| what are drugs? | imitate substances already present in our nervous system, particularly those that affect transmission at synapse |
| 2 ways that drugs affect transmission at synapse? | antagonist
agonist |
| what is an antagonist? | blocks neurotransmitter |
| what is an agonist? | increase effects of neurotransmitters, mimic neurotransmitter |
| high affinity drugs.. | bind to the receptor |
| Order of drug stimulation on the release of dopamine | 1. drug
2. sustained burst of dopamine (inhibitory)
3. inhibit GABA (inhibitory transmitter)
4. increases activity in nucleus accumbens |
| high efficacy drugs.. | activate receptor |
| effects of speed? | stimulates dopamine synapses by increasing release of dopamine from presynaptic terminal |
| effects of cocaine? | block reuptake of dopamine, prolonging effects |
| what are opiates? | heroin
morphine |
| how do opiates work? | increase relaxation
decrease sensitivity to pain
mimic endorphins
attach to specific endorphin receptors
inhibit GABA= increase dopamine
blocks hindbrain area= releases norepinephrine (memory storage & stress) |
| effects of marijuana | contains cannabinoids
bind to specific cannabinoids receptors
inhibit GABA release
cannabinoid receptors abundant in hypothesis= increased appaetite |
| what is Botox? | deadly neurotoxin released by bacteria in decaying body
antagonist
blocks release of acetylcholine neurotransmitter junction- paralysis
small doses used to reduce muscle tremors& cosmetically |
| sensitisation of nucleus accumbens? | becomes more sensitive to substances after repeated use
increased ability to release dopamine in response to substance
reduced sensitivity to other things |
| facts about withdrawal? | craving for drug
relapse causes increased sensitivity
user learns drug will relieves distress associated with withdrawal
crave drug even more |
| describe the 2 types of alcoholism | type 1:
late onset (after 25)
gradual onset
equal men & women
less severe
type 2:
early onset (before 25)
rapid onset
more men than women
severe |
| how do genes effect alcoholism? | coding for an increase in risk taking beh.
coding for an increased stress response= more likely to relapse after quitting |
| what is depression? | clinical/ major depression
feeling extreme sadness & helplessness
interfere with daily life
twice as common in women than men
5% adults have clinically sig. depression |
| what causes depression? | some heritability
relatives more likely to suffer from anxiety, substance abuse, bulimia
more common among family of women with early onset depression
low serotonin turnover
genes controlled serotonin (MAOA) implicated |
| how does MAOA affect ppl? | short & long types
having 2 short types= more likely to be depressed in response ton stressful events |
| postnatal depression | 20% women
0.1% long lasting
runs in families
normal reaction after childbirth |
| 2 types of bipolar disorder | unipolar disorder
bipolar disorder |
| what is unipolar disorder? | varying between normality & depression |
| what is bipolar disorder? | varying between mania & depression |
| what is mania? | restless activity, excitement, confidence
increased metabolism
treated with limbic salts |
| what is seasonal affective disorder? (SAD) | depression associated with one season (usually winter)
common near poles- long nights
less severe than major depression
light therapy as treatment |
| what is schizophrenia? | split mind
refers to division between emotional & intellectual experiences & beh.
not related to multiple personality disorder
show inappropriate emotional expression |
| positive symptoms of schizophrenia? | delusions
hallucinations
odd emotional displays
thought disorder |
| negative symptoms of depression? | poor social interaction
poor speech
absent facial expression |
| neurodevelopmental hypothesis in schizophrenia | abnormalities in development of NS before & after birth
infections, poor nutrition, complicated delivery
slight brain abnormalities |
| what are ventricles? | fluid filled space in the brain |
| why do brain abnormalities occur? | 1. ventricles larger, less space for brain cells
2. prefrontal cortex damaged
3. cell bodies smaller in hippocampus & prefrontal cortex
4. less lateralisation than most ppl |
| what is lateralisation? | the development of specialised functioning in each hemisphere of the brain |
| dopamine hypothesis of schizophrenia? | excess activity of dopamine synapses
schizophrenia patients have twice as many receptors than other ppl
normal levels of dopamine are found when measured |
| glutamate hypothesis for schizophrenia | deficient activity at glutamate synapses
related to dopamine- dopamine inhibits glutamate release
glutamate activates neurons that inhibit dopamine
PCP & angel dust inhibit glutamate receptors & produces similar symptoms to schizophrenia |
