Biology - Lecture 8 (Psychopharmacology)
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- Created on: 08-04-16 17:14
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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
- e.g. the tetanospasmin toxin does this at inhibitory, GABAergic, synapses disrupting the natural balance of excitation and inhibition
- 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
- Certain substances simply bind to receptors but without opening the channel
- 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
- Heroin - modified form of morphine - agonist of endorphins, natural body chemicals that bind to opiate receptors
- can interfere with the release of the transmitter by shutting some calcium channels, one reduce the amount of released neurotransmitter
- 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
- Many of the neurons that release catecholamines also release (at same time) a self-inhibiting transmitter = adenosine
- Alcohol
- 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)
- Anxiety
- Neurotransmitter inactivation and recycling
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