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PS2061 Lecture 6: Biological Basis of Psychological Abnormality (Methods…

- - - - Process at a synapse: 1. AP arrives at presynaptic membrane; 2. voltage gates calcium channels open and calcium ions diffuse into cell; 3. Ca increases causes vesicles to move to presynaptic membrane, where they fuse, releasing NT into cleft; 4. NT binds to receptors on postsynaptic membrane, causing opening of ion channels - if opens sodium channels then causes depolarization (excitatory postsynaptic potential EPSP), if opens chlorine channels then causes hyperpolarization (IPSP); 5. EPSP or IPSP propagated along membrane towards the axon hillock
      - Postsynaptic receptors - each receptor only binds to a specific NT (lock and key principle); when NT binds with receptor, the receptor changes shape, causing an ion channel to open; there are 2 types receptors: ionotropic - receptor is ion channel, metabotropic - receptor causes separate ion channel to open using G-protein coupling; when these ion channels open, causes influx of either Na or Cl which leads to either de- or hyperpolarization
      - When AP reaches axon hillock: If net charge (sum of EPSP's and IPSP's) is above threshold potential (-40mV) then an AP is elicited and travels along axon to axon terminal, where causes release of NT and passes signal to next neuron etc.
      - Neurotransmitters: many different NT's; they can be excitatory or inhibitory; each neuron synthesizes and releases one NT; NT's can be monoamines e.g. acetylcholine, dopamine, adrenalin, amino acids e.g. GABA and neuropeptides e.g. endorphins
      - Re-uptake: NT is either metabolised by enzymes in the cleft or moved back into presynaptic membrane by re-uptake pumps; continued presence of the NT in cleft would lead to persistent EPSP's or IPSP's, even without further APs
- - - - Monoamine Oxidase Inhibitors: inhibit enzymes that break down monoamine NTs, raising the levels of NT in the synaptic cleft; led to Catecholamine theory of Depression (Schildkraut, 1965) - depression caused by poor or failed expression of catecholamine at synapses, treatment can stop enzymes breaking down NTs which are not bound to a receptor
      - Tricyclic Antidepressants: similar effect to MAOIs but different action, these act to inhibit reuptake of NTs, again leaving more to bind with receptors
      - SSRIs: most modern drug for treatment of depression, more effective than MAOIs and have fewer side effects, they take up space where the seraotonin would be taken back in (block re-uptake channels) therefore increasing serotonin levels in cleft
      - MAOIs work on Catecholamines - Noradrenaline and Dopamine; however, not still believed to be sole cause of depression as there is no evidence of reduced levels in the brains of depressed people; therefore, believed they ignore another important NT - serotonin; therefore, a more broad Monoamine theory of depression established
      - MAOIs - affect NA/DA, highly effective, v bad side effects; TADs - affect NA/DA, highly effective, some side effects, suicide risk; SSRIs - affect serotonin, safe, few side effects; therefore suggests that both NA/DA and serotonin are important in depression - could be because low serotonin disrupts NA/DA system which causes depression; so correction of serotonin system would lead to correction of NA/DA system and depression symptoms alleviated
      - Problems with SSRI model: SSRIs increase serotonin in matter of hours, but takes weeks for relief from depression; could be because SSRI effect is via an intermediary response e.g. a secondary response in the brain in response to increased levels of serotonin --> more complex than just simple higher serotonin levels