A5 Neuropharmacology Flashcards
Excitatory nerve impulses
Some neurotransmitters generate excitatory post-synaptic potentials (EPSPs) by causing depolarisation (e.g. glutamate)
the neurotransmitter causes positively charged ions to enter postsynaptic neuron
Inhibitory nerve impulses
Some neurotransmitters generate inhibitory post-synaptic potentials (IPSPs) by causing hyperpolarisation (e.g. GABA)
the neurotransmitter causes negatively charged ions to enter postsynaptic neuron
Summation
The combination of graded potentials (EPSPs and IPSPs) in the post-synaptic neuron is known as summation
Cancellation occurs when excitatory and inhibitory graded potentials cancel each other out (no threshold potential reached)
Spatial summation occurs when EPSPs are generated from multiple presynaptic neurons simultaneously to reach threshold
Temporal summation occurs when multiple EPSPs are generated from a single presynaptic neuron in quick succession
These summative effects determine which nerve pathways are activated and hence lead to alternate decision-making processes
Slow-acting neurotransmitters
trigger second messenger pathways within the post-synaptic cell, which allows for:
A longer, more sustained duration of action (i.e. ion channels remain open for longer to mediate greater depolarisation)
Long term alterations to cellular activity to improve synaptic transfer (i.e. increased expression of ion channels)
Slow-acting neurotransmitters are called neuromodulators because they can modulate the efficiency of synaptic transfer
By modulating the efficiency of synaptic transfer, slow-acting neurotransmitters can regulate fast synaptic transmission
Psychoactive drugs
affect the brain and personality by either increasing or decreasing postsynaptic transmissions
Drugs that increase neurotransmission levels are called stimulants and increase psychomotor arousal and alertness
Drugs that decrease neurotransmission levels are called depressants and slow down brain activities and relax muscles
Stimulants
mimic the stimulation provided by the sympathetic nervous system (i.e. ‘fight or flight’ responses)
Examples of stimulants include caffeine, cocaine, amphetamines, ecstasy (MDMA) and nicotine
Depressants
reduce stimulation of the central nervous system and may induce sleep (sedatives)
Examples of sedatives include benzodiazepines, barbiturates, alcohol and tetrahydrocannabinol (THC = cannabis)
Nicotine
Nicotine stimulates the cholinergic pathways by mimicking the action of acetylcholine (binds Ach receptors)
Nicotine is not broken down by the enzyme acetylcholinesterase, resulting in overstimulation of Ach receptors
Nicotine raises dopamine levels in the brain (leading to addiction) and activates parasympathetic pathways (calming effect)
MDMA (ecstasy)
MDMA binds to reuptake pumps on presynaptic neurons and blocks the recycling of dopamine and serotonin (5-HT)
MDMA also enters the presynaptic neurons via the reuptake pumps and triggers the secretion of neurotransmitter
This increases levels of neurotransmitter in the synaptic cleft, prompting feelings of euphoria and heightened sensation
Benzodiazepine
Benzodiazepines bind to GABA receptors on the post-synaptic neuron and increase the efficiency of GABA action
GABA triggers the opening of chloride channels to cause hyperpolarisation – benzodiazepines enhance this effect
Benzodiazepines promote sleep-inducing and muscle relaxing responses by the body
Tetrahydrocannabinol (THC)
HC mimics the neurotransmitter anandamide by binding to cannabinoid receptors on presynaptic neurons
Anandamide (and THC) blocks the release of inhibitory neurotransmitters that prevent dopamine secretion
By preventing the inhibition of dopamine secretion, THC causes a sense of euphoria and emotional well-being
Anaesthetics
act on ion channels to block the conduction of sensory nerve signals to the central nervous system
This results in the loss of sensation (numbness) in the affected region, allowing for surgical interventions to occur
Anesthetics can be grouped into two classes – local anesthetics and general anesthetics
Local anesthetics only affect a localised region – usually by blocking axonal sodium influx (conduction block). They will not result in a loss of consciousness and only cause a reversible loss of sensation to the affected area
General anesthetics affect the whole body – this may involve blocking calcium influx to prevent neurotransmitter exocytosis. They will induce a temporary loss of consciousness as they interfere with neural transmissions in the brain
Endorphins
are endogenous neuropeptides produced by the pituitary gland that functions as the body’s natural painkiller
Endorphins are typically released by the body during periods of stress, injury or physical exercise
How do endorphins act as painkillers
Pain is perceived in body tissues when impulses are sent from pain receptors (nocireceptors) to sensory areas of the brain
Endorphins bind to opiate receptors on pre-synaptic neurons to block the transmission of pain signals
Endorphins differ from anesthetics in that they reduce pain perception but do not necessarily block all sensory perception
Endorphins can also promote feelings of euphoria (as they target opioid receptors)
Addiction
is a dependence on a substance or an activity which results in its repeated and compulsive use
Stopping is very difficult and can cause severe mental and physical reactions (withdrawal symptoms)
Addictions can be affected by genetic factors, social factors and dopamine secretion
