Bio Psych Exam #3 Flashcards
Psychopharmacology
the study of drugs that affect the nervous system and behavior
What is a drug?
An exogenous (made outside of the body) chemical not necessary for normal cellular functioning that significantly alters the functions of certain cells of the body when taken in relatively low doses
(exogenous, low doses, not necessary
Drugs and behavior
The changes a drug produces in an animal’s physiological processes and behavior
- Ex: morphine/heroine and other opioids are pain relievers
Drugs have sites of action
each drug has a unique effect and a site of action
**Ex: there are specialized receptors for opioids; when molecules of heroin activate these opioid receptors the activity of the neuron changes
Pharmacokinetics
what the body does with the drug
Absorption types
1) Intravenous (IV) injection - into a vein
2) Intraperitoneal (IP) injection - into space surrounding stomach, liver → usually in animals
3) Intramuscular injection (IM_: vaccines
4) Subcutaneous injection (SC) = into the space beneath the skin
5) Orally = swallow pill
Sublingual - under the 6)tongue
7) Inhalation - smoked
8) Intranasal - snort
9) Topical - into skin
Cocaine absorption
1) IV: strong high immediately
2) smoking: similar to IV, less higher
3) snorting: takes a bit to kick in, less high but lasts longer
4) oral: takes an hour to kick in, less high but lasts very long
Oral dose vs. Sublingual
1) Oral: Has to go through many steps to get to the brain
2) Sublingual: under the tongue
- Dissolve and can get into the blood system immediately: travel through the capillaries in your mouth
Goes to the brain almost immediately
Distribution of drugs within the body
After absorption, the drug distributes to interstitial and intracellular fluids → depends on some physiological factors and physicochemical properties
Body parts with high drug distribution
The liver, kidneys, brain, and other well-irrigated (have the most blood supply) organs receive most of the drug
Body parts with low drug distribution
Release to muscles, most viscera, and adipose tissue (fat) is slower
What prevents drugs from getting to the brain?
- Blood-brain barrier: a barrier that restricts the indiscriminate access of certain substances in the bloodstream to the CNS
- A layer of astrocytes that prevents substances in the circulating blood from freely entering the extracellular fluid of the brain
lack of blood brain barrier in:
1) Pituitary gland
2) Pineal gland (day/night cycle) → drugs can easily impact sleep
3) Area postrema (vomit toxic substances): in the brain stem
Metabolism
Set of reactions and transformations that drugs undergo in the body
Excretion
Elimination by the body of residues of drug metabolism
Kidney and excretion
Take blood and filter out waste products
**most important excretory organ
Excretion pathways
1) Renal (kidneys)
2) Biliary (bile) and fecal (poop)
3) Pulmonary (lungs)
4) Sweat, saliva, and tears
5) Breast milk
Dose response curve
Systematically titrate the dose of the drug: see what the effect of the drug is at each dose
Left: The dose is too low to have any therapeutic benefit
Right: point where the dose plateaus → If you give the patient a larger dose, the therapeutic benefit does not increase
The margin of safety on a dose response curve
1) The effective dose (orange)
2) Where it becomes lethal (purple) → opioids will stop respiration
Tolerance
A decrease in the effectiveness of a drug administered repeatedly
- Once someone has developed tolerance, they will likely show withdrawal symptoms
- Decrease in effectiveness of binding, **receptors become less sensitive or receptors decrease in overall numbers
Sensitization
An increase in the effectiveness of a drug that is administered repeatedly
Less common than tolerance
Can get both tolerance and sensitization
Example of sensitization and tolerance
Example: movement effects of cocaine show sensitization → repeated use leads to movement disorders./convulsions whereas euphoric effects don’t show sensitization, maybe even tolerance
Can develop tolerance to the euphoria
Can develop sensitization for movement disorders
Agonists
A drug that mimics or facilitates the effects of a neurotransmitter on the postsynaptic cell
- a drug that helps the system
Birth of agonists
some neurotransmitters need raw/precursor materials
*If we administer more of the precursor, we get more neurotransmitters → our effects are enhanced
Antagonists
A drug that opposes or inhibits the neurotransmitter on the postsynaptic cell – harms the system
Antagonist birth
Birth: some of the synthesizing steps are controlled by enzymes
*if we neutralize the enzymes with a drug, it prevents the neurotransmitter from being produced (effects blocked)
Competitive binding
only one spot (for drug or neurotransmitter)
- Direct agonis or Direct antagonist
Noncompetitive binding
It is possible for NT to bind to one part and the drug to bind to another part
- Indirect agonist or Inverse agonist
Psychotropic
drugs that impact behavior
1) Antidepressants:
used to lift mood out of a depressive episode
Antidepressants treat
Depression (mainly)
Anxiety disorders
OCD
Panic disorders
Phobias
Bulimia
PTSD
Neurotransmitters involved in mood disorders
Dopamine
Noradrenaline
Serotonin
Mood disorders
symptomatic issues in people’s affect
Symptoms of mood disorders
1) Reduction in positive affect: loss of happiness, loss of interest less and/or energy (nor and dop affected)
2) Increase in negative affect: more depressed mood, more guilt, more anxiety, etc. (nor and serotonin affected)
Types of antidepressants
1) Selective serotonin reuptake inhibitors (SSRIs)
2) Serotonin-norepinephrine reuptake inhibitors (SNRIs)
3) Norepinephrine and dopamine reuptake inhibitors (NDRIs)
4) Tricyclics: not used anymore due to side effects / MAOs
mood stabilizers:
regulate mood so it doesn’t get too low (depression) or too high (mania)
Types of mood stablizers
Lithium:
Mechanism of action not known
Effective for manic episodes and maintaining remission
Helpful for suicide prevention
Anticonvulsants (anti-epileptic):
Uncertain mechanisms of action (might act on GABA)
Effective for acute manic phases of bipolar disorders
Inconclusive for bipolar depression
Many side effects (exhaustion)
anti-anxiety medications
high overlap with depression
SSRI and SNRI
Anticonvulsants
Benzodiazepines
Benzodiazepines
Depressants and sedatives → feelings of calm drowsiness, GABA agonists
Inhibits the arousal system
People tolerate well but risk of dependence, abuse, and withdrawal reactions
Examples: Xanax, Valium, Ativan
** do not combine with alcohol
Benzodiazepines and alchol
Chloride channel: when GABA binds, it opens the channel; why it is inhibitory (lets more negative in)
Alcohol increases GABA binding → chloride channel open for longer
Noncompetitive binding: Benzodiazepines can bind and open the channel even more
Effects summate (level up)
stimulants
Usually used to treat ADHD and some sleep disorders
Types of stimulants
Amphetamines
Adderall: blocks the reuptake of norepinephrine and dopamine
Ritalin: non-competitively blocks the reuptake of dopamine and noradrenaline
Major potential for abuse
**do not combine with alcohol
typical antipsychotics
First generation → 1950s
Generally, they are blocking dopamine at D2 receptors → tight binding
Useful but prescribed out of desperation → high risk of side effects
Ex: Haldol and Thorazine
Psychosis
a condition where people lose touch with reality
- Hard to tell what is real and what is not
Delusions and hallucinations
Atypical antipsychotics:
Second generation (1990s)
Also blocking dopamine at D2 receptors → use loose binding (not as stuck into the receptor)
Very useful
Side effects are not as bad as typical antipsychotics
Ex: Risperdal, Olanzapine
Order of operations: what should be treated first?
1)alcohol/stimulant/substance abuse
2) mood disorders
3) anxiety disorders
4) ADHD
5) nicotine dependence
Substance abuse disorder
The compulsion to seek out and take the drug
Impaired control in limiting intake (can not stick to having “just one”)
Persistent despite very clear evidence of overtly harmful consequences
Progressive neglect of alternative pleasures or interests
Relapse → not required for substance use disorder but common
Positive reinforcement
something good is added
A positive consequence will increase behavior
Ex: rapid euphoria after taking a drug will increase drug-taking behavior
Neural mechanism of positive reinforcement
Synaptic strengthening in the ventral tegmental area (green pathway is strengthened)
VTA: sits next to SN → also dopaminergic
Mesolimbic pathway (from VTA to the ventral striatum (aka nucleus accumbens))
**Ventral striatum (nucleus accumbens) → inital stages of addiction behaviors
Dorsal striatum (caudate + putamen): habit-formation; cue induced
Negative reinforcement
A response/behavior is strengthened when you remove/avoid the aversive thing
Ex: feeling of alleviated pain after drug taking will increase drug-taking behavior
Incentive-sensitization theory of substance abuse
Wanting and liking are different and mediated by different brain circuitry
- wanting: based on cues from the environment, becomes hyperactive over time (compulsive)
- liking: actual pleasurable impact of the reward consumption
Neural pathways of wanting and liking
Striatum (midbrain) to nucleus accumbens
White: liking pathway
Gray: wanting pathway
Risk factors of addiction
Age: older adults more likely to abuse certain styles of drugs
Genetics
Environment:
- Adverse childhood experiences (ACEs)
Neurological disorders definition
diseases of the central and peripheral nervous system
Mental disorder
generally characterized by a combination of abnormal thoughts, perceptions, emotions, behavior, and relationships with others
Psychiatrist
able to conduct psychotherapy and prescribe medications and other medical treatments
Psychologist
often has extensive training in research or clinical practice
Psychologists treat mental disorders with psychotherapy and some specialize in psychological testing and evaluation
Research PhD
DSM
Lists symptom checklists for many disorders → have to see where your symptoms cluster as there is no physiological test for a disorder
What you need for a mental health disorder diagnosis
Impairment of functioning that impacts quality of life
Duration → needs to be persistent
Pros of the symptom checklist approach
Measures the invisible
Standardization
Can help rule things out
Cons of the symptom checklist approach
Wrong way of measuring?
Different clinical presentation earns the same diagnosis → depression can be different for everyone
Is it helpful for understanding?
History of depression
-not a diagnosis until the early 1900s
-1930s: benzine was marketed as a treatment for fatigue and mild depression-like symptoms (not depression)
-1940s: ECT to treat depression, don’t know why it works but it is effective
1950s: drugs for anxiety came out but they didn’t really help with depression
Late 1950s: first drugs that do seem to treat depression (meant to treat tuberculosis)
Serotonin hypothesis of depression
If we block the reuptake of MAO and people get happier, there must be low levels of these neurotransmitters in people with depression
Is the serotonin hypothesis of depression correct?
**NO evidence to suggest that low levels of neurotransmitters cause depression → These drugs do help but this is not the root cause
Neurotrophic
related to the growth/survival of neurons
Neurotrophic hypothesis
**depression is caused by low lebels of neurotrophins (BDNF) which leads to neuronal loss
increased 5-HT (serotonin) and NE activity at certain synapses → leads to important downstream actions that may underlie the observed antidepressant effects
**metabatropic receptors: downregulation of post synaptic receptor
Downregulation
decreased response and/or decreased number of or sensitivity of receptors
BDNF
BDNF: brain-derived neurotrophic factor → involved in plasticity for learning and memory
**When stress hormones increase, BDNF decreases - antidepressants may work to reverse this
Transcription
the process by which a cell makes an RNA copy of a piece of DNA → this RNA copy (messenger RNA, mRNA) carries the genetic information needed to make protein in a cell
Why is it hard to treat depression?
Other symptoms
Underlying mechanisms
Max efficacy
Prescription of drugs
SSRIs are usually tried first because they are generally well-tolerated
Choose a low dose (often not even therapeutic) and slowly ramp up
Adequate trial is at least 6 weeks at a therapeutic dose
Biorhythm
natural rhythm in behavior or a bodily process
Circannual biorhtyhms
yearly
ex: migration of birds
Infradian
more than a day
- ex: human menstrual cycle
Circadian
daily
- ex: human-sleep wake cycle
Ultradian
less than a day
- human eating cycles
diurnal
the opposite of nocturnal (active during the day)
Circadian rhythms are not just sleep but…
pulse, blood pressure, body temperature, alertness, feeding behavior and more
Are biorhythms endogenous (internal) or exogenous (external)
Biorhythms are endogenous (internal) - we have a biological clock in the neural system that times behavior by producing biorhythms
Bunker sleep study
Over time: sleep times shift but are not chaotic → stays constant but shifts a bit (a slow progressive shift that is not linked to external cues)
Over time: getting up when the night was → the rhythm did not go away but it was not synced to the world
Biological clock
Synchronized behavior to the passage of a real day and make predictions about tomorrow
Anticipate events, and prepare for them physiologically and cognitively
Regulates feeding times, sleeping times, etc
What impacts circadian rhythms
Light pollution (phones)
Jet lag (going west to east is more challenging than going east to west)
Master clock neurology
Superchiasmic nucleus of the hypothalamus (SCN)
** above the optic chiasm
Retinohypothalamic pathway
We get visual information which hits photoreceptors (tells us light or dark
Activates RGCs → produce melanopsin (hormone) → talks directly to the suprachiasmatic nucleus
If dark is signaled to the SCN
signal goes to the Ventrolaterial preoptic area
If light is signaled to the SCN
signaled to Orexin neurons (lateral hypothalamus)
SCN sends information to …
Hypothalamus
Thalamus
Pituitary
Autonomic neurons in the spinal cord
Master Clock Summary
1) special photopigment in ganglion cells
2) relevant information travels to SCN (retinohypothalamic pathway)
3) SCN is the master clock: daily rhythms observed in firing rate of cells
4) SCN exerts control by: direct synaptic connections with other regions, secreting neuromodulators (melatonin)
Sleep stages
1) awake
2) non REM (N1, N2, N3)
3) REM
awake EEG
alpha activity + beta activity
- Alpha: higher amplitude → resting/relaxing
- Beta: smaller amplitude → alert, attentive, thinking
N1 EEG
theta activity
Alpha activity decreases, slow rolling eye movements, motor activity slightly reduced, partial awareness of surrounding
N2 EEG
sleep spindle → k complex
Eye movements are rare, not much motor movement, some bursts of waves, sleeping soundly
N3 EEG
delta activity:
Aka SWS (slow-wave sleep): high voltage waves, eye movements rare, not much motor movement
**deepest sleep
REM (rapid eye movement) sleep
theta activity → beta activity
EEG reverts to a mix of beta and theta, bursts of eye movements, muscle paralysis
EEG output is very similar to when you are awake
Full night sleep cycle
90 minutes → go through 5-6 of these cycles per night
REM happens around the end of the 90-minute period
Adults who sleep 8 hours spend about 2 hours in REM sleep
Changes in sleep over the lifespan
As we get older:
We get less sleep overall
Less REM sleep
What happens in N sleep
Dreaming occurs in N-sleep but is not as vivid
Sleepwalking
Sleep-talking
Night terrors (40% of children): the only type of vivid dream in N sleep
Talking or grinding teeth
Flailing, banging an arm, kicking a foot
Maintaining muscle posture
Maintaining muscle posture
Sleep may occur in a variety of positions → standing up, sitting, or several reclining positions – in N sleep
REM sleep: (R-sleep)
Atonia: no muscle tone; conditions of complete muscle inactivity produced as sleep regions of the brainstem inhibit motor neurons
Mechanisms that regulate body temperature stop working → body temp moves towards room temp (gets higher)
Dreaming
Dreaming
Vivid dreams in REM
Everyone dreams a number of times each night
Dreams appear to take place in real-time; dream sessions get longer throughout a sleep session
Histamine
keeps you awake
Orexin
How we control staying awake (motivation)
What area controls sleep patterns?
Ventrolateral preoptic area (VLPOA)
Ventrolateral preoptic area (VLPOA)
GABAergic neurons (inhibitory)
Inhibits the around brain systems (flip-flop circuit)
**see images here
Why do we sleep?
Energy conservation
Restoration
Learning and memory
Sleep for energy conservation
Reduces a person’s energy demand during part of the day/night when it’s least efficient to hunt for food
Support: body has decreased metabolism when sleeping
Sleep for restoration
Sleep lets the body repair and replete cellular components necessary for biological functions that become depleted throughout an awake day
Clears out waste products of neural activity
Sleep for learning and memory
Patterns that you experience during the day reactive when sleeping (almost reliving) → keeping important memories and reliving to better remember them (neurons that fire together wire together)
Sleep disorders
Narcolepsy
REM sleep behavior disorder
Narcolepsy
Slow-wave sleep disorder in which a person uncontrollably falls asleep at inappropriate times
Symptoms of narcolepsy
1) Cataplexy: sudden loss of muscle tone → slurred speech, weakness → often triggered by a strong emotion
2) Sleep paralysis: temporary inability to move or speak while falling asleep or upon waking → can remember these events
3) Hypnagogic hallucinations: particularly vivid and frightening because you may not be fully asleep when you begin dreaming and you experience your dreams as reality
Neural Features of narcolepsy
Low levels of orexin/hypocretin
Genetic: 20-40x more likely to get it if you have a family member with narcolepsy
REM sleep behavior disorder
Physically act our vivid, often unpleasant dreams
- Sleep talking, shouting, screaming, hitting, punching, etc. → can be dangerous
- no atonia of muscles
- Seems to be linked to Parkinson’s and other neurodegenerative disorders but it is unclear why
Manipulations technique definition
Manipulation technique: the structure or function of the brain is altered and the resulting effects on behavior are observed
*hard
Measurement technique definition
brain activity is measured during a task to identify brain areas that might be involved in the performance of that task
Manipulations
1) lesions
2) Brain stimulation (DBS, TMS, optogenetics)
Lesions
Assumption: The function of a brain area can be inferred from the behavior that can no longer be performed after the area is damaged
Cons of lesions
Control: something bad has to happen
non-specific/diffuse damage
Cortical reorganization
Was the behavior localized to begin with?
Deep brain stimulation (DBS)
Place an electrode into the brain → invasive for research only
Used to treat:
Parkinson’s disease
OCD
Cons of DBS
Usual surgery risks (risks increase with age): can outweigh the benefits
What if the placement isn’t exactly perfect
Transcranial magnetic stimulation (TMS)
Place a coil over a particular area
Current passes through, causing cortical cells to depolarize (in a semi-local way → not perfect but ok)
Pros of TMS
Noninvasive
Clinically used for depression
Used in research
Cons of TMS
How localized is it really?
Makes interpretation quite difficult
Reproducibility issues
Safety if doing it at home
Optogenetics
Genetically engineered mice → to express membrane channels that are light-sensitive
Light triggered: depolarization of hyperpolarization of cells
Can insert these proteins into particular areas and then apply light
**understanding neural circutry in living organisms
Cons of Optogenetics
Cells are responding to light, nut not how they would normally respond (validity)?
Trying to get more precision for the subtypes of neurons → What kind of membrane channels can you engineer
Not at the human level → no genetic engineering
Measurement examples
1) electrical activity (single/multi cell recordings, EEG, ECog, MEG)
2) functional brain imaging (PET, MRI, fMRI)
3) structural methods (CT/CAT, MRI)
Intracellular recording
tiny electrode inserted directly inside a neuron to record its electrical sensitivity
Extracellular recording
tiny electrodes inserted into the fluid surrounding neurons to record electrical currents generated by the neuron in the electrode’s vicinity
Electroencephalography (EEG)
Put electrodes on the scalp to record “brain waves”
Measuring the summed graded potentials from thousands of neurons
Done while someone does something/something is happening (like a seizure)
- When ions flow in and out, they cause distortions in the electrical field
Pros of EEG
Really great temporal resolution (order of milliseconds)
Event-related potentials (ERP)
EEG that is synchronized with a task
cons of EEG
Poor spatial resolution → can be hard to figure out where exactly electrical signals came from
The skull distorts signals → since measuring from outside, bone distorts electrical activity
Electrocorticography (ECoG)
Intracranial EEG → remove the skull and directly place electrodes on the brain
See the prosopagnosia video from vision 2 lecture
For research purposes → often paired with some form of stimulation (manipulation)
Both manipulation and measurement
Usually people who are undergoing brain surgery anyway (often for epilepsy)
Magnetoencephalography (MEG)
Very similar to EEG, but magnetic waves are not distorted by the skull
Used MEG is overlaid on top of high-resolution MRI
Better spatial resolution
Cons of MEG
Need to should out any other magnetic fields → including Earth’s magnetic field
Have to create a room that blocks all magnetic fields
Have to keep the room cold: requires liquid helium to cool some of the sensors
~100 machines in the whole world → $2 billion each (2007 data)
Mobile MEGs are in the works
Positron emission tomography (PET)
Different radioactive agents can be used with biomarkers of disorders and pathologies
Radioactive things decay over time: can attach the radioactive agents to some construct of interest and follow it over time
Types of tracers in PET
FDG: analog of glucose
Oxygen-15: blood flow
Can also label chemicals such as neurotransmitters (e.g. dopamine)
Pros of PET
good for studying…
Task-related activations
Brain metabolism and neurochemistry
Cons of PET
ack of structure → can overlay this with a structural image
Lower spatial resolution (mm-cm)
Slower temporal resolution (tracer needs to watch out between experimental conditions)
Doesn’t image brain structure
Dealing with radioactive isotopes → hard to get past IRB and have a nurse on-site to inject and monitor the patient
MRI
Relies on magnets (~60,000x stronger than Earth’s magnetic field) → generally 3T sometimes 7T/11T
VERY strong
Pros of MRI
Non-invasive: subjection only exposed to magnetic field and radio waves
High spatial (~1mm voxels) → very clear and crisp
What does an MRI show?
White/gray matter
Bone shown, but CT is better for this
Cortical thickness (distance between gray matter and white matter)
fMRI
Most often measures the blood oxygen level-dependent (BOLD) signal
Indirect measure of neural activity
BOLD signal
When neurons fire, they require additional oxygen → BOLD relies on the different magnetic properties of oxygenated and deoxygenated blood
BOLD: ratio of oxygenated to deoxygenated blood
Decrease in BOLD: the area just used oxygen and now replenishing
Deoxy-hemoglobin
Paramagnetic iron → attracted to the magnet
Low BOLD signal
Oxy-hemoglobin
Diamagnetic iron → repelled by the magnet
Normal BOLD signal
Hemodynamic response function (HRF)
Time 0: when the stimulus is shown → immediately uses up a bit of oxygen
Time 4: overcompensation (increase in BOLD signal) → peaks about 5 seconds after activity happened
Comes back down
Undershoots
**see graph in notes
voxel
a 3D pixel: usually 1-3mm cubes and contain 100,000+ neurons
About 1,000,000 voxels in a brain scan
Cons of MRI AND fMRI
Movement matters → in order to get a clear image, the person has to be very still
- Who are we scanning → if you can’t move, you have to scan people who can lie still (not good for people with Parkinson’s or kids) + claustrophobia
Expensive
Statistical woes
Computerized tomography (CT/CAT)
Rotates an X-ray around the patient’s head
Pros of CT/CAT
Feaster and cheaper than MRI, but lower resolution
Can be used in situations where magnets cannot (implanted metal devices in the body)
Can detect major structural problems (tumor, bleeding, TBI)
Mind as a blank slate
nothing is given to us and everything is determined by our sensory experiences
Mind as a black box
stimuli comes in (sensations) and something happens that we can not see (mental processes) and then we get a product (behavoir)
Consilience
conceptual integration - hierarchy and similarities of information
Mind as a sponge
Given a tool to soak up information but not built in
Proximate vs. ultimate explanations
Proximate explanation: mechanisms and developmental history
- Immediate cause
Ultimate explanation: adaptive functions and phylogenetic history
Evolutionary cause (functional advantage)
- The “why
Mild depression and evolution
“survival value” as a social-emotional hibernation that allows humans to:
- Conserve energy
- Avoid conflicts and other risks
- Let go of unattainable goals
- Take time to contemplate (rumination)
- Signal to others the need for assistance
Actigraphy
Actigraphy looks at:
Sleep activity
Sleep variability
Sleep timing
Sleep duration
Sleep onset latency: how long it takes to fall asleep
- collected on watches
Pros of actigraphy
measures biological sleep data
Cons of actigraphy
can not measure the subjective “goodness” of sleep
Social disadvantage and brain structure of infants
Greater irregularity in mothers’ sleep schedule = smaller cortical brain matter volume, white matter volume, smaller cortex ** sleep may be a mediator
Increased Chronodisruption = smaller brain volumes
Increase chronotype = smaller brain volumes
Social disadvantage and chronodisruptions
sleep less/more varied due to stress, jobs, unpredictability of where you will sleep etc.
Chronodisruption
irregularity in the sleep period as indexed by variability in daily sleep duration
Sleep and depression
90% of adults and 73% of youth diagnosed with major depressive disorder report sleep disturbances
- May predict and precede depression symptoms and depression episodes
*depression does NOT cause sleep disturbances
Childhood depression
Depression onset at ages 3-5
- difficult for caregivers to detect
Subjective vs. objective measures of sleep
More sleep problems = more likely to show depression symptoms (concurrent association)
Caveat: not on subjective interviews (parents)
- you need to have both to get the full picture on sleep
Sleep disturbances and early childhood depression
- Sleep disturbances in infancy and toddlerhood precut the emergence of early childhood depression (at age 3)
- More sleep problems = more likely to show depression symptoms (concurrent association)
**early sleep disturbances and later depressive symptomology
Pharmacodynamics
What the drug does to the body
3 categories of symptoms for clinical disorders
1) emotional
2) neurovegatative
3) neurocognitive
