Lecture 7: Drugs and Behavior Flashcards
Electrochemical signal
- Synthesis of neurotransmitter
- Chemical packaging of neurotransmitter
- Release of that chemical from vehicles in the synaptic terminal of the presynaptic neuron, neurotransmitter is the synaptic cleft
- Reception/ activation of receptors
–> different types of receptors and different types of mechanisms as a result of that receptor activation - Inactivation of the neurotransmitter either through degradation or reuptake.
Tetrodotoxin
- block sodium channels —> don’t have any action potential take place
- Sodium channels can’t open —> sodium can’t come on in —> can’t get to the threshold of excitation —> can’t get that big rapid depolarization that is needed for the first part of our action potential
- actually making sure that you neurons don’t talk to your muscles —> end up poisoning you —> will ultimately be fatality question
Agonist –> synthesis of neurotransmitter
drugs that increase the synthesis of the neurotransmitter —> increasing the neurotransmitter amounts
Parkinson’s
- a result of having decreased amounts of a neuron that works with dopamine as a neurotransmitter
- potential treatment: L-dopa (a precursor to dopamine —> dopamine can’t cross the blood brain barrier)
- give the precursor to it —> your body, your brain can start to make dopamine
- Drug L-dopa —> able to increase synthesis
Agonist –> Drugs that facilitate release
- making it so that you’re releasing more neurotransmitter —> got a lot more neurotransmitter hanging out in the synaptic cleft
- Black widow spider venom –> when they release their venom, their drug (toxin their venom) —> causes the release of acetylcholine
- have a lot of acetylcholine in your synaptic cleft —> going to actually result in like excessive contraction of your muscles
- everything was contracting against it —> those muscles were receiving a whole bunch of acetylcholine at that time
- if you’re receiving all that signal, your muscles keep on contracting for extended periods of time —> cramp on steroids —> getting into like tetanus
- agonist —> increasing neurotransmitters or is mimicking the neurotransmitter
Agonist –> Receptor activation
- Receptors that we find on the postsynaptic neuron –> ionotropic or metabotropic
- if you bind to them and activate them –> circumstance of mimicry —> something pretending to be a neurotransmitter and able to activate them
- Nicotine can pretend to be acetylcholine –> nicotinic receptors also get activated by nicotine — works on your muscles as well
- acetylcholine crossing over the synaptic cleft —> muscle contractions
- In some circumstances the presence of nicotine can also help out with muscle contraction
Agonist –> Neurotransmitter inactivation
- if you block the breakdown of neurotransmitter —> your neurotransmitter levels increase
- Esterase usually breaks down acetylcholine —> drug that comes in and inhibits acetylcholine —> acetylcholine levels will go up —> type of treatment that’s used in myasthenia gravis
- whatever receptors on the postsynaptic neuron are available —> have a higher chance of getting activated by whatever acetylcholine wasn’t broken down because of this drug blocking the breakdown
Antagonist
Drug that will decrease levels of neurotransmitter or inhibit their action in any way, shape, and form
Agonist
Drugs that mimic a neurotransmitter, increase the neurotransmitter itself, or increase the neurotransmitter’s activity
Auto receptors
if they get activated on our presynaptic neuron, tell presynaptic neuron —> less synthesis or less release
Mesolimbic Dopaminergic Reward System
- nucleus accumbens filled with neurons that release dopamine —> talks to your frontal lobe, specifically prefrontal cortex
- Becomes activated and releases dopamine so that you can feel good —> you will do that particular behaviour again —> need this area in the first place
- reward system activation over and over again —> learned response in that way —> you want to have that feeling of dopamine flooding over your brain
How Addiction Happens
- All about like flooding your brain with dopamine gets you that first initial hit —> you want to keep on having that particular flood of euphoria attributed to the dopamine —> that’s how a lot of these drugs work
- even though not contributing to your survival —> how they’re ultimately resulting in increased dopamine around your mesolimbic dopaminergic system sometimes directly, sometimes indirectly
Increase dopamine indirectly
- GABA —> Main inhibitory neurotransmitter. —> go with VTA(ventral tegmental area)
- Usually VTA neurons, since it’s GABA neurons —> inhibiting dopamine neurons —> can no longer release dopamine —> levels of dopamine go down —> usual circumstance where we don’t have activation of our system
- opiates —> producing endorphins —> can get those not just from opiates, but exercise —> got natural endorphins as opposed to like morphine
- Endorphins are inhibiting the VTA neurons —> activity is going to go down —> releasing less GABA—> not so much with the inhibition of the dopamine neurons —> dopamine levels go up
- That’s how those other drugs are working with regards to indirectly increasing dopamine —> inhibition of an inhibitor results in increased dopamine
- agonists —> not a good agonist by any means
- net increase in the neurotransmitter dopamine —> result in reinforcement wanting to have increased levels of dopamine for future use
Addiction
- compulsive use of the drug
- We all want to have big amounts of dopamine running through our brain
- There’s a lot of different types of stimuli that can help with that particular circumstance —> doesn’t always lead to addiction per se
- Reason —> your brain changes with the continued drug use (whatever drug of abuse it might be) —> compulsive use of the drug is trying to help us out against the brain changes that have occurred
Brain Changes
- Amounts of dopamine receptors went down —> shows you have decreased numbers of dopamine receptors
- If that continued drug use —> have less dopamine receptors on your postsynaptic neuron —> need more and more of that drug in order to have the same effect
- If you have less receptors —> less EPSPs —> want that postsynaptic neuron to fire later on to release dopamine
- All the neurons themselves using it too much —> because of the huge amount of dopamine that your brain physiologically —> you’ve got too much of this neurotransmitter, you don’t need that much, so we’re going to decrease the number of receptors —> like a balance
- Homeostasis —> in order to maintain those normal physiological processes
- Detrimental for the drug addict —> just trying to survive —> without the normal release of dopamine from that postsynaptic neuron —> they’re full of pain
- Brain changes —> why drug addicts are always really feeling pain —> their amount of dopamine being released is at much decreased levels than the normal subject —> drug addiction is a brain disease
- if able to abstain —> not to do with dopamine receptors per se, but to do with like activity levels from this MRI scan —> after 100 days of abstaining from the particular drug abuse, activity levels can come back
- Metaprotropic receptors —> can induce more receptors to be created later on —> takes time