1. How Do Drugs Affect Synapses? BY RUI XIAO

2. Psychoactive Drugs  Psychoactive drugs are chemical substances that can alter brain functions and result in changes in mood, performance, consciousness, this can be expressed by changes in behaviour and personality.  They are divided into 5 different groups according to their effect 1) Anxiolytics which are drugs that inhibit the feeling of anxiety 2) Euphoriants which can induce the sense of Euphoria 3) Stimulants are drugs that can temporarily increase mental and physical awareness and result in enhanced alertness 4) Depressants, calmative effects but also changes in perceptions 5) Hallucinogens are drugs which cause hallucinations and major changes in perceptions.

3. Agonists  Drugs which can amplify the process of synaptic transmission and increase post-synaptic stimulation are called agonists.  The two main type of agonists which are direct-binding agonists and indirect-acting agonist. Direct binding agonists act just like neurotransmitters in that they directly bind to receptors on the post- synaptic membrane and opening the corresponding ion channels causing an action potential. Indirect-acting agonists are substances which enhances the release of a neurotransmitter with no effect on the receptors themselves. There are various mechanisms for which indirect –acting agonists can work such as inducing transmitter release, inhibiting the breakdown of transmitters.

4. Direct-Binding Agonists  An example of a direct-binding agonist is nicotine which can bind to nicotinic acetylcholine receptors causing ion channels to open and positive ions such as sodium to enter and depolarising the plasma membrane and potentially cause other neurotransmitters to be released in parts of the brain.

5. Indirect-Acting Agonists Cocaine is an example of indirect- acting agonist as it binds to dopamine transporter (DAT) which prevents the removal of dopamine from the synaptic cleft therefore increasing the number of dopamine binded on the receptors and amplifying the signal.

6. Antagonists  Antagonists in contrast block neurotransmitters and they can be split into two types as well, competitive antagonists and non-competitive antagonists.  Examples of competitive antagonists are atropine and beta-blockers which ‘compete’ with neurotransmitters for the same binding site on the receptors. In other words they have affinity for the receptor but once they do bind to it they do not activate the receptor thus the channel ions are closed. Competitive antagonists are usually reversible and the receptor is free to bind with a neurotransmitter after the antagonist molecule leaves.  Non-competitive antagonists such as reserpine irreversible binds to a protein called VMAT which normally transports neurotransmitters to the receptors on the post-synaptic membrane. Without these VMAT, neurotransmitters are oxidised and broken down in the synaptic cleft before they can bind to the receptors.

7. L-Dopa  Parkinson’s disease is caused by decreasing supplies of the neurotransmitter Dopamine in the brain due to neuronal loss.  The L-Dopa is a precursor of dopamine  The main reason why dopamine injections by itself is not used in treating PD is because dopamine cannot cross the blood-brain barrier.

8. MDMA  MDMA (ecstasy) is a psychoactive drug that can induce the feeling of euphoria and diminished feel of fear and anxiety. Long terms effects of the drug are depression and anxiety.  -MDMA most prominent effect on the synapses is at the neurotransmitter serotonin. Serotonin molecules when released into the synaptic cleft bind to the receptors and are transported back afterwards. MDMA binds to serotonin molecules preventing the removal of the neurotransmitter enhancing the effect of the neurotransmitter as the action potential is constantly generated in the post synaptic parts of the brain controlling mood.