gaps

Alzheimer’s disease

(5)

•gradual loss of memory

–affects 50% of people over 85

–early onset influenced by genes

–99% of cases are late onset

–about half of all patients with late onset have no known relative with the disease

Alzheimer’s Brain Damage

•clumping of brain proteins

–Amyloid beta protein 42 which produces widespread atrophy of the cerebral cortex, hippocampus and other areas

–an abnormal form of the tau protein, part of the intracellular support system of neurons

Accumulation of tau protein results in (2)    

–Plaques

•formed by degenerating neurons

–Tangles

•formed by degenerating structures within a neuronal body

major area of Alzheimer’s damage is

•basal forebrain

treatment includes enhancing acetylcholine activity

experimental Alzheimer’s treatment 

stimulation of cannabinoid receptors that limits overstimulation by glutamate    

•possibility of immunizing by stimulating the production of antibodies against amyloid beta protein

–there can be deficiencies of very different aspects of memory

–there are independent kinds of memory

–various kinds of memory depend on different brain areas

Other cortical/subcortical brain areas important in learning (5)    

–amygdala

•associated with fear learning

–parietal lobe

•associated with piecing information together

–anterior and inferior region of the temporal lobe and semantic memory

–prefrontal cortex

•rewards and punishments

–basal ganglia, anterior cingulate cortex

Malignant tumor

Benign tumor

Metastasis

udistinct border between the mass of tumor cells and the surrounding tissue

uborder = benign tumor; surgeon can cut it out, and it will not regrow

uno clear-cut border = tumor infiltrating surrounding tissue; if surgeon removes the tumor, some cells may be missed; these cells will produce new tumor

directly destroy brain tissue, or it can do so indirectly by blocking flow of cerebrospinal fluid and causing hydrocephalus

uCells that originate from transformations of neural stem cells, rapidly proliferate, and give rise to a glioma

uMalignant gliomas (starts in brain or spine) contain tumor initiating cells, which originate from transformations of neural stem cells

uBecause they are more resistant to chemotherapy and radiation than most tumor cells, the survival rate from these tumors is very low

stroke

2.5 million

•Brain damage may be caused by excessive release of glutamate during seizure

•Most common cause is

-scarring produced by injury, stroke

-developmental abnormality in the brain

-irritating effect of a growing tumor

uHigh fevers most common in children

u3 % of children under age of 5 years sustain seizures associated with fevers

uThe sudden release from the inhibiting effects of the alcohol or barbiturate leaves the brain in a hyperexcitable condition

uIn the past, many cases considered idiopathic

uof unknown causes’ literally “one's own suffering”

uMRIs with more resolution and sensitivity means that small brain abnormalities responsible for triggering seizures are more likely to be seen

many work by increasing effectiveness of inhibitory synapses

well enough so patient can lead a normal life

uin a few instances drugs provide little or no help

uSometimes, seizure foci remain so irritable that despite drug treatment, brain surgery is required

uIn the U.S. alone, millions treated and released from an emergency dept

u270,000 people hospitalized

u52,000 people die from TBI

umany more go undiagnosed

uAlmost a third of deaths caused by injury involve TBI

•Caused by a blow with a blunt object against right side of person's forehead

TBI how it manifests 

TBI

results in 

uobvious physical trauma to brain

uresults in increased levels of adenosine and glutamate in traumatized brain tissue

TBI 

treatment

uTreatment with a drug that inhibits the release of glutamate can prevent this switch in role of extracellular adenosine

uTreatment of long-term behavioral and cognitive effects TBI involve same strategies as those employed in treatment of brain damage caused by cerebrovascular accidents

uCommon cause of mental retardation (intellectual disabilities) is the presence of toxins that impair fetal development during pregnancy

drugs affect on fetal development

uvarious drugs can adversely affect fetal development

uingestion of alcohol during pregnancy, especially during the third to fourth week

ubabies born to alcoholic women typically smaller than average & develop more slowly

uBirth defects caused by ingestion of alcohol during pregnancy

ucharacteristic facial anomalies and faulty brain development

uMost important abnormalities are in the development of the brain 

uCaused by degeneration of nigrostriatal system

udopamine-secreting neurons of substantianigra that send axons to basal ganglia

uSeen in approximately 1% of people over 65 years of age

uPrimary symptoms are muscular rigidity, slowness of movement, a resting tremor, and postural instability

uAnother basal ganglia disease caused by degeneration of caudate nucleus and putamen

uProtein that may serve to facilitate the production and transport of brain-derived neurotrophic factor

uNeurotropic factor: Family of proteins responsible for growth and survival of developing neurons and maintenance of mature neurons

uAbnormal huntingtin is cause of Huntington's disease

Dementia

cause

symptoms 

uCommon causes are multiple strokes and Alzheimer's disease

uLoss of cognitive abilities such as memory, perception, verbal ability, and judgment

uOccurs in approx. 10% of the population above 65 and almost 50% of people older than 85

Alzheimer's degeneration

uProduces severe degeneration of the hippocampus, entorhinal cortex, neocortex (especially the association cortex of the frontal and temporal lobes), nucleus basalis, locus coeruleus, and raphe nuclei