Biology - Lecture 8 (Psychopharmacology)

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  • Lecture 8 - Psycho pharmacology
    • Neurotransmitter inactivation and recycling
      • 1. Diffusions: the transmitter is "lost" in the inter-cellular space
      • 2. Enzymatic degradation: enzymes break down the transmission
      • 3. Re-uptake: the transmitter is recycled either in the pre-synaptic or the post neuron
        • Thi is the most economical way to inactivate the transmitter
    • Substances
      • can interfere with the release of the transmitter by shutting some calcium channels, one reduce the amount of released neurotransmitter
        • e.g. the tetanospasmin toxin does this at inhibitory, GABAergic, synapses disrupting the natural balance of excitation and inhibition
          • This leads to very strong muscle contractions (tetanus) which can be lethal
      • can alter how the transmitter interacts with its receptors
        • Certain substances simply bind to receptors but without opening the channel
          • e.g. plant toxin curare acts as antagonist, and occupies acetylcholine's receptors in excitatory synapses, blocking them and causing paralysis
      • Agonists imitate the behaviour of the neurotransmitter, increasing its effect
        • Heroin - modified form of morphine - agonist of endorphins, natural body chemicals that bind to opiate receptors
          • = reduce pain + produce relaxation
    • Neuro transmitters
      • Acetylcholine (Ach) is a neurotransmitter that has two types of receptors: nicotinic (excitatory) and muscarinic (inhibitory)
      • Botulinum toxin (formed by bacteria in improperly canned food) interferes with the release of Ach at nicotinic synapses
        • by preventing the vesicles from fusing with the membrane
      • Due to its similarity to dopamine, amphetamine can enter the dopamine-releasing neuron either directly through the membrane or binding to dopamine transporter
        • Once inside the cell, mph facilitates release of dopamine from the vessel when these fuse with the membrane
    • Psychoactive substances
      • Alcohol
        • Low doses: is agonist of GABA (typically found in inhibitory synapses), thus increasing feeling of relaxation
        • High doses: binding of alcohol to GABA channels leads to sedation, higher doses can lead to destruction of cell membranes
          • = brain cell death
      • Coffee
        • Many of the neurons that release catecholamines also release (at same time) a self-inhibiting transmitter = adenosine
          • This binds to its receptors in the pre-synaptic neuron and inhibits release of catecholamines
        • Caffeine competes with adenosine for its receptors, reducing its inhibitory effect
          • Caffeine inhibits enzyme that breaks down cAMP = high glucose metabolism in cell
        • Caffeine acts on cyclic adenosine monophosphate (cAMP), which controls the energy levels in the cell via regulation of glucose metabolism
          • Caffeine inhibits enzyme that breaks down cAMP = high glucose metabolism in cell
    • Medication
      • Anxiety
        • BZs are GABA agonists, they do not bind to same receptor sites as GABA itself (non-competitive agonist)
      • Depression
        • MAO inhibitors: interfere with MAO enzyme, breaks down serotonin, dopamine + noradrenaline
        • Tricyclic antidepressants: inhibits transporters of serotonin, nor + adrenaline
      • Schizophrenia
        • Neuroleptics: anti-psychotic drugs that block transmission of dopamine by binding to dopamine receptors without opening ion channels (antagonists)

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