Prelim 2 Flashcards
Five tasks of the brain for all animals
1- Eating and drinking
2- Fighting
3- Courting
4- Mating
5- Caring for offspring
Brain stem structures
Medulla, pons, midbrain, cerebellum, basal ganglia
?
Medulla
Sits on top of spine and regulates heart rate, blood pressure, rate of respiration, basic essential functions
Pons
Switch for sleep and wakefulness
Midbrain
Sits on top of pons, controls body movement in fight and sex, lowers pain during both, carries out orders from cortex, calls shots in lower mammals
Cerebellum
Takes sensory info from nervous system and communicates with frontal lobes, makes physical motion precise and nuanced, when damaged movements are jerky
Basal ganglia
Higher level of motor control, involved with control of slow movements, large muscles, learning specific actions
Thalamus
Evolved to process sensory information more deeply and with more detail before sending it on to frontal lobes, has two parts- one for each hemisphere
Hypothalamus
Smaller than thalamus, takes info from sensory organs, regulates pituitary gland which releases hormones, so involved with eating, drinking, sexual behavior
Limbic system
Border of cerebral hemispheres and brain stem, bringing information from cerebellum, routing it to the centers of the brain generating conscious thought while also contributing to awareness, emotion, aggression and memory
Hippocampus and amygdala
Hippocampus
Episodic memory, directs memory storage and retrieval, encodes spatial memories, in rats hippocampi shown responsible for remembering way through mazes
Amygdala
Instinctive aggression, fight or flight in lower mammals, plays a role in our response to threats or trauma, increased activation in PTSD
Cerebral cortex
Two hemispheres connected by corpus callosum, each hemisphere has four lobes
Occipital lobe
Visual cortex, generates images from information sent up through brain stem, and visual association cortex which generates visual memories, categories, focus
Temporal lobe
Primary auditory cortex and its association area
Parietal lobe
Primary somatosensory cortex and somatosensory association area
Frontal lobes
Fine movement, language, thought, judgement generated, prefrontal cortex rewires during adolescence and results in abstract thinking and higher orders of analysis and creativity
Computed tomography
Images from narrow x-rays passed through the brain
Magnetic resonance imaging
Magnetic field around brain agitated by radio waves, scanner measures rate by which molecules return to resting state
fMRI
Detects levels of oxygen in brain’s blood vessels
Micro-electrodes
Measure electrical charges of individual neurons
EEG
Sensors placed on forehead measures seizure activity and stages of sleep
PET
Images brain activity by measuring positrons emitted by radioactive particles injected into brain, scientists combine specific chemicals with radioactive material to observe specific brain activity
Functioning system
Luria
You learn a complex action by first learning the separate actions which compose it
Once you’ve mastered the separate actions, your brain writes a “macro” for the whole action
This is stored in a different part of the brain
Ways to misuse brain imaging
- Reverse mind/body dualism to “prove” “brain theory” ie using neuroimaging to show that a difference in behavior has an associated difference in the brain
- Using data to reduce complexity of brains to something simply physical
- Ignoring that fact that the brain constructs itself from experience (if time come back to practice slide 35), what we learn in adolescence constructs the brain
To use brain imaging well
- Think of brain as a collection of verbs, parts derive meaning from experience and contribute to awareness
- Explore how brain constructs itself
Brain organization
Nervous system and sensory organs feed information to spinal column which goes to hindbrain, hindbrain gives info to midbrain, where information is processed and refined and shared with cortex through clusters of neurons that project from midbrain to lobes of brain, bringing information that is experienced as thought, anxiety, and mood
Neuron structure
Dendrites receive messages to other cells, connect to cell body (soma) which connects to axon which passes messages away from cell body to other cells
How neurons are build
Fluid inside- cytoplasm- and outside- extracellular fluid
Generating energy with ATP?
Myelin coating made by glial cells, thicker coating faster conduction
Chromosomes inside
Neuron firing
Neurons change the polarity of other neurons by flooding them with ions until they fire or sending neurotransmitters into synapses that switch on genes in other neurons causing them to produce proteins that change them- generate new receptors, make more NTs, etc
Why and how neurons fire
Neuron has resting electrical charge, high levels of potassium in cell, when sodium enters cell, charge rises, neuron fires and releases NTs or passes charge to another neuron
Excitatory post synaptic potential
Charge builds and then stops before charging
Inhibitory post synaptic potential
Charge drops lower than resting
Ionotropic receptors
NTs open channels at the receptor’s center allowing ions to enter the cell
Metabotropic receptors
NTs cause the receptors to create a G-protein which opens ion channels or creates a second messenger that switches on DNA in the neuron leading to cellular changes
Basic mechanism is activation of G protein followed by simulation or inhibition of effector enzyme in the membrane of the postsynaptic cell, followed by increased synthesis or breakdown of a second messenger, followed by biochemical changes in the postsynaptic cell due to altered levels of the second messenger, biochemical cascade causes a wide variety of changes in the neuron including long-lasting changes in gene expression
Neurotransmission
Neurons respond to input from other neurons and chemicals
Amino acid transmitters
Glutamate-made in glial cells, excitatory neurotransmitter, precursor to GABA- inhibitory neurotransmitter
Acetylcholine
Involved in lots of things, found throughout body
Catecholamines
Dopamine, norepinephrine, epinephrine
Dopaminergic neurons
Create vesicles and move into membrane, releasing DA into synapse, have autoreceptors that receive DA and if these take in enough, stop releasing, also have transporters that vacuum excess, help neuron maintain a precise amount of DA in synapse
DA/NE balance
Contribute to regulation of function in body, severe consequences if too much or little of either- behavioral depression in rabbits with low supplies of these
DA pathways
Midbrain to striatum- nigrostriatal, gross motor movements, shortage is tremors and Parkinsons, VTA to limbic system- mesolimbic, affects emotion and memory, VTA to prefrontal area- mesocortical, high order thought etc affected by LSD marijuana etc
NE pathways
Brainstem to every part of forebrain, role in hunger, sex, arousal, sleep, fear, pain, anxiety, etc
Serotonin
Functions throughout nervous system, crosses blood brain barrier, made from tryptophan which if depleted makes people more sad
Sero neurons
Vesicles release Sero, autoreceptors, and transporters, maintain precise amount in synapse like DA
Sero pathway
Midline of brainstem to every part of brain
Serotonin receptors
Many kinds of receptors, 5-HT 1A contributes to mood and anxiety, mice without the receptor have high anxiety
Serotonin and depression and anxiety
If increase, by adding agonists that power receptors or block reuptake of transporters or forcing release from neurons can decrease A and D
Class assessment
Rarely say feel depressed even if other answers show depressed, 60 for mild depression, 42 clinically relevant, more unhappy than prison inmates, narrative completion test predicts CESD depression, as a whole this and early memory do, both projectives predict self report depression
Roy Baumeister escape theory
Suicidal ideation, escaping negative affect by cognitive deconstruction- time perspective constricted, concreteness- focus on immediate stuff, proximal goals- immediate goals
Depressed teen study
Depressed adolescent girls, matched, one group suicidal one group not, father’s mood powerfully predicted suicidal thoughts
3 kinds of suicide
- Thoughtfully planned out
- Done impulsively with hope of being stopped
- Committed bc of psychotic thinking during a severe depressive episode
What prevents suicide?
Love and attachment to others, a sense that one can change their life, restored hope in a future self, ability to appreciate life philosophically, learning that loss is a part of life
Bi-Polar Depression
Strongly heritable, 50% with identical twins
BP 1- full blown mania, includes psychotic elements
BP 2- more variable, major depression followed by hypomania- lesser manic states without psychosis
Manic episode diagnostic criteria
At least a week of persistently elevated, expansive, irritable mood and more
Treating BP1
Lithium reduces manic psychotic thinking and behavior
Seems to stimulate a neurotropic factor that maintains healthy dendrites and is an agonist of an enzyme the regulates transmission
Anticonvulsive medicines are even better, support BDNF production and growth of GABA neurons
GABA agonist alsot helps
But BP patients, when manic, don’t believe they are sick
BP2 criteria
1 or more major depressive episode
1 or more hypomanic episode
Never manic
Hypomanic episode- 4 days
Kinds of depression
Dysthymia- mild dep
Unipolar dep- only dep
Bipolar dep 1- dep and mania
B dep 2- dep and hypomania
Cyclothymia- dysthymia and hypomania
Dysthymia/Persistent Depressive Disorder diagnosis criteria
Depressed mood for 2 years, most of day for more days than not
Major depressive disorder criteria
2-week period, 5 symptoms w one being depressed mood or loss of interest/pleasure
Cognitive model of emotions
Event, thought (interpretation), emotion
Attributional style of depression
People with depression think things happen for reasons that are:
Internal
Permanent
Global
Non-depressed:
External
Single Event
Specific Domain
Multi-Hit Model
Multiple risk factors lead to depression- life events, personality, genetic vulnerability
Three kinds of people - depression
- People w/o dep
- People who usually don’t have dep but develop symptoms when stressed beyond a certain point, fine when crisis resolves
- People who are chronically depressed, only experience relief with meds
Brain structure + depression
HPA Axis- when threatened, hypothalamus sends hormone CRH to release ACTH from pit gland, ACTH causes stress hormones like cortisol from adrenal gland, hypot should shut off CRH when cortisol reaches level, but this fails in depressed people, excess CRH, dendrite damage to hippocampus neurons that have CRH receptors
Brain circuit of depression
Prefrontal cortex- less volume more activity
Hippocampus smaller
Amygdala larger
ACC activated by extreme sadness
NA less active, linked to adaptability
Neuronal pathways of depression
Serotonin/NE- depressed people don’t make enough of these
BDNF keeps dendrites healthy, unhealthy ones don’t work well and absorb lower levels of Se and NE, symptoms of depression lessen with more BDNF
MAO inhibitors
First antidepressant, blocks MAO which breaks down excess Se and NE, so more NT in synapse, but also down-regulates receptors on post-synaptic neuron, also serious side effects and diet issues can’t eat things
Tricyclics
Reuptake inhibitors, block transporters (vacuums), but also blocked other receptors which caused bad side effects, esp with histamine receptors
SSRIs
Target receptors more carefully, reduced side effects, blocks reuptake which leads to an increase in Se which causes autoreceptors to downregulate which causes neurons to release more Se and increase in Se causes post synaptic receptors to downregulate which reduces side effects (?)
Schizophrenia diagnostic criteria
2 or more present for significant period of time during 1 month period-
Delusions
Hallucinations
Disorganized speech
Grossly disorganized or catatonic behavior
Negative symptoms
Acute onset schizophrenia
Happens suddenly, late teens/early 20s for men and a little later for women
Prodromal onset schizophrenia
Person always had odd characteristics, often socially isolated, slides in schizophrenic episode
Positive symptoms
Mental features that shouldn’t be there
- Delusions
- Hallucinations
- Bizarre speech
- Inappropriate affect
- Perseverations or clang associations
- Violent or threatening behavior
Negative symptoms
Loss or absence of mental functioning
- Flattened affect
- Paucity of thought
- Catatonia- restriction of movement
- Lack of social awareness
- Poor hygiene
Schizophrenia as a neurodevelopmental disorder
Genetic liability
Intrauterine trauma, infection, stress
Environmental, psychological stress
Leads to schizotype- expressing symptoms of neurological deficits or schizophrenia- prodromal or acute onset
Developmental model of schizophrenia
Gene, schizotypy, stressors- second hit leads to schizophrenia or schizotypal PD or deviance on lab tests
Schizotypes
People with schizophrenic liability
Endophenotypes
Ways schizotypes differ from healthy comparison subjects
A measurable component unseen by the naked eye along the pathway between disease and genotype
Could be neurophysiological, endocrinological, neuroanatomical, cognitive, neuropsychological
Represents a simpler clue to genetic underpinnings than the disease syndrome itself
Confirmed deficits in schizotypes
Sustained attention/vigilance
Abstraction ability
Working memory
Attentional inhibition
Smooth pursuit eye movement
Antisaccade performance
Thought disorder
Personality/psychopathology
Schizophrenia neuroanatomy
During second trimester of pregnancy, when neurons migrate to what will develop into the ventricles of the brain, neurons don’t set up properly and lead to a cascade of deficits which, during anatomical and hormonal changes in adolescence, leads to schizophrenic episode
Four subgroups of schizophrenia
Sensitivity psychosis- solitary, minor stress, negative symptoms
Drug-related psychosis- initial presentation is drug-induced, recurrence when drugs not present
Trauma-related psychosis- associated with PTSD and depression
Anxiety psychosis- acute onset, stress-related, further episodes in response to stress
Antipsychotic meds
Excess of DA involved in hallucinatory experiences, medications lowering DA lead to reduction in positive symptoms
Mesolimbic area is related but can’t target specific areas of the brain with meds so meds lower DA everywhere
Dopamine levels
Too much in mesolimbic- pos symptoms
Too little in mesocortical- neg symptoms
Too little in nigrostriatal- parkinsons symptoms
Too little in tuberoinfundibular- breast milk secretion
Atypical antipsychotics
Targets specific DA receptors, and serotonin-dopamine antagonist: blocks serotonin receptors that inhibit DA release in adjacent DA neurons, so DA is released
DA antagonists inhibit release of DA in key pathways, SDA inhibitors cause release of DA in those neurons, so lower DA overall, but not too much
RD Laing categories schizophrenic experience
Engulfment, implosion, petrification and depersonalization
Ontological insecurity
Absence of assurances derived from firm sense of own and other people’s sense of reality and identity
