Neuropsychology
Lecture 12-Mechanisms of drugs Question 1
TCAs-Tricyclic antidepressants
Blocks reuptake of norepinephrine and serotonin ie they linger for longer in the synapse and interact with receptors longer
SSRIs-Selective serotonin reuptake inhibitors
Block only serotonin (not NE) reuptake
MAOIs-Monoamine oxidase enzyme inhibitors (MAOIs) * Block action of MAO enzymes – presynaptic terminal has increased levels of monoamine transmitters for release * Decrease in MAO activityIncrease in NT presynaptic terminalincreased concentration of NT transport of NT outside (high concentration) into neuron (normally low) slows down
MAOs * Present in liver, intestines & brain monoamine (serotonin, dopamine & norepinephrine) releasing neurons * Inactivates monoamines
Barbiturates
Mimics GABA on the GABA-A receptor (binds and activates it)
This increases the time that GABA-A channels open
More Cl- comes in
Benzodiazepines
Binds to GABA-A receptor, but can’t activiate it if GABA is not bound on receptor at the same time) This allows for increased frequency of channel opening
Cl- influx a bit over what GABA does alone
Opiates
MorphineSlow to get across BBB
Heroin=2xMorphine+O2 Also crosses a lot faster through BBB
HeroinMore rapid + delivers more morphine into brain
THC/Rimonabant/Endocannibaniods
CB1 receptor activates G-protien which activates Ca2+ channels allowing for homeostasis
THC-CB1 receptor agonist
Rimonanbant-CB1 receptor antagonist
Nicotine * Found mainly in tobacco * Binds acetylcholinergic nicotinic (nACh) receptors * Widespread in the CNS with ‘neuromodulatory’ ability * Main ‘addictive’ constituent in tobacco
Cocaine
In CNS: * Blocks the dopamine, norepinephrine and serotonin transporters * Prevents NT reuptake
Amphetamines
Main mechanisms: 1. Block dopamine (DAT), norepinephrine (NET) & serotonin (SERT) transporters 2. ‘Reverse transport’ of NTs via reuptake
TCAs-Tricyclic antidepressants
Blocks reuptake of norepinephrine and serotonin ie they linger for longer in the synapse and interact with receptors longer
SSRIs-Selective serotonin reuptake inhibitors
Block only serotonin (not NE) reuptake
MAOIs-Monoamine oxidase enzyme inhibitors (MAOIs) * Block action of MAO enzymes – presynaptic terminal has increased levels of monoamine transmitters for release * Decrease in MAO activityIncrease in NT presynaptic terminalincreased concentration of NT transport of NT outside (high concentration) into neuron (normally low) slows down
MAOs * Present in liver, intestines & brain monoamine (serotonin, dopamine & norepinephrine) releasing neurons * Inactivates monoamines
Barbiturates
Mimics GABA on the GABA-A receptor (binds and activates it)
This increases the time that GABA-A channels open
More Cl- comes in
Benzodiazepines
Binds to GABA-A receptor, but can’t activiate it if GABA is not bound on receptor at the same time) This allows for increased frequency of channel opening
Cl- influx a bit over what GABA does alone
Opiates
MorphineSlow to get across BBB
Heroin=2xMorphine+O2 Also crosses a lot faster through BBB
HeroinMore rapid + delivers more morphine into brain
THC/Rimonabant/Endocannibaniods
CB1 receptor activates G-protien which activates Ca2+ channels allowing for homeostasis
THC-CB1 receptor agonist
Rimonanbant-CB1 receptor antagonist
Nicotine * Found mainly in tobacco * Binds acetylcholinergic nicotinic (nACh) receptors * Widespread in the CNS with ‘neuromodulatory’ ability * Main ‘addictive’ constituent in tobacco
Cocaine
In CNS: * Blocks the dopamine, norepinephrine and serotonin transporters * Prevents NT reuptake
Amphetamines
Main mechanisms: 1. Block dopamine (DAT), norepinephrine (NET) & serotonin (SERT) transporters 2. ‘Reverse transport’ of NTs via reuptake