Psychopharmacology

Question 1

What is the relation of drugs and the synapse?

Answer 1

-various substances alter synaptic transmission

Question 2

What is synaptic transmission?

Answer 2

• once the vesicles containing neurotransmitter reach the membrane they open and release into synaptic cleft
• neurotransmitter then binds to receptors in postsynaptic neuron, if those receptors are ion channels they’ll open
• if not ion channels they interact with specific ion channels to open them
• ion enters postsynaptic neuron causing post-synaptic potential

Question 3

What is neurotransmitter inactivation and recycling?

Answer 3

• where the effect of drugs usually occur
• diffusion: the transmitter is lost in the inter-cellular space
• enzymatic degradation: enzymes break down the transmitter
• re-uptake: the transmitter is recycled either in the pre-synaptic or the post-synaptic neuron (most economical way to inactivate the transmitter: saves synthesis resources)
• drugs can influence transmitter inactivation and recycling:
• reuptake of neurotransmitters into the original cell is done by specialised proteins: transporters, cocaine blocks the transporter of noradrenaline and dopamine, thus interfering with re-uptake and boosting effect

Question 4

How do substances influence different phases of the synaptic sequence?

Answer 4

• some act as early as the propagation of the action potential
• others influence release of transmitter
• others modulate how transmitter interacts with post-synaptic channels
• others alter presence of transmitter by modulating activation and recycling

Question 5

How do some chemicals interfere with the signals going through the axon?

Answer 5

• by blocking sodium channels in the axon’s membrane, TTX (tetrodotxin) can produce paralysis and respiratory failure
• Tetanospasmin toxin interferes with the vesicles of the neurotransmitter GABA fusing with the cell membrane, reduces amount of GABA released into synapse, is an inhibitory neurotransmitter so imbalance between excitation and inhibition neural signals. leads to very strong uncontrollable muscle contractions (tetanus) which can be lethal.
• Acetylcholine is a neurotransmitter that has 2 types of receptors: nicotinic (excitatory) and muscarinic (inhibitory). Botulinum toxin (formed by bacteria in improperly canned food) interferes with the release of Acetylcholine at nicotinic synapses, by preventing the vesicles from fusing with the cell membrane. This toxin is used in the cosmetic agent BOTOX, treat wrinkles by reducing synaptic effectiveness at the neuromuscular junction in facial muscles.
• Amphetamine is very similar in structure to the neurotransmitter dopamine. Due to its similarity to dopamine, amphetamine can enter the dopamine-releasing neuron either directly through the membrane or by binding to dopamine transporter (molecule that ‘recycles’ dopamine back into the cell from the synaptic cleft). Once inside the cell, amphetamine facilitates the release of dopamine from the vesicles when these fuse with the membrane (enhances the release of the transmitter rather than blocking it).
• Amphetamine and other drugs have a profound effect on dopaminergic pathways in the brain. One pathway is seen as particularly crucial in explaining the potent effects of these drugs: the projections from the Ventral Tegmental Area (VTA, group of cells in brain stem) to Nucleus Accumbens (group of cells in Basal Ganglia). VTA and Nucleus Accumbens are though to be involved in pleasure, reward and motivation.

Question 6

How can substances alter how the transmitter interacts with its receptors?

Answer 6

• certain substances simply bind to receptors but without opening the channel
• curare acts as antagonist (occupies channel but doesn’t open), used as anaesthesia
• agonists imitate behaviour of neurotransmitter, increasing effect

Question 7

What are the different psychoactive substances?

Answer 7

• chocolate
• coffee
• alcohol

Question 8

What is the relation of anxiety and GABA?

Answer 8

• anxiety disorders are in part characterised by deficits in GABA-ergic transmission
• Benzodiazepines (Valium) are GABA agonists used to treat anxiety disorders
• although their effect may seen similar to that of alcohol, they bind to different sites on GABA receptors
• they also don’t bind to the same receptor sites as GABA itself: such an action is one of a non-competitive agonist

Question 9

What is the relation of depression and MAO?

Answer 9

• depression is associated with reduced monoamine transmission
• MAO inhibitors: interfere with the enzyme MAO, which breaks down serotonin, dopamine and noradrenaline
• Tricyclic antidepressants: inhibit the transporter of serotonin, dopamine and noradrenaline (prevent reuptake)

Question 10

What is the relation of depression and serotonin?

Answer 10

• been found that serotonin is in fact the neurotransmitter closely linked to depression and less so dopamine and noradrenaline
• selective serotonin reuptake inhibitors inhibit the transporter of serotonin without affecting other neurotransmitters

Question 11

What is the relation of schizophrenia and dopamine?

Answer 11

• schizophrenia is associated with a surplus of dopamine
• its symptoms include paranoia and hallucinations
• Neuroleptics: anti-psychotic drugs that block the transmission of dopamine by binding to dopamine receptors without opening ion channels
• they’re dopamine antagonists

Question 12

What are methamphetamine and amphetamine derivatives?

Answer 12

• as cocaine, these substances reduce the transport of monoamine neurotransmitters
• also attach to enzymes that break down these neurotransmitters
• overall effect is a boost in neurotransmitter transmission
• cocaine as well as amphetamine and its derivatives: by increasing dopaminergic transmission, they can induce schizophrenia-like symptoms in high doses.
• the medication for Parkinson’s and schizophrenia push dopamine in the opposite direction and can cause each others’ symptoms in high doses.