Brain and Behavior - Rest of Info for Exam 3

Major Depressive Disorder (MDD) vs. situational depression

2 categorically different disorders; situational depression is a reaction to an event, is temporary, and is less severe than MDD

relationship between the development of situational depression and the development of MDD

every time someone experiences situational depression, their likelihood of experiencing MDD increases

DSM-5 criteria for MDD

must experience at least 5 of the listed symptoms within a 2-week period

8 main DSM-5 symptoms of MDD

depressed mood, anhedonia, vegetative symptoms, psychomotor retardation, trouble concentrating, thoughts of suicide, agitation/increased stress hormones, and obsessive feelings of worthlessness/hopelessness/grief/guilt/etc.

anhedonia

loss of interest and pleasure in nearly all activities one used to enjoy

2 main sets of vegetative symptoms

under- or over-eating (most commonly under-eating) and hypersomnia or insomnia (most commonly insomnia - early morning awakening)

early morning awakening

a common pattern of insomnia (and a clear marker) in people with MDD in which they have no trouble falling asleep, but they wake up really early (around 3-4am) and they can't go back to sleep

psychomotor retardation

extreme fatigue and experiences in which everything feels more physically and psychologically difficult, which can result in minimal activity or people slowing down (even their speech can slow)

agitation

lots of stress hormones and lots of activation of the stress-related parts of the PNS and CNS

when suidice is most common and why

soon after patients have been medicated for MDD and their symptoms begin to slightly improve, because at that point, they are still suffering greatly and remember their worst suffering, but have regained enough strength and energy to act on suicidal thoughts

3 main biological bases of MDD

neurotransmitters, brain structure, and hormones

prevailing theory about the development of MDD

the monoamine hypothesis and biological base of neurotransmitters

Monoamine Hypothesis

low levels of monoamines nd/or dysfunction of monoamine signaling cause MDD

3 main monoamines involved in MDD

serotonin (5-HT), norepinephrine (NE), and dopamine

how most antidepressants work

they boost levels of monoamines, most commonly, by preventing the reuptake of serotonin (5-HT)

natural/unmedicated process of serotonin reuptake

serotonin is released from the vesicles of the pre-synaptic neuron, then some of it binds to receptor sites on the post-synaptic membrane, then proteins reuptake (i.e. recycle) the excess serotonin back into the pre-synaptic neuron

how antidepressants interfere with serotonin reuptake

they block serotonin reuptake, which boosts levels of serotonin in the synapse until more receptor sites clear, and then that excess serotonin can bind to those sites and create more EPSPs

why we need to take SSRIs (selective serotonin reuptake inhibitors) and not just serotonin supplements

serotonin is a large molecule and cannot pass through the blood-brain barrier

ratio of SSRIs as antidepressants

most antidepressants are SSRIs; 5 of the 7 most common antidepressants

5 most common SSRIs

zoloft, celexa, prozac, lexapro, paxil

what kind of antidepressant is desyrel (one of the 7 most common antidepressants)

serotonin antagonist and reuptake inhibitor (SARI)

what kind of antidepressant is cymbalta (one of the 7 most common antidepressants)

serotonin-norepinephrine reuptake inhibitor (SNRI)

according to the school of thought that believes certain MDD symptoms are linked to low levels of or dysfunction of specific neurotransmitters, what neurotransmitter is anhedonia tied to

low levels of dopamine

according to the school of thought that believes certain MDD symptoms are linked to low levels of or dysfunction of specific neurotransmitters, what neurotransmitter is psychomotor retardation tied to

low levels of norepinephrine (NE)

according to the school of thought that believes certain MDD symptoms are linked to low levels of or dysfunction of specific neurotransmitters, what neurotransmitter is obsessive thoughts of sadness tied to

low levels of 5-HT (serotonin)

Substance P and its role in MDD

a neuropeptide (not a monoamine) used in the communication of neurons that results in the feeling of psychological pain

biological bases of MDD: brain structure

less prevalent, but some people understand depression as a result of abnormalities in brain structures (not neurotransmitters)

the brain structures believed to contribute to MDD

the cortex convinces the limbic system to activate stress responses

bilateral cingulotomy

an operation that disconnects the cortex and the limbic system to treat depression that has not responded to medication, psychotherapy, or electroconvulsive therapy

general results of bilateral cingulotomies

they can help treat severe MDD symptoms, but the patients still often come out of surgery without their original, larger channel of affect (they're more dull - could just be a result of being depressed for so long)

biological bases of MDD: hormones

thyroid dysfunction and the resulting abnormal hormone levels can create symptoms that closely mimic MDD (about 20% of people diagnosed with MDD actually have a thyroid disorder)

what the symptoms of thyroid disorders suggest

there is likely some overlap between thyroid hormones and the causes of the symptoms of MDD

role of estrogen/progesterone in MDD

we don't fully understand the role of estrogen/progesterone in MDD, but we believe there may be some link because women are 70% more likely to be diagnosed with MDD, but that does not necessarily mean they are 70% more likely to experience it

other possible explanation for MDD diagnoses being more common in women

women are more likely to report their symptoms and seek treatment

evidence that suggests there is a link between estrogen/progesterone and MDD

women are more likely to develop MDD in 3 main contexts, all of which are times when estrogen and progesterone are significantly changing: after they have given birth (around 2 weeks after), during menopause, or during the perimenstrual period

glucocorticoids (GCCs)

stress hormones that activate the adrenal glands (cortisol = main stress hormone in humans)

how GCC levels change with MDD

50% of people with MDD have elevated GCCs

important role of GCCs in MDD

GCCs impair dopamine signaling in the brain

the 4-step process that shows how repeated stress predisposes people to MDD

an environmental stressor causes the pituitary glands to release glucocorticoids into the blood, which then bind to glucocorticoid receptors, which epigenetically alters genes, some of which regulate dopamine in assisting communication between neurons, which can cause neuropsychiatric disorders

epigenetics

changes in gene expression without altering the DNA sequence

what can happen when the glucocorticoids epigenetically alter genes

it can cause dysfunction in dopamine signaling, which can cause neuropsychiatric disorders

2 pieces of evidence that suggest the more cortisol you take, the higher the probability of developing MDD

Cushing's Disease and people taking GCCs as anti-inflammatories

Cushing's Disease and its connection to MDD

when the adrenal glands secrete excessive GCCs; people with this disease are more likely to develop MDD

connection between MDD and people taking GCCs as anti-inflammatories

people who take these are also more likely to develop MDD

how to maximize efficacy of MDD treatments

using both pharmacological (biological - medication) treatment and psychotherapy

why the psychology of MDD is important

medication is only effective in 30-40% of MDD cases

2 major psychological theories of depression

Freud's Mourning and Melancholia theory and learned helplessness

Freud's Theory of Mourning and Melancholia

a theory that is still living today that says there are 2 varieties of depression: mourning and melancholia, which are both about loss (of a person, concept, object, etc.), but melancholia is more severe

Freud's Theory: mourning

when a person is able to accept the reality of the loss of something/someone important to them

Freud's Theory: melancholia

when a person is not able to accept the reality of a loss and instead holds onto what they've lost by internalizing the lost person/thing, and it becomes part of their self/identity

Freud's general idea of depression

he believed that depression was aggression turned inward because the anger that someone had over the loss of an object becomes directed at the self (depression as aggression turned inward is still a living theory)

Mourning and Melancholia in relation to situational/reactive depression and MDD

mourning is more similar to situational/reactive depression because it is less severe and the person mourns for a temporary period of time before accepting the loss; melancholia is more similar to MDD because it is long-lasting and more severe

learned helplessness theory of depression

MDD is more common in people who experience pathological loss compared to normal loss

learned helplessness theory - pathological loss

when people generalize the loss/pain of one situation to different following situations and believe they won't have any control over following situations

learned helplessness theory - normal loss

when people recognize that the situation in which they experienced loss/pain is different from the following situations, and they can still control their actions and other situations apart from the 1 harmful one

classic example of pathological loss

people who lose a parent by age 10 don't recognize the power and control they have or realize that not everyone they love will leave them, which can appear as MDD later (MDD more common in these people)

our current best progress on understanding depression

depression is partly genetic and starts with heritability, but many other factors contribute as well

evidence that something in DNA predisposes some people to MDD

identical twin experiments when separated at birth and raised in different environments showed that when 1 twin developed MDD, the other had a 60% chance of developing it as well (if there was no genetic involvement, that number would be around 17% cause that's the prevalence of MDD in the U.S.)

the gene that may contribute to the development of MDD

there are two versions of a gene linked to 5-HT (serotonin) that seem to interact with environmental stressors

"good" version of the 5-HT gene

stressors increase risk of depression

"bad" version of the 5-HT gene

stressors increase risk of depression 30x more than people with the "good" version

contribution of hormones to the 5-HT gene

glucocorticoids regulate the function of this 5-HT gene, which demonstrates the intersection of the 3 factors contributing to MDD

intersection of the 3 factors contributing to MDD

genetics, environmental stressors, stress hormones in the body

how the DSM-5 revamped our understanding of Schizophrenia

the DSM-5 now explains Schizophrenia as a spectrum instead of having subtypes

general explanation of Schizophrenia

primarily a disorder of thinking and speech

DSM-5 criteria for Schizophrenia

must experience 2 or more of the listed symptoms within a 4-week period: disorganized speech, hallucinations, delusions, negative symptoms, grossly abnormal psychomotor behavior (e.g. throwing arms around at random points)

specificities of Schizophrenia symptoms - concrete thought

thought becomes totally complete and people are unable to abstract out of the concreteness of the stimuli

proverb tests

used to test this concrete thought in people who may have schizophrenia, in which they are asked to explain a proverb (e.g. birds of a feather flock together) and people with schizophrenia genrally answer literally (e.g. "well all birds have feathers and fly in groups") instead of giving the generalized meaning of the proverb

coherency of schizophrenic delusions

can be internally coherent (make sense), but just not reality

most common schizophrenic delusion

paranoia

most common type of schizophrenic hallucination

almost exclusively auditory (visual is much less common)

positive symptoms

symptoms that include how someone is involved/contributing to society (i.e. what people are doing)

negative symptoms

symptoms that include what people are not doing; social withdrawal (become much more prominent as age advances)

self-injury and self-mutilation in people with schizophrenia

another symptom of schizophrenia in which (similarly to MDD) people are more likely to attempt suicide just after they have begun treatment and are slightly improving

prevalence of suicide attempts in people with schizophrenia

50% of people with schizophrenia attempt suicide and the more they attempt and "fail" and are treated, the more likely they are to try again (viscious cycle)

age of onset of schizophrenia

late adolesence - early adulthood; precipitated by a major stressor

why we're most vulnerable to schizophrenia at this point in life

it is one of the points of huge rewiring in the brain with frontal cortex maturation, this puts the brain in a more "fragile" place and a major stressor combined with this rewiring in people who are predisposed to schizophrenia can trigger it

prevalence of schizophrenia in the U.S.

1-2%

implication of the prevalence of schizophrenia being similar worldwide

implies that schizophrenia is much more genetic than environmental

gender differences in schizophrenia

seems to be no gender differences; there is some evidence that women may develop it later in life (25-29 compared to 20-24 in men), but it's not proven

treatment of schizophrenia

primarily treated pharmacologically; psychotherapy is less helpful than it is in people with other psychological disorders

prognosis 10 years after diagnosis of schizophrenia

prognosis is poor - 10% are dead (mostly suicide), 15% are hospitalized and unimproved, 25% are improved but need substantial support

2 biological bases of schizophrenia

neurotransmitters and brain structure

dopamine hypothesis

the proximal cause of schizophrenia is elevated dopamine levels in the brain

3 pieces of evidence supporting dopamine hypothesis

people with schizophrenia have: elevated dopamine breakdown products in blood/urine/cerebrospinal fluid (CSF), when autopsied, they're found to have more dopamine receptors than usual in frontal areas, and antipsychotic medications block dopamine receptors and can be effective