Biopsychology Exam 3

Front 1

Schizophrenia

Back 1

Called dementia praecox
- Eugene Bleuler coined the term "schizophrenia" in 1911, and it means split mind
- A pattern of extremely disturbed thinking, emotion, perception, and behavior that seriously impairs the ability to communicate and relate to others and disrupts most aspects of functioning

Front 2

Schizophrenia + positive symptoms

Back 2

Symptoms that add to your personality
1. delusions - false beliefs based on incorrect inferences about external reality
2. hallucination - perceptions with no clear external cause (can be visual or auditory, but auditory are more prevalent)
3. disorganized speech - loosening of associations, shifting between topics
4. disorganized behavior
5. inappropriate affect/movement - emotions are hard to reconcile with the stimulus.

Front 3

Schizophrenia + types of delusions

Back 3

1. persecution - belief that others are persecuting, spying on, or trying to harm you
2. reference - the belief that objects, events, or other people have particular significance to them
3. grandeur - the belief that you have great power, knowledge, or talent
4. identity - the belief that you are someone else, such as jesus or the president
5. guilt - the belief that you have committed a terrible sin
6. control - the belief that their thoughts and behaviors are being controlled by external forces.

Front 4

Schizophrenia + negative symptoms

Back 4

Take away from personality and behavior
1. social withdrawal
2. mood disturbances
3. flattened affect - lack of emotional response
4. memory alterations - impaired working memory
5. motor disturbances - such as paucity of movement and catatonia
6. grossly disorganized and inappropriate behavior, such as wearing three coats and gloves on a hot day

Front 5

Prevalence of schizophrenia

Back 5

men and women are equally likely to be diagnosed with schizophrenia.
age:
- usually after 6 years of age
- mode: 18-25 years
- some occur even as late as a person's 40's

Front 6

Schizophrenia + law of thirds

Back 6

1/3 okay
1/3 functional with a support system
1/3 need to be institutionalized

Front 7

Schizophrenia + genetics

Back 7

1. lifetime risk of developing schizophrenia is highest in identical twins (48%) and then kids who have 2 parents with schizophrenia (46%)
2. concordance rate in identical twins is 50%
- so there is a genetic component, but there must be something else going on as well
3. Adoption studies support a strong genetic role
4. As many as 70 genes may be involved with schizophrenia
- disrupted in schizophrenic gene (DIS-1 gene)

Front 8

Schizophrenia + possible genetic marker

Back 8

A majority of patients and 40% of their relatives show abnormal intrusions of saccades in smooth pursuit tasks. People with schizophrenia do not have fluid eye movement pursuit

Front 9

Schizophrenia + environmental influences

Back 9

1. stress - changes brain make up
- brain derived neurotrophic factor (BDNF) keeps a healthy neuronal environment. BDNF decreases with stress, leading to unhappy neurons
2. Difficult labor and delivery, abnormal fetal development (with cell migration specifically)
3. Maternal exposure to viruses during pregnancy
- kids with moms who had the flu during the second trimester
- seasonality effect - winter
- geographical patterns - parts of the world where its dark increases stress

Front 10

Schizophrenia + enlarged ventricles

Back 10

Enlarged ventricles represent a loss of neurons in adjacent areas. The hippocampus and amygdala may be smaller in the case of schizophrenia.

Front 11

Schizophrenia + hippocampus

Back 11

Using a Nissl stain (which counts the number of cell bodies), they found that
1. the cell bodies in the hippocampus of a control participant are arranged neatly
2. the cell bodies in the hippocampus of a participant diagnosed with schizophrenia are relatively disorganized.
--- messed up connections? could alter/affect behavior.

Front 12

Schizophrenia + structural differences

Back 12

People with schizophrenia have:
1. a thicker corpus callosum
- so there are a lot more connections going from the right to left hemisphere
2. decreased gray matter in the frontal cortex
- frontal lobe is responsible for personality, cognition, etc.
- many people are schizophrenics because they have an under active frontal lobe but the same amount of gray matter
- people with schizophrenia also have a more significant loss in gray matter

HOWEVER, not everyone develops these structural changes.

Front 13

Schizophrenia + activity differences + hypofrontality hypothesis

Back 13

Using PET scans, they found that people with schizophrenia tend to have lower frontal lobe activity in comparison to normal controls. This could account for the negative symptoms of schizophrenia, because the frontal lobe is responsible for personality and cognition, so an under active frontal lobe would take away from personality, etc.
- At rest, patients with schizophrenia have lower frontal lobe activity
- During a card sorting task, schizophrenic patients do not show a change from baseline. Normal patients increase frontal lobe activity. This could mean that the schizophrenic participants are not engaged, etc.

Front 14

Schizophrenia + neurochemical differences + auditory hallucinations

Back 14

In a study, they had schizophrenic patients listen to auditory speech and auditory hallucination, and they took a baseline of brain activation.
- then, they gave the patients LSD and asked the patients if they could differentiate between a schizophrenic hallucination and an LSD hallucination
--- LSD + serotonin in the occipital lobe = visual hallucinations
--- regular schizophrenic hallucinations are more auditory. They could tell the difference.

Front 15

Schziophrenia + magnetic stimulation

Back 15

Transcranial stimulation changes the electrical communication/electrical firing in the brain. It can be used to help reduce auditory hallucinations in patients with schziophrenia

Front 16

Schizophrenia + dopamine

Back 16

1. dopamine agonists (such as cocaine and amphetamines) produce symptoms of psychosis
- people were taking up to 3000mg of adderall and they were showing up to the hospitals with schizophrenic symptoms
2. Dopamine antagonists reduce psychotic behavior
- dopamine antagonists are good at helping reduce the positive symptoms of schizophrenia
3. Patients with schizophrenia may also have abnormalities involving dopamine auto receptors
- which help reuptake dopamine back into the cell when it is no longer needed.

Front 17

Schizophrenia + dopamine + psychosis

Back 17

1. Psychosis may result from conditions associated with high levels of dopamine activity
- schizophrenia
- LDOPA, methamphetamine, cocaine
2. Normal levels of dopamine activity
3. Motor disturbances and relief from psychotic symptoms may result from conditions associated with low levels of dopamine activity
- Parkinsons disease
- dopamine antagonists

Front 18

Schizophrenia + treatment

Back 18

There was no effective treatment of schizophrenia until 1950. Then, a french surgeon gave chlorpromazine to his patients as an antihistamine. He noticed that his patients became subdued, mild mannered, and calm. He then gave the drug to his agitated schizophrenic patients, and it helped them as well.
- It was a neuroleptic. neuroleptics have a greater effect on the positive than the negative symptoms of schizophrenia

Front 19

Schizophrenia + treatment + neuroleptics

Back 19

"typical antipsychotics" They function by blocking the dopamine D2 (inhibitory) receptor because they have a higher affinity for the D2 receptor than dopamine.
- neuroleptics have a greater effect on the positive than the negative symptoms of schizophrenia

Front 20

Schizophrenia + neuroleptics + side effects

Back 20

If taken for a long time, neuroleptics can cause tardive dyskinesia (esp in the face), involving tremors and involuntary movements
- because they lower dopamine activity everywhere, including the basal ganglia and substantia nigra (mesostriatal pathway responsible for fluidity of movement)
- decreased dopamine or GABA activity may be the cause of tardive dyskinesia
- age, gender, and ethnicity may influence a person's response to neuroleptics
- because of this negative side effect, approximately 50% of people being treated for schizophrenia prefer to use atypical antipsychotics, such as clozapine

Front 21

Schizophrenia + treatment + atypical antipsychotics

Back 21

These bind to serotonin receptors better than D2 receptors, and they treat the positive and negative symptoms of schizophrenia without tardive dyskinesia.

Front 22

Schizophrenia + problems with a dopamine hypothesis

Back 22

1. 25% of patients do not respond to a dopamine antagonist
2. Atypical antipsychotic medications (like clozapine) act primarily on neurotransmitters other than dopamine
3. Drugs change dopamine activity immediately, but the patient may not improve for weeks
4. Drugs lead to an increase in D2 receptors when really, you expect a down regulation in a regular brain
5. PCP produces symptoms similar to schizophrenia by blocking the NMDA (ionotropic) glutamate receptor
- PCP hallucinations are most similar to real, schizophrenic hallucinations
- Normally, glutamate (major excitatory NT in the cerebellum - motor control) receptors open and let Ca+2 come in. PCP acts as a noncompetitive antagonist (blocking at a location other than the binding site)

Front 23

Parkinsons + intro study

Back 23

People with parkinsons have a bad substantia nigra, which affects dopamine (LDOPA increases basal ganglia activity)
- new solution: implanting fetal tissues in the brain
- In an experience, they did a double blind procedure. They injected fetal cells in the substania nigra of 1/2 of the participants. The people who evaluated progress were in NY.
--- People with PD have an inability to start and stop goal-oriented movements. The fetal cells helped
--- Some people in the control group got better, so the placebo effect is important as well.

Front 24

PD + general information

Back 24

First described in 1817 by James Parkinson as "shaking palsy"
- .5% of the population is diagnosed with Parkinson's (1-2% of the population over age 65)
- Typically exhibited between 5-60 but it is probably present much earlier. It just takes a long time for degeneration to be so severe that you exhibit symptoms of it.
- Progressive, with death within 10-20 years of diagnosis.

Front 25

PD + positive symptoms

Back 25

1. Rigidity
2. Resting tremor
3. involuntary movements
- oculogyric crisis - looking up and to the left

Front 26

PD + negative symptoms

Back 26

1. hypokinesia (little movement) or akinesia (no movement)
2. monotonic speech

Front 27

PD + other symptoms

Back 27

1. cognitive deficits
2. affective changes - reflective, rigid, stoic, slow-tempered, frugal, orderly, low novelty-seeking, depressed

Front 28

PD + neurochemistry/brain regions affected

Back 28

1. Destruction of the substantia nigra (the mesostriatal dopamine pathway, where dopamine cell bodies are located; responsible for movement)
2. Leading to 97% loss in striatum at diagnosis
- 80% loss probably takes place 20 years before the preclinical stage. So, that makes PD hard to predict.
- Evidence that there is a large reserve of dopamine and that there are compensatory mechanisms in the brain that allow you to cope with substantial dopamine neuron degeneration and still function
--- compensatory changes in dopamine receptors (down regulation in dopamine receptors to keep the overall action the same) and transporters

Front 29

PD + etiology + MPTP incident

Back 29

A guy trying to sell heroin on campus missed a step and ended up making MPTP instead. The kids that he sold it to ended up in the hospital with PD-like symptoms, and they were also depressed and suicidal.
- In a completely unrelated study, nonhuman primates that were exposed to pesticides containing MPTP displayed PD-like symptoms as well

Front 30

PD + etiology + MPTP model

Back 30

MPTP is not harmful on its own, but it is oxidized in the brain by monoamine oxidase to MPP+
- MPP+ is toxic to dopamine cells in the substantia nigra. MPP+ is attracted to melanin, and melanin is what gives the substantia nigra its brownish color. MPP+ is taken up by dopamine neurons, esp in the presence of melanin, and then MPP+ kills the dopamine neurons by inhibiting metabolism

Front 31

PD + etiology + idiopathic PD

Back 31

Has no genetic component and its caused by an environmental toxin

Front 32

PD + etiology + pugilistic PD

Back 32

Muhammed Ali has PD because he has taken too many blows to the head

Front 33

PD + etiology + genetic component

Back 33

They looked at Italian families and there genes -
1. gene called "Parkin" - if there were any alternations or mutations to the "Parkin" gene, members in the family developed PD
2. gene called "α synuclein" - when this gene was not present, individuals developed PD
So, parkin gene + α synuclein gene = good
- when you lack one or the other, you increase the probability of developing PD.

Front 34

PD + basal ganglia

Back 34

- Motor nuclei (dopamine) are located here
- Part of the loop that receives information from the cortex and transmits it back via the thalamus
--- the basal ganglia is responsible for coordinating the motor loop
- The selection and initiation of motor sequences, motor learning, and learning non-motor cognitive tasks takes place in the basal ganglia
- The basal ganglia plays a major role in huntingtons and parkinsons disease

Front 35

PD + treatment

Back 35

1. LDOPA
- increases dopamine production, so the substantia nigra has a greater chance of transiently activating the striatum
2. Coffee
- caffeine blocks dopamine autoreceptors
3. Cigarettes
- cigarette smoke inhibits monoamine oxidase, so MPTP can no longer be converted into toxic MPP+
4. MAOIs (depranyl)
- prevent the enzymatic degradation of dopamine, so you keep more dopamine in the cleft
5. electrode implantation
- can help produce more dopamine by directly stimulating the substantia nigra
6. tissue implant
7. gene therapy

Front 36

Tourettes + history

Back 36

- First described in 1885
- previously thought to be a symptom of hysteria
- progressive, degenerative
- three stages:
1. multiple tics (more stress = more tics)
2. inarticulate cries
3. echolalia (repeating what other people say) and coprolalia (unprovoked cursing)

Front 37

Tourettes + symptoms

Back 37

97% tics involving eye, head, and face
81% tics involving upper limbs
55% tics involving lo wer limbs/body
35% complex movements (hitting, touch bbb

Front 38

Tourettes + incidence

Back 38

- affects .001-1% of the population
- more prevalent in males than females (x-linked)
- probably x-linked, transmitted by mothers
--- polygenetic
--- someone with tourettes has a 50% chance of passing it onto offspring
- age of onset: 2-15
--- median: 7
--- evident by age 11 in 97% of all cases

Front 39

Tourettes + neurobiology

Back 39

1. Pathological studies of tourettes are virtually nonexistent because of the young age of onset and because it is hard to use brain imaging techniques on people who are aways twitching.
2. EEG is normal
3. Lack of evoked potential (a little dip before an action potential) indicates that movements are involuntary
4. basal ganglia is implicated (perhaps dopamine/movement related)
- 2 autopsies - one was normal and the other had smaller cells in the basal ganglia
5. Neuroleptic (dopamine antagonist) drug therapy
- haloperidol
- possibly due to abnormal metabolism of dopamine

Front 40

Tourettes continued

Back 40

There are a lot of motor problems with tourettes, so perhaps the basal ganglia is implicated. However, it is hard to do research because:
1. People get diagnosed with they are very young, so it's hard to find the doctor from diagnosis
2. it is hard to do brain imaging studies because they have to move. Those people who can control their movements are not the same.
- no evoked potential for people with tourettes, so its involuntary

Front 41

OCD

Back 41

OCD is comorbid with tourettes (there is a 68% concordance rate) - perhaps a strong genetic component?
- characterized by repetitive, intrusive thoughts (obsessions) accompanied by repetitive, ritualistic behaviors (compulsions)
- could be because of brain abnormalities
- could also be because of birth trauma, infection, and injury
--- strep throat is highly correlated with OCD. if you're already susceptible to OCD, maybe step turns on the gene.

Front 42

OCD + brain regions

Back 42

brain regions:
1. orbitofrontal cortex
- responsible for decision making
2. prefrontal cortex
- responsible for decision making
3. caudate nucleus of the basal ganglia
- initates what the PFC and OFC think should happen. In OCD, there is a problem with feedback
4. cingulate gyrus
- responsible for learning, and mediates decision making and movement

Front 43

OCD + treatment

Back 43

1. antidepressants
2. behavioral treatment
3. both antidepressants and behavioral treatment together are most effective

Front 44

Depression

Back 44

Most common mood disorder, characterized by:
- unhappy mood
- loss of interest, energy, and appetite
- difficulty in concentration
- restless agitation

Front 45

Unipolar depression

Back 45

Depression that alter natures with normal emotional states
- depression may last several months
- inheritances is a factor in depression (60%)

Front 46

Depression + brain changes

Back 46

1. increased blood flow to the frontal cortex and the amygdala
- PET scans
- frontal cortex related to impulsivity and racing thoughts
- amygdala related to strong associations with what makes you depressed even when the person is no longer depressed

Front 47

Depression + impulsivity

Back 47

80% of the people who commit suicide are depressed - impulsivity?
- serotonin 2A impulsivity gene - if there is a decrease in these serotonin 2A receptors, there is an increase in impulsivity
--- people who actually commit suicide have lower serotonin levels and higher circulation of cortisol (stress)

Front 48

Depression + neurochemical theories of depression

Back 48

1. monoamine hypothesis
2. electroconvulsive shock therapy
3. vagal nerve stimulation
4. deep-brain stimulation

Front 49

Depression + monoamine hypothesis

Back 49

The monoamine hypothesis suggests that depression is caused by reduced synaptic activity of norepinephrine and serotonin
1. decreased dopamine, increases depression
2. monoamine oxidase (MAO) is an enzyme that inactivates monoamines
- treatment with MAO inhibitors raises the level of monoamines (serotonin, dopamine, norepinephrine) at the synapse
3. reserpine - a drug which reduces monoamines in the brain - can cause depression

Front 50

Depression + electroconvulsive shock therapy (ECT)

Back 50

Induction of a seizure.
ECT induces the release of monoamines

Front 51

Depression + transcranial magnetic stimulation (TMS)

Back 51

TMS appears to alter the metabolism of monoamine transmitters

Front 52

Depression + vagus nerve stimulation

Back 52

Depression increases heart rate, so just have an increased heart rate (maybe from exercise) may make you feel depressed
- vagus nerve stimulation decreases heart rate, so you are less likely to associate the two. the decreased association could take your body out of the learned association

Front 53

Depression + deep brain stimulation

Back 53

Could also be used to help with depression

Front 54

Depression + serotonin

Back 54

Serotonin deficiency is important in depression.
- SSRIs are antidepressants that block the reuptake of serotonin at the synapse
- tricyclic antidepressants block the reuptake of serotonin and norepinephrine

Front 55

Depression + problems with serotonin reduction as the cause of depression

Back 55

1. it takes 3 weeks for SSRIs to affect behavior and reduce depressive symptoms
2. not everyone is cured or even helped
3. SSRIs increase the risk of suicide in children and adolescents

Front 56

Depression + Cushings syndrome

Back 56

People with cushiness syndrome have high levels of glucocorticoids (cortisol) and are prone to depression
- the high levels of cortisol are present before symptoms
- symptoms include depression, obesity, body hair. these symptoms suggest a dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis

Front 57

Depression + increased glucocorticod circulation

Back 57

When you increase glucocorticoid circulation (more cortisol), this decreases brain-dervied neurotrophic factor (BDNF), which is important in keeping neurons nourished and maintaining a healthy neuron environment.
- A lot of the drugs used to treat depression aim to increase BDNF production

Front 58

Depression + problems with HPA axis

Back 58

The HPA axis is responsible for communication during the fight or flight response. possibly due to the HPA axis, depressed people show elevated levels of:
1. growth hormone
2. thyroid hormone
3. cortisol

Front 59

Depression + HPA axis functioning

Back 59

Normally:
1. trigger; sensory information about a perceived threat
2. amygdala
3. hypothalamus releases cortisol releasing hormone (CRH)
4. anterior pituitary releases ACTM
5. adrenal glands release cortisol
6. prepares body for fight or flight response
7. Hippocampus has receptor sites for cortisol. It takes the cortisol and acts to inhibit the excessive release of CRH
8. The hypothalamus stops releasing CRH


THE FEEDBACK LOOP where the hippocampus tells the hypothalamus to stop making more CRH may not function in people with mood and/or anxiety disorders

Front 60

Depression + how did they know about HPA axis dysfunction?

Back 60

There was an abnormal response to exogenous, synthetic cortisol during a dexamethasone (DST) suppression test.
- When you give normal controls DST, cortisol production is suppressed the next day because the body knows that there is already enough cortisol present and that it does not need to produce any more
- When you give DST to depressed people, this does not suppress cortisol production throughout the day. There is excess cortisol release (and it is seen in suicide victims as well as depressed patients)
--- Normal cortisol levels start to rise around 3-4am but normal individuals are able to sleep through that. people with depression will respond to the cortisol released around 3-4am by waking up and thinking about what has been making them depressed

Front 61

Depression + women

Back 61

More women than men suffer from depression
- may reflect help seeking patterns
- may have a psychosocial explanation, such as social discrimination
- gender differences in endocrine physiology
- women talk, men self medicate

Front 62

Depression + abnormal sleep patterns

Back 62

Depressed people:
1. fall asleep faster
2. enter REM earlier
3. spend little time in stage 3 or 4 sleep
4. awaken frequently
- so, they may appear to sleep a lot but the sleep doesn't allow them to feel rested
- studies have shown that disrupting depressed people's REM sleep can help improve their depressed mood

Front 63

Seasonal affective disorder (SAD)

Back 63

A type of depression that is brought on by the shorter days of winter

Front 64

SAD + treatment

Back 64

1. phototherapy is administered in the morning and can suppress melatonin, a hormone that may be important in controlling sleep
2. SAD may also respond to SSRIs

Front 65

Depression + animal models

Back 65

In animals, we can used learned helplessness to mirror depression in humans. During learned helplessness, an animal is exposed to a repetitive, stressful stimuli.
- Learned helplessness is linked to a decrease in serotonin function, like depression

Front 66

Depression + olfactory bulb ectomy

Back 66

When you remove the olfactory bulb in rats, they can no longer smell anything. Since smell is an important sense for them, losing the sense of smell makes them depressed because they can no longer interact with the environment.

Front 67

Bipolar disorder

Back 67

Is characterized by periods of depression alternating with expansive mood, or mania.
- the rate of cycling varies from person to person.
--- rapid cycling occurs when a person goes through 4 or more cycles in a year, but some people may cycle several times a day.

Front 68

Cyclothymia

Back 68

Is a milder form of bipolar disorder, during which patients cycle between dysthymia (mild depression) and hypomania (increased energy)

Front 69

Biopolar disorder + treatment + discovering lithium

Back 69

A guy put the urine of manic patients in guinea pigs guinea pigs and then inject lithium. the lithium managed to calm the guinea pigs

Front 70

Bipolar disorder + treatment + lithium

Back 70

Lithium is a mood stabilizing drug used to treat bipolar disorder. It seems to interact with the circadian clock
- It has little effect on people who do not have bipolar disorder
- it does not directly affect serotonin levels, but it may influence related enzymes and second messengers
- lithium enhances norepinephrine reuptake
- if lithium cannot be tolerated, patients may use SSRIs, benzodiazepines, neuroleptics, and anticonvulsant drugs.

Front 71

Phobic disorder

Back 71

Intense, irrational fears centered on an object, activity, or situation that a person avoids

Front 72

Panic disorder

Back 72

Recurrent attacks of intense fearfulness

Front 73

Generalized anxiety disorder

Back 73

persistent, excessive, anxiety, and worry

Front 74

Correlates of panic disorder with depression

Back 74

1. sodium lactate can initiate a panic attack
2. antidepressants that work in treating panic disorder reduce the activity of the locus coeruleus
3. A circuit connecting the hippocampus, orbitofrontal cortex, and cingulate gyrus may mediate panic attacks

Front 75

Correlates of panic disorder + sodium lactate

Back 75

sodium lactate (hypoxia - from not enough oxygen) can initiate a panic attack in someone with panic disorder, probably by stimulating the locus coeruleus
- the cell bodies for the neurons that make norepinephrine are located in the locus coeruleus (located in the pons, responsible for arousal and alertness)
- anxiety may be the result of increased norepinephrine production

Front 76

Correlates of panic disorder + antidepressants

Back 76

The antidepressants that are effect in treating panic disorder generally reduce activity in the locus coeruleus
- reduced activity = less norepinephrine = less arousal and alertness

Front 77

Correlates of panic disorder + circuit

Back 77

A circuit connecting the hippocampus, orbitofrontal cortex, and cingulate gyrus may mediate panic attacks
- hippo - memory of what produces anxiety may cause more anxiety
- orb - fight or flight
- cing - more associations

Front 78

Anxiety + treatment

Back 78

1. Benzodiazepines are anxiolytic drugs used to treat anxiety. They are a non-competitive agonist.
- They bind to GABA receptors at a site other than the binding site and they enhance GABA's inhibitory actions (basically, it makes the GABA receptor's gate open wider, so even more Cl- can come into the postsynaptic neuron.
2. Allopregnalanone - an inhibitory steroid transmitter that provide a way for the body to deal with stress internally by regulating or decreasing stress (like how alcohol works)
- modulates GABAa receptors
3. serotonin agonists and SSRIs are also used to treat anxiety

Front 79

Post traumatic stress disorder

Back 79

Unpleasant memories repeatedly plague the victim. Victims show
- memory changes, such as amnesia
- flashbacks
- deficits in short term memory

Front 80

PTSD + hippocampus

Back 80

People with PTSD have lower volume in the right hippocampus. However, this may be a risk factor for PTSD and not a consequence of PTSD
- In a study with twins, they thought that one of the twins had low right hippocampal volume because he was repeatedly exposed to stressors during war. BUT, both twins had low hippocampal volume. Maybe it was the low hippocampal volume that predisposed the twin and made him much more susceptible to stress and more likely to develop PTSD

Front 81

PTSD + fear conditioning

Back 81

Fear conditioning is a type of learning in which fear is associated with a neutral stimulus

Front 82

PTSD + symptoms

Back 82

Persistent memories and fears in PTSD may be the result of a failure to forget
- projections to the amygdala may lose effectiveness in suppressing fear. The original stressor/event may have formed such a strong cue in the brain that anything even remotely close or similar to that cue makes a person go back to that memory and the anxiety associated with it
- PTSD victims may have an increased response to stress hormones

Front 83

Sensation

Back 83

The process of transducing physical energy from the environment into electrical energy in neurons
- helps with survival

Front 84

Perception

Back 84

Selection, organization, and interpretation of sensations
- happens in the brain
- gives a quality of the external experience

Front 85

Steps to get to perception

Back 85

1. sensory receptors
2. transduction - taking external energy and transforming it into a neuronal impulse
3. coding - interpreting in the brain

Front 86

Functions of sensation and perception

Back 86

1. sense environment
2. control movement
3. maintain arousal

Front 87

Labeled lines

Back 87

All senses use the same type of energy - action potentials (mechanically-gated receptors)
- Action potentials for distinct senses travel along separate nerve tracts
--- The brain codes each labeled line separately and then interprets them together for perception

Front 88

Pacinian corpuslce

Back 88

A receptor that detects vibration.
- A stimulus to the corpuscle produces a graded electrical potential that is proportionate to the strength of the stimulus
- When the potential is big enough, the receptor reaches threshold and generates and action (spike) potential
- there are some pacinian corpuscles located in the stomach as well. when they stretch, you feel full

Front 89

Coding

Back 89

Patterns of action potentials in a sensory system that reflect a stimulus
- a single neuron can convey stimulus intensity by changing the frequency of its action potentials (but neurons generally only fire 150 action potentials in a second)

Front 90

Range fractionation

Back 90

Takes place when different cells have different thresholds for firing, over a range of stimulus intensities
- multiple neurons can act in parallel. as the stimulus strengthens, more neurons are recruited and their action potentials are essentially added together in the brain to equate an increase in intensity

Front 91

Adaptation

Back 91

Occurs because our information processing is selective and analytical. Adaptation is the progressive loss of response to a maintained stimulus
- tonic receptors do not show adaptation, but phasic receptors do show adaptation

Front 92

Tonic receptors

Back 92

Show slow or no decline in action potential frequency

Front 93

Phasic receptors

Back 93

Display adaptation and decrease frequency of action potentials

Front 94

Sensory pathways

Back 94

Each sensory system has a distinct sensory pathway in the brain.
- all pathways (except olfaction) pass through regions of the thalamus
- the pathways terminate in the cerebral cortex

Front 95

Tactile sensation + center on/surround off mechanism

Back 95

We have receptive fields - where external sensation will result in an electrical potential in the neuron. there is:
1. a receptive center
2. an inactive mid field
3. a tonically active outer field

The brain focuses on stimuli that hit the receptive center. This allows for us to be able to discriminate sensation (more in the fingers than in calves) and helps us to not muddle sensations coming from different areas/receptive fields

Front 96

Receptive fields in the cortex + primary sensory cortex

Back 96

The parietal lobe; exists for each modality; it is the first place that information goes to after it goes through the thalamus.
- the primary somatosensory cortex (S1) receives tactile information from the opposite side of the body

Front 97

Receptive fields in the cortex + secondary sensory cortex

Back 97

Gets information from the primary sensory areas for that specific modality
- the secondary somatosensory cortex (S2) maps information from both sides of the body

Front 98

Association areas

Back 98

Areas in the brain that show a mixture of inputs from different modalities
- provide a way for sensory systems to influence each other
- work through polymodal cells

Front 99

Polymodal cells

Back 99

Allow for intersensory interactions and are located in specific association areas
- for example, when you have a cold and food doesn't taste good

Front 100

Synesthesia

Back 100

A condition in which a stimulus in one modality creates a sensation in another
- for example, a person may perceive colors when looking at letters or a taste when hearing a tone.