Biological Bases Of Behavior: Exam 3

Front 1

Cranial Nerve 1: Olfactory Nerve

Back 1

o Fibers come from the nose.
o Goes to the olfactory bulbs.
o Olfactory tract
o Olfactory system is part of the limbic system.
o Olfactory cortex is a core limbic area.
o Does not go to thalamus- primitive

Front 2

Name the three cranial nerves of the oculomotor system.

Back 2

Cranial Nerve 3: Oculomotor Nerve
Cranial Nerve 4: Trochlear
Cranial Nerve 6: Abdusence

Front 3

Cranial Nerve 3: Oculomotor Nerve

Back 3

 has autonomic functions
 parasympathetic connection to the eye.

Front 4

Cranial Nerve 4: Trochlear

Back 4

moves eye laterally (side to side)
Only nerve that emerges from the brain stem posteriorly.

Front 5

Cranial Nerve 6: Abducens

Back 5

attaches to eyeball in oblique fashion- responsible for superior oblique movement

Front 6

Cranial Nerve 5: Trigeminal Nerve

Back 6

• This is both a sensory and motor nerve.
• Primarily sensory.
 Sensory to three divisions:
• Eyes (opthalmic division)
• Maxillary
• Mandibular
 Motor component: chewing/mastication

Front 7

Cranial Nerve 7: Facial Nerve

Back 7

• Both motor and sensory.
• Primarily motor.
• Provides muscles of the face, eyelids, forehead.
• Sensory:
 Taste from the anterior two thirds of the tongue.
 Taste divided between two nerves.

Front 8

Cranial Nerve 9: Glossopharyngeal

Back 8

• Mixed sensory and motor.
• Taste from the posterior 1/3 of the tongue and the throat.
• Sensation from the back of the throat and the upper respiratory tract.
• Motor: shape of the esophagus.

Front 9

Cranial Nerve 10: Vagus

Back 9

• Information from the visceral

Front 10

Cranial Nerve 12: Hypoglossal

Back 10

• Allows for speech; controls all the muscles of the tongue.

Front 11

Bells Palsy

Back 11

Facial Nerve Problem
• Flaccid paralysis on one side of the face.
• Usually caused by various viral infections (including herpes simplex virus)
• One side of the mouth droops.

Front 12

Ptosis

Back 12

Facial Nerve Problem
Droopy eyelids.

Front 13

Which cranial nerves originate above the brainstem?

Back 13

Olfactory
Optic

Front 14

Which cranial nerves emerge from the brainstem at the level of the midbrain?

Back 14

Oculomotor
Trochlear

Front 15

Which cranial nerves emerge from the brainstem at the level of the pons?

Back 15

Trigeminal
Abducens
Facial
Vestibulochoclear

Front 16

Which cranial nerves emerge from the brainstem at the level of the medulla?

Back 16

Glossopharyngeal
Vagus
Spinal Accessory
Hypoglossal

Front 17

Purely Sensory Nerves

Back 17

Optic
Olfactory
Vestibulocochlear

Front 18

What is the only cranial nerve that does not go to the thalamus?

Back 18

Olfactory
Goes to olfactory cortex (core limbic area).

Front 19

Purely Motor Nerves

Back 19

Oculomotor
Trochlear
Abducens
Spinal Accessory
Hypoglossal

Front 20

BOTH Motor and Sensory Nerves

Back 20

Trigeminal
Facial
Glossopharyngeal
Vagus

Front 21

Cranial Nerve 1

Back 21

Olfactory

Front 22

Cranial Nerve 2

Back 22

Optic

Front 23

Cranial Nerve 3

Back 23

Oculomotor

Front 24

Cranial Nerve 4

Back 24

Trochlear

Front 25

Cranial Nerve 5

Back 25

Trigeminal

Front 26

Cranial Nerve 6

Back 26

Abducens

Front 27

Cranial Nerve 7

Back 27

Facial

Front 28

Cranial Nerve 8

Back 28

Vestibulococlear

Front 29

Cranial Nerve 9

Back 29

Glossopharyngeal

Front 30

Cranial Nerve 10

Back 30

Vagus

Front 31

Cranial Nerve 11

Back 31

Spinal Accessory

Front 32

Cranial Nerve 12

Back 32

Hypoglossal

Front 33

Reticular Formation

Back 33

Heart/center of brainstem.
Two primary functions: control of vital functions (breathing, heart rate- rhythmic- pacemaker cells), and control of arousal.

Front 34

Reticular Activating System

Back 34

Includes cells which use monoamine neurotrasmitters.
Sends neurotransmitters all over the system.
Responsible for arousal and activation.
Stimulate the thalamus and cortex.

Front 35

Monoamine Neurotransmitters

Back 35

Serotonin
Dopamine
Norepinephrine
Histamine
Acetylcholine

Front 36

Nuclei of the Reticular Formation

Back 36

Locus Coeruleus
Ventral Tegmental Area
Rafae Nucleus
Tubulomammilary Nucleus

Front 37

Neurotransmitter used by Locus Coeruleus?

Back 37

Norepinephrine or Noradrenaline

Front 38

Neurotransmitter used by Ventral Tegmental Area?

Back 38

Dopamine

Front 39

Neurotransmitter used by Rafae nucleus?

Back 39

Serotonin

Front 40

Neurotransmitter used by Tubulomammilary nucleus?

Back 40

Histamine

Front 41

Coma

Back 41

Results of damage to the reticular activating system in the brainstem.

Front 42

Saccades

Back 42

Vision is one of the main senses that allows us to pay attention. In visual system we pay attention by focusing on an object (“the object of attention”) (keeping it on our foveal vision- visual acuity- cones located here). Visual system performs saccades to allow you to shift your attention- moving the eye to shift your focus on something else (see Fig 29-2 on page 640). Saccades are generated in the superior colliculus. The superior colliculus is where visual information terminates in the brain stem. Area of the motor cortex responsible for the saccades is the frontal eye fields.

Front 43

What is the main cortical area that allows us to direct attention?

Back 43

Inferior Posterior Parietal Cortex
Where Pathway
This is where integration of information takes place.

Front 44

Hemispatial Neglect

Back 44

Neglect is usually seen on the left (damage is on the right). Right hemisphere damage causes left side neglect. What about left side neglect? Right side actually contributes to both (controls attention on both left and right of the body). Left side only controls the right side of the body. Just know that the reason is because the right hemisphere is redundant. If right hemisphere is damaged you still have attention on the right because the left hemisphere is also controlling attention there. If left hemisphere is damage the right hemisphere is still controlling attention on the right side of the body
Loss of the "where" information.

Front 45

Masking

Back 45

• Part of the field we were paying attention to are sharp and part of the fields we shift our attention to are sharp but do not see blur when we shift our attention.
• Visual constancy.
• Important principle of sacccades is visual constancy.

Front 46

Which hemisphere of the brain is dominant for attention?

Back 46

Right

Front 47

Unilateral Neglect

Back 47

Results of lesions to the inferior parietal cortex.

Front 48

What happens to the neurotransmitter systems of the reticular formation during sleep?

Back 48

o During sleep these systems are decreased in activity, except in REM.
o Cholinergic system (diffusely projecting cholinergic neurons of the brain stem) is actually more active during REM sleep.
• Special function in inducing REM sleep.

Front 49

Where is the nucleus that controls circadian rhythms?

Back 49

• Part of the hypothalamus.
• Suprachiasmatic nucleus responsible for circadian rhythms.

Front 50

EEG Activity in Wakefulness vs. Sleep

Back 50

Awake= Beta Waves
Resting= Alpha Waves
Falling asleep --> frequency of waves decrease and amplitude increases.
4 non REM stages of sleep and 1 REM stage.
Stage 1= low amplitude, high frequency
Stage 4= high amplitude, low frequency
REM= low amplitude, high frequency waves (but NOT most similar to wakefulness)
No muscle tone during REM sleep. REM sleep is longer usually. REM= dreams

Front 51

How does the superchiasmatic nucleus control rhythmic systems?

Back 51

Suprachiasmatic nucleus is in the hypothalamus which controls the pituitary gland.
o Suprachiasmatic nucleus secretes transcription factors which transcribe the DNA, allowing RNA to be produced.
o Has own rhythm.
o Connected to pineal glad.
o Connected to the eyes- when there is a lot of light coming in it performs differently.

Front 52

Disorders of Sleep

Back 52

Insomnia
Sleep Apnea
Obstructive Sleep Apnea
Central Sleep Apnea
Hypersomnia
Narcolespy
Catolepsy
Sleep Paralysis
Restless Leg Syndrome
Parasomnias: Sleep walking, sleep talking, night terrors

Front 53

Insomnia

Back 53

• Most common.
• General cause is not really a physiological dysfunction.
• Usually related to stress; depression can cause insomnia.
• Inability to sleep.

Front 54

Sleep Apnea

Back 54

• Second most common type of sleep disorder.
• Symptom:
 person is asleep, they stop breathing, and then they snore.
 The snoring wakes the person up → cyclic depravation of the brain and depriving the body of oxygen.
• Can cause cardiac problems in people with severe sleep apnea.
• May be the basis of lot of neurodegenerative disorders.

Front 55

Obstructive Sleep Apnea

Back 55

Caused by the collapse of the muscles at the back of the throat.
• Back Pressure: force air through the throat
• Can be treated with oxygen mask or with surgery.

Front 56

Central Sleep Apnea

Back 56

Mediated by the central nervous system.
• Much harder to treat.
• Happens more during REM sleep.

Front 57

Hypersomnia

Back 57

Excessive daytime sleepiness (counterpart of insomnia).
• Can also be a counterpart of sleep apnea (don’t sleep well at night).

Front 58

Narcolepsy

Back 58

Abnormal activation of the sleep inducing system.
• No voluntary component
• Symptoms (narcolepsy usually has a composite of some of those symptoms):
 Catolepsy: catatonia= inability to move.
• Loss of muscle tone.
 Sleep attacks.
 Dream-like episodes while awake.
• Dreams start intruding into wakefulness.
o Like hallucinations.
 Disturbed nocturnal sleep.
 Sleep paralysis: awake but there is no muscle tone (can’t move).

Front 59

Treatments for Insomnia

Back 59

Treatments:
 Use benzodiazapines→ increase release of GABA (inhibitory neurotransmitter).
• Antimuscorinic agents also help with sleep

Front 60

Treatments for Narcolepsy

Back 60

Amphetamines.
Anti-depressants for the catolepsy (particularly tricyclics).

Front 61

Multimodal Association Areas

Back 61

• Inferior parietal lobe- where pathway.
o There are others but they don't integrate as many senses.
• Prefrontal cortex.
• Orbitofrontal cortex.
• Inferior temporal and middle temporal gyrus- what pathway.
• Superior parietal cortex is also a multimodal association area.

Front 62

Connectivity of the Cerebral Cortex

Back 62

• Unimodal association areas primarily connected to primary areas and multimodal association areas.
• There is ordering of areas and how they are connected.
• Multimodal areas talk to unimodal areas and paralimbic areas.
• Paralimbic areas get their information from the core limbic areas.
• Integration of information→ cognition
• Information on the internal environment comes from the hypothalamus.

Front 63

Cognitive Processing

Back 63

• Sensory info processed through two pathways: dorsal and ventral
• Dorsal pathway primarily goes to parietal and frontal cortex.
• Ventral pathway primarily goes to the temporal lobe and the frontal cortex.

Front 64

Dorsal Pathway

Back 64

Upper pathway
Where
o Integrates visual, somatosensory, and auditory.
• This information is crucial for motor function (could not coordinate movement without knowing where things are).
o Intimate connections between parietal lobe and the motor/premotor cortex.

Front 65

Ventral Pathway

Back 65

Lower pathway
What
o Inferior temporal gyrus= facial recognition (most important in humans)
• Also called the fusiform cortex.

Front 66

Agnosia

Back 66

Inability to recognize or perceive.

Front 67

Apraxia

Back 67

Difficulty performing movements.

Front 68

Ataxia

Back 68

Lack of control of necessary movements.

Front 69

Disorders Caused by Superior Parietal Cortex Lesions

Back 69

Somatoagnosia
Idea Apraxia
Opticataxia

Front 70

Somatoagnosia

Back 70

Lesion to superior parietal cortex.
 Agnosia= inability to recognize or perceive.
 Somato= body
 Inability to perceive your own body.
 Representation of own body is messed up.
 Foreign limb syndrome.
 Damage dorsally to the dominant hemisphere.
• For sensory and motor have dominant hemisphere (ex/ motor- right handedness vs. left handedness)

Front 71

Ideamotor Apraxia

Back 71

 Apraxia= difficulty performing movements.
• Not because of paralysis.
• Cognitive difficulty in performing movements.
• Able to move muscles appropriately but difficulty performing cognitive commands to move.
• Ex/ Can spontaneously wave hand but can’t do so when asked to or asked to imitate.

Front 72

Opticataxia

Back 72

Ataxia: Cannot properly control the movements that are necessary.
Ex/ reach
Cerebellum helps with this type of function. There are cerebellar ataxias but this is not the same.
Person can not look at something and reach and grab it instantly. This is a visual problem. Problems with visual guidance of movement. Lesion disrupts integration of motor and visual information.
Reaching difficulties for objects that are not in the center of the vision. BUT could touch knee if instructed in the dark.

Front 73

Constructional Apraxia

Back 73

• Individuals with inferior parietal lesions also have problems with the integration of components.
• Can’t draw an object when asked.

Front 74

Acalcaria

Back 74

Parietal lesion
Inability to calculate

Front 75

Agraphia

Back 75

Parietal lesion
Inability to write

Front 76

Alexia

Back 76

Parietal lesion
Inability to read

Front 77

Disorders caused by damage to the temporal cortex.

Back 77

Propsopagnosia
Object Agnosia
Semantic Dementia

Front 78

Prosopagnosia

Back 78

Inability to recognize faces.
• Result of the lesion of the inferior temporal gyrus aka fusiform gyrus.
o Right under the temporal lobe.

Front 79

Dorsolateral Prefrontal Cortex

Back 79

Allows for cognitive control of behavior.
• Wisconsin Card Sorting Test
 Sorting by color vs. shape vs. number
 People with damage to the prefrontal cortex cannot do this task as it has to do with cognitive control over behavior.

Front 80

Orbitofrontal Cortex

Back 80

Social Emotions
• damage to that area can cause sociopathy or disengagement.
• Appropriate decision making about appropriate behaviors are associated with this cortex.

Front 81

Damage to Dorsolateral Prefrontal Cortex

Back 81

• Trouble planning (going to the grocery store is difficult)
• Problems with sequential activities
• Working memory is lost
• Decision making- both dorsolateral and ventral prefrontal cortex

Front 82

Where is the primary motor cortex located?

Back 82

Precentral Gyrus

Front 83

Functions of the Supplementary Motor Cortex

Back 83

 context of movement
 rules of movement
• executive function
o must follow rules
o Sequences
• there is a lot of coordination that this area needs to do; not just initiation of movements.

Front 84

Movement is initiated by....

Back 84

the primary motor cortex.
the caudate nucleus of basal ganglia.

• if there’s damage to the Substantia Nigra- problems with movement
o Parkinson’s Disease (overcontrols)
• Akinesia/Diskinesia
 Problems initiating movement

Front 85

Intimate connection between the premotor and supplementary motor cortex and the ___________.

Back 85

Parietal Cortex

• Connection between the parietal cortex and premotor and supplementary motor cortex is very important.
• Parietal lobe has an even greater role in cognitive aspects of motor function than PM and SM cortex.
 Parietal lobe coordinates information and then tells PM and SM cortex what types of actions are possible.
 Parietal cortex= contemplation of action
 PM and SM cortex then consider the context and tell the motor cortex what to do.

Front 86

Cortical Areas Involved in Language

Back 86

Posterior and inferior aspects of the frontal cortex.
Primary Motor Cortex
Basal Ganglia (particularly caudate nucleus)
Superior Temporal Sulcus
General aspects of the temporal lobe.

Front 87

Prosity

Back 87

Speaking
Intonation
Some of the emotional aspects of language
facial expressions
Emphasizing something
Two components to prosity:
Emotional (tone of voice matters-emotional content)- right hemisphere
Semantic: emphasizing meaning; changing tone (same word can carry different meanings)- left hemisphere

Front 88

In general, language is located in what hemisphere?

Back 88

Left (attention is right hemisphere).

Front 89

Mediational Areas of Language

Back 89

• not immediately involved in the production of language
• when damage occurs can use language properly
• connection between language and thought is lost
• conception of language can be lost (ideas, concepts)

Front 90

Broca's Area

Back 90

• Inferior and posterior frontal cortex

Front 91

Broca's Aphasia

Back 91

o language production
o left hemisphere (for most individuals)

Front 92

Wernicke's Area

Back 92

Located in temporal and parietal lobe.

Front 93

Wernicke's Aphasia

Back 93

o Occlusion of the middle cerebral artery would cause this.
o Damage leads to problem with meaning and use of proper grammar (verbal diarrhea)
o Production of language is intact.
o comprehension/understanding of language is lost
• Makes sense because this area is close to the auditory cortex

Front 94

Conduction Aphasia

Back 94

Lesions in parietal cortex.
• Conduction aphasia
o thought to disrupt the connection between Broca’s area and Wernicke’s area
o Symptoms:
• cannot repeat what you ask them to
 “Say ‘dog.’”
• Understand what you said but cannot say it.
• Can spontaneously produce the word dog and can understand the word dog.

Front 95

Two Components of Short Term Memory

Back 95

Rehearsal component
Broca’s area- inferior and posterior frontal cortex
Visuospatial component
Knowing where things are, what sequence they’re in.

Front 96

Storage Area for Rehearsal Component of Short Term Memory

Back 96

Posterior Parietal Cortex

Front 97

Storage Area for Visuospatial Component of Short Term Memory

Back 97

Prefrontal Cortex

Front 98

HM

Back 98

Removed medial aspect of temporal lobe (hippocampus and parahippocampal gyrus) due to seizures.
Suffered anterograde (after surgery) LT memory loss.
ST memory intact.
Implicates hippocampus in processing of LTM (NOT storage).

Front 99

Two types of LTM

Back 99

Implicit
Explicit

Front 100

Implicit Memory (and involved brain systems)

Back 100

Unaware of this.
Ex/ Mirror Drawing
Brain Systems: NOT hippocampal-dependent, basal ganglia (striatum), cerebellum, neocortex (premotor, motor, parietal), cerebellum

Front 101

Explicit Memory (and involved brain systems)

Back 101

Episodic (events)
Semantic (facts/meaning of words)
Hippocampus and connections between hippocampus and prefrontal cortex important in episodic memory (PFC=planning, sequencing).
These are not the sites of storage.

Front 102

Two Types of Implicit Learning

Back 102

Habituation & Sensitization

Front 103

Cellular Basis of Habituation

Back 103

 System no longer responds to stimulation as the organism learns the response is not essential for survival.
 Based on synaptic depression
• depression of synaptic activity
 Neuron that is receiving the stimulation goes through changes that make it not release the neurotransmitter the way it used to.
• For sensory system where touching is taking place the neurostransmitter would be glutamate
 Fewer synapses

Front 104

Cellular Basis of Sensitization

Back 104

 Opposite of habituation.
 Ex/ deliver a shock
 Synaptic activity is enhanced
 Milder and milder stimulus will result in a much larger/exaggerated response
• synaptic transmission increases – more synapses

Front 105

What building block is needed for memory storage?

Back 105

Protein

Front 106

Long Term Potentiation

Back 106

Makes depression and sensitization permanent.
 Equivalent to sensitization
• But longer in effect
 Opposite of long term depression
• Long term depression
 Talking about synaptic activity- potentiated.
 Bases of the storage of information/formation of LTM.

Front 107

Brain structure responsible for aversive conditioning.

Back 107

Amygdala

Front 108

Habit Formation

Back 108

One type of implicit memory.
Requires the basal ganglia.
• Striatum in particular.
• Long term potentiation is required for the formation of habits as well.

Front 109

Working Memory

Back 109

Resides in PFC. During working memory the same neurons maintain depolarization- sustained activity- continually firing action potentials. Neurotransmitter: Acetylcholine is one neurotransmitter that helps with the sustained activity of neurons during WM. Network of neurons is also important:
If there is excitatory sustained activity: Glutamate
If there is inhibition sustained activity: GABA
All of this gives rise to the cellular basis of sustained activity. This stops when person shifts attention.

Front 110

Brain structures involved in explicit memory.

Back 110

Hippocampus
Amygdala
Parahippocampal gyrus
Amon's Horn

Front 111

Storage site for LTM.

Back 111

Association Cortical Areas

Intricate connections (of Amon’s horn) allow the hippocampus to store LTM in the association cortical areas.

Front 112

Long Term Potentiation

Back 112

Potentiated synaptic activity.
• Don’t need a lot of repetition
• enhanced response of the connected neuron
• amygdala
• caudate
• hippocampus

Front 113

Main NT involved in LTP

Back 113

Glutamate
Involved in both long term potentiation and long term depression.
• Released either directly or by secondary mechanisms (calcium channels that cause it to be released)
• When the receptors are antagonized (antagonists- prevent NT from binding to receptor)
 NMDA
 Can knock out the gene for the NMDA receptor.
• If glutamate can’t bind to the receptor, long term potentiation can’t take place.

Front 114

Negative Symptoms of Schizophrenia

Back 114

presence of behavior that "normal people" do not exhibit.
• Hallucinations and Delusions

Front 115

Positive Symptoms of Schizophrenia

Back 115

Something "normal people" do have but in people with schizophrenia it is suppressed.
• flat affect
• disorganized thought and speech

Front 116

Cognitive Symptoms of Schizophrenia

Back 116

slower cognitive processing; memory problems (working memory) → problems with executive function → disorganization
• What is different about the cognitive symptoms of schizophrenia than the positive and negative symptoms?
 Medications do not treat these symptoms.

Front 117

Heritability of Schizophrenia

Back 117

o Strong genetic influence.
o Identical Twins= 50%
• Not TOTALLY genetic.
o Adopted individuals- more like birth family
• More influence of the blood family than the adopted family.
• Points to a stronger genetic component.
o First degree, second degree and third degree relatives all have greater risk than the general population.
• Second degree relatives have much lower risk than first degree relatives. See figure 62-1 on page 1392.

Front 118

Genetic Causes of Schizophrenia

Back 118

• Very few specific genes/genetic changes have been identified in schizophrenia.
• Two have been proposed:
o focal changes in nucleotides (mutations)
o translocations and deletions
• Translocation:
o Disc-1: Dysfunction in Schizophrenia Gene
o Gene was discovered the gene in a family the same gene caused many different disorders.

Front 119

Environmental Correlates of Schizophrenia

Back 119

o SES
o Urban Birth
o Season of Birth
o Maternal Exposure to Viral Illness
o Paternal Age
o Perinatal Complications

Front 120

Where does the brain show problems in individuals with schizophrenia in MRI studies?

Back 120

Thinning of the Gray Matter= loss of volume- Occurs in: Prefrontal cortex → working memory functions; organization (executive functions)
Temporal lobe → auditory hallucinations.
Hippocampus → memory problems
Hallucinations more associated with negative affect (makes sense in terms of thinning of the amygdala)
Temporal pole (a paralimbic cortex)-Thinner gyri; wider sulci; widening of the ventricles
More dense dendritic spines in normal individuals than in individuals with schizophrenia (fewer synapses)

Front 121

Synaptic Pruning in Schizophrenia (Developmental Aspect)

Back 121

During development, everything develops to an excess→ we then prune this back. Loss of synapses and neurons is actually part of neural development. Despite this, brain continues to grow:Myelination leads to brain growth. Connections increase.
Synaptic pruning is accelerated in schizophrenia.
Part of the pruning taking place in the frontal cortex is associated with dopaminergic cells.

Front 122

Treatment for Schizophrenia

Back 122

First line of treatment- tranquilizers (ex/ Chlorpromazine)
• Get rid of positive symptoms.
• Primary side effect- Parkinsonian Symptoms (rigid movement)
 Also tardive dyskinesia.
• primarily in face, mouth, and tongue.
• These drugs are dopamine receptor antagonists- block dopamine receptors.

Front 123

Two Types of Dopamine Receptors Involved in Schizophrenia

Back 123

D1- lost in schizophrenia
o decreased particularly in the prefrontal cortex.
• Prefrontal cortex decrease in D1 receptors correlates with working memory loss in patients with schizophrenia.
D2- Overactive in schizophrenia- blocked by tranquilizers.

Front 124

Glutamatergic System and Schizophrenia

Back 124

Glutamatergic System:
 It is known that the antagonist of one type of glutamatergic receptor (NMDA receptor) causes psychosis (Ex/ Ketamine)

Front 125

Primary Brain Structure Involved in Anxiety

Back 125

Amygdala

Front 126

Brain Structures Involved in Depression

Back 126

o Orbitofrontal cortex- involved in social emotions/interactions.
o Anterior Cingulate Cortex*
o Amygdala*
o Hippocampus
o Prefrontal Cortex (Medial aspect of the prefrontal cortex)
o Insula
*Primary areas that show differential activation in patients with depression and their connections.

Front 127

Correlate of Success with Antidepressant Therapy

Back 127

The lower the activity (greater the depression of activity) in the area where the cingulate cortex curves around, the better the outcome of antidepressant therapy.

Front 128

Two Monoamines Involved in Depression

Back 128

Serotonin
Norepinephrine
(Part of Reticular Activating System)

Front 129

Antidepressants

Back 129

SSRIs
Monoamine Oxidase Inhibitors (MAOIs)
Tricyclics

Front 130

SSRIs (Selective Serotonin Reuptake Inhibitors)

Back 130

 Impact reuptake and degradation of serotonin at the synapse.
 Enhance synaptic activity of serotonin but do not directly effect the receptors.
 Few side effects.

Front 131

Monoamine Oxidase Inhibitors

Back 131

 Monoamine oxidase degrades all monoamines.
 Inhibition of monoamine oxidase→ more monoamines available
 Side effects:
Peripheral effects because they bind throughout the body.
Food restrictions- dietary control is very important.

Front 132

Tricyclics

Back 132

 Effect both the epinephrine and serotonin transporters (inhibit them).
 Block receptors from functioning.
 In blocking these receptors they then sometimes block other receptors leading to side effects:
Some types of cholinergic receptors or histamine receptors.
Cause drowsiness, dryness of the mouth, attention problems.

Front 133

Brain Structure Implicated in OCD

Back 133

Basal Ganglia

Front 134

Anxiety Medication

Back 134

Benzodiazepines- Enhance gabaergic transmission (through GABA A receptors)
GABA=inhibitory neurotransmitter
Enhance entrance of chloride through a chloride channel in the complex.
Chloride=negatively charged- Hyperpolarizes the cell. More chloride enters.
Problem with benzos= addiction/dependence.

Front 135

Male to female ratio for Autism

Back 135

4:1

Front 136

Genetics and Autism

Back 136

Sibling pair showed X-linked types of mutations in genes- the portion of the gene deleted relates to synaptic structure. This is why more males have this disorder.
Sporadic Mutations: In Autistic individuals a number of mutations have been discovered that are sporadic:
o Deletion mutation: gene not active
o Duplications: too many copies of one gene.

Front 137

Brain Structures Involved in Autism- Attention Deficits

Back 137

Emotional component of attention in the cingulate cortex.

Front 138

Brain Structures Involved in Autism- Social Emotions

Back 138

Orbitofrontal Cortex

Front 139

Brain Structures Involved in Autism- Facial Recognition

Back 139

Fusiform gyrus/anterior temporal gyrus

Front 140

Brain Structures Involved in Autism- Recognizing Emotional Content in Faces

Back 140

Medial Temporal Lobe

Front 141

Brain Structures Involved in Autism- Language Deficits

Back 141

Inferior Frontal (Broca’s Area), Inferior Parietal/Inferior Temporal (Wernicke’s Area), striatum and cerebellum (fine motor aspects)

Front 142

Ectopia

Back 142

More general problem with the cerebral cortex
• During development cells are produced in a particular area of the brain and then they migrate to where they are supposed to be.
• End up with cells out of place.
• Happens in autism and schizophrenia.

Front 143

X-linked Disorders

Back 143

Rhet's Syndrome
Fragile X Syndrome
Downs Syndrome

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Rhet's Syndrome

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X-linked
Initially development is fine and then something goes wrong. Start to develop speech normally and then lose it.
Lose ability to manipulate things with their hands effectively. Gene that is responsible interferes with transcription (conversion of RNA to protein). Gene encodes for one transcription factor.
Seen only in girls. All males that get the mutation die; females have another gene that does some of the transcription.

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Downs Syndrome

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Trisomy of chromosome 21 (there are three chromosomes instead of the normal 2). Tons of proteins are encoded on chromosome 21. When Downs Syndrome individuals live long enough (into their 40s) they develop Alzheimer’s disease. Too much amyloid causes Alzheimer’s disease. Genes have a lot to do with physical characteristics: Eyes, Short stature, Overweight (different lipid metabolism). Mental retardation:caused by problem with a calcium channel and a glutamate receptor on chromosome 21- normal nerve transmission is difficult (Glutamate)

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Brain Structure Changes Due to Aging

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Enlargement of the ventricles. Frontal gyri thin.
White matter problems. Part of normal aging is loss of gray matter. In abnormal aging there is demyelination of the oligodendricites. Loss of plasticity with aging. Microglia come to clean up the mess caused by demyelination.

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Major Signaling System Contributing to Aging

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Insulin Growth Factor Receptor (IGF): When this receptor is disrupted animals live longer.
Growth hormone:
 The system that mediates the growth hormone system is disrupted by aging. Interrupting this system during aging can cause people to living longer.
Caloric Restriction: Permanent reduction in calorie intake- Reduces IGF -Increases life span. Impossible in humans.

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Brain Changes in Alzheimer's Disease

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Loss of gray matter
Gyri are thin
Sulci are widened
Thin temporal lobe
Hippocampus is almost gone and Para hippocampal gyrus (happens very early and is very extreme)

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Two Types of Lesions in Alzheimer's Disease

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Plaques (made of amyloid; amyloid deposits)
Tangles (these are what correlate with the clinical symptoms of autism). First place that tangles form is where long term memory is encoded (para hippocampal gyrus)
These are hallmarks of Alzheimer’s disease (need to be present for the person to be diagnosed with Alzheimer's.

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Amyloids

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Amyloid-B (AB) Peptide
Amyloid Precursor Protein (APP; located on chromosome 21). Problem with misfolding of proteins (aggregates formed). The proteins form very small soluble (float around and get stuck in synapses and dendrites) aggregates. Plaques and tangles are causing problems but small soluble proteins might be more problematic.

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Tau

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Involved in tangles.
Tau are microtubule associated proteins. Should be located in cell axons. Become phosphorylated. Instead, you have a tangle inside the cell. First see soluble phosphorylated cell and then aggregates form.
Initially have tangles inside the cell and then you later see just a tangle and the cell is gone.

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Genetic Causes of Alzheimers

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Apolipoprotein E (APOE)- risk gene for Alzheimer’s
Different variants: 2, 3 and 4
If you have one APOE 4 gene allele your risk for developing Alzheimer’s jumps, if you have 2 APOE 4 gene alleles your risk is even higher.

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First NT System Effected by Alzheimer's

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Acetylcholine- Basal forebrain cholinergic system- a bunch of neurons at the base of the brain but send axons all over the cerebral cortex. Involved in memory. This system is effected very early in Alzheimer’s. Came up with treatment by increasing availability of Acetylcholine. Inhibits acetylcholine esterase (AChE)(which breaks down acetylcholine). Three approved drugs for Alzheimer’s all inhibit Acetylcholine esterase. These drugs treat symptoms but at this stage they don’t influence the disease process.

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Motor Neurodegenerative Diseases

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ALS- Symptoms: flaccid paralysis, hyporeflexes (reduced reflexes)
Parkinson's - Symptoms: dyskinesia/akinesia (can’t initiate movements), resting tremors
Huntingdons: choreic movements

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Cognitive Neurodegenerative Diseases

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Alzheimer’s, Parkinson's
Frontotemporal Dementia- Symptoms: disinhibition (because of orbitofrontal problems), apathy
Lewy Body Dementia - Symptoms: related to Parkinson’s disease, can experience visual hallucinations, fluctuating cognition.
Vascular Dementia- Caused by strokes. There is a vascular event that happens that causes abnormalities. Stepwise progression.