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Created by Elizabeth Then
over 8 years ago
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| Question | Answer |
| 2 main CNS pathways | serotonin and 5-HT important for sleep, mood, hallucinations, sensory transmission mostly g-protein coupled receptors |
| Main dopamine pathways in the CNS | mesolimbic pathway- brain reward system, facilitates learning, activated by drugs of dependence (DA release or blocks DA uptake) nigrostriatal pathway- deficiency of dopamine in this pathway, associated with parkinsons |
| Acetylcholine, Ach | CNS, brain stem, cortex and hippocampus, involved in parkinsons and alzheimers |
| Amino acids | glutamate and aspartate= excitatory neurotransmitters invloved in neurogenerative disorders, brain damage, strokes |
| GABA | inhibitory neurotransmitters GABA -A ligand receptors bind benzos, CNS depressants, alcohol GABA-B G-protein linked receptors inhibit neurotransmitter release |
| Depression | neurotransmitters: NA, 5-HT depletion |
| Depression treatments | alter amine storage, release or uptake within CNS SSRI= 5-HT uptake Tricyclics (TCA)= 5 HT > NA uptake Selective MAOI type A= prevents breakdown of 5-HT, NA, reversible, mainly CNS |
| Adverse effects of depression treatments | SSRI= headache, nausea TCAs= dry mouth, blurred vision, sedation, confusion MAOI type A= negligible cardiovascular effects |
| Schizophrenia | neurotransmitter: DA, 5 HT overactivity |
| Treatments for schizophrenia | control positive symptoms, hallucinations, delusions but not always negative symptoms mood antipsychotics- CNS effects Typical: block DA receptors, mainly the D2 (chlorpropazine) Atypical: mostly block 5 HT receptors (clozapine) |
| Adverse effects of schizoprenia treatments | Typical: can cause movement disorders, dry mouth, postural hypotension, sedation Atypical: reduction in white cell numbers |
| Parkinsons disease | progressice degeneration of DA neurons in the substantia nigra |
| Parkinson treatment | levodopa (precursor of DA) and carbidopa (peripehral dopa-decarboxylase inhibitor) |
| Parkinson treatment adverse effects | nausea, confusion, nightmares, with prolonged use of levodopa (2 years), it becomes less effective. |
| Alcohol CNS depressant | Alcohol causes activation of GABA-A receptor and inhibition of glutamate (NMDA type) receptor in brain. alcohol indirectly stimulates the release of endogenous opiods and dopamine int he brain reward system via inhibition of GABA neurons |
| BAC | blood alcohol concentration, amount of gram per 100 mililitres of blood, vary in genders, age, body size, liver, genetics |
| alcohol is metabolised by | mostly in liver and acetaldehyde is a toxic short lived metabolite, at low BAC, euphoric effect, loss of emotional restraint, mild impairment of judgement at high BACs, memory is affected, coma, death, stupor |
| Nicotine | improve cognitive function, mood, anxiety, decrease appetite is a nAch receptor agonist and stimulates the dopamine reward pathway in brain, therefore enhancing dependency |
| chronic use with nicotine | tolerance, withdrawal syndrome, mood, dysphoria, irritability, anxiety |
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