Lecture 7: Drugs and Behavior Flashcards
1
Q
Electrochemical signal
A
- 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.
2
Q
Tetrodotoxin
A
- 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
3
Q
Agonist –> synthesis of neurotransmitter
A
drugs that increase the synthesis of the neurotransmitter —> increasing the neurotransmitter amounts
4
Q
Parkinson’s
A
- 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
5
Q
Agonist –> Drugs that facilitate release
A
- 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
6
Q
Agonist –> Receptor activation
A
- 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
7
Q
Agonist –> Neurotransmitter inactivation
A
- 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
8
Q
Antagonist
A
Drug that will decrease levels of neurotransmitter or inhibit their action in any way, shape, and form
9
Q
Agonist
A
Drugs that mimic a neurotransmitter, increase the neurotransmitter itself, or increase the neurotransmitter’s activity
10
Q
Auto receptors
A
if they get activated on our presynaptic neuron, tell presynaptic neuron —> less synthesis or less release
11
Q
Mesolimbic Dopaminergic Reward System
A
- 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
12
Q
How Addiction Happens
A
- 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
13
Q
Increase dopamine indirectly
A
- 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
14
Q
Addiction
A
- 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
15
Q
Brain Changes
A
- 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
16
Q
Central Nervous System
A
Brain + spinal cord
17
Q
Peripheral Nervous System
A
- nerves being like your axon —> sending information to your muscles
- nerves are considered to be also part of your nervous system, part of the peripheral nervous system
- Can see they actually make up a larger proportion of your nervous system compared to your brain and spinal cord
18
Q
Frames of Reference:
- Superior
- Inferior
- Ventral/Anterior
- Dorsal/Posterior
- Laterial
- Medial
- Rostral
- Caudal
A
- Superior vs inferior
- Superior —> going above
- Inferior —> below would mean
- ventral vs dorsal
- Dorsal/posterior —> towards the back
- Ventral/anterior —> towards the front
- Lateral vs medial
- pretend that you have this imaginary mid line that divvies up your body into symmetrical left and right
- Towards that mid line —> medial
- Away from the mid line —> lateral
- Rostral vs Caudal
- Rostral —> towards the head
- Caudal —> towards tail
19
Q
Planes of Reference
- Sagittal
- Longitudinal planes of section —> coronal or frontal
- Transverse plane of section/cross section
A
- Sagittal
- divide up your body into left and right —> if it’ symmetrical left and right —> known as a midsagittal plane
- Cut through my left shoulder —> parasagittal plane
- para —> parallel to that mid sagittal circumstance
- Longitudinal planes of section —> coronal/frontal
- Ventral and dorsal
- When you cut your body into ventral, dorsal, or anterior/posterior —> creating frontal plane/coronal plane
- corona —> crown || when you’re making that cut —> you’re putting on a crown
- Transverse plane of section/cross section
- creating a superior end, inferior portions of your body
- virtual slices happening through our body —> also true for when we’re looking at the brain
20
Q
somatic nervous system
A
You have voluntary movement
21
Q
autonomic nervous system
A
no voluntary or overt control —>autonomic similar to automatic —> all the things that don’t require overt control besides your heart
22
Q
sympathetic nervous system
A
- fight or flight —> faced with a mountain lion —> heart rate/breathing increases, blood flow to your brain increases
- besides fight or flight —> freeze
- Not just about exciting particular types of muscles like your heart muscle or your respiratory tract —> actively inhibiting messages to other systems that you should not be using at that time
- Blood flow to your digestive system should be —> Involuntary —> blood flow to your stomach during a situation like this should go down —> not important to be doing any digesting at that time, not important to be feeling hungry
- urinary system —> not important to create urine/filtering your blood —> don’t want to be wasting that energy that blood supply to your kidneys at that time
- blood flow should decrease
- Reproductive system —> blood flow to your reproductive system should go down
- starts at middle of spinal cord
- act on all systems of the body
23
Q
parasympathetic nervous system
A
- Trying to rest and digest, conserve energy/ to bring on board energy —> get energy by eating
- blood flow to your digestive system should go up —> get much more muscle contractions in your stomach + your intestines —> in order to facilitate
- heart rate should go down, breathing should go down, blood flow to your brain should go down
- start at ends of spinal cord
- act on all systems of the body
24
Q
Protection
A
- Skull
- CSF (Cerebral Spinal Fluid)
- Meninges
- BBB (Blood-Brain Barrier)
25
Q
Skull
A
Hard and hard bone structure –> most obvious form of protection
26
Q
CSF
A
- brain is floating in CSF —> helps to stop any of that like sudden impact or momentum that can occu –> helps to slow it down —> frontal lobe won’t hit the front of your skull
- Ventricles (two lateral ventricles, three, four) –> full of CSF
- Choroid Plexus –> Helps to create CSF in first place
- CSF in of itself —> primarily protecting you —> making that bath, also where nutrients and the light can come back and forth between the brain tissue —> pretty useful in that way
27
Q
CSF Process
A
- Cerebellum —> roof of the fourth ventricle
- After the fourth ventricle —> CSF actually leaves your brain —> goes down the middle of your spinal cord
- Cut through the spinal cord from left to right (A) —> transverse
- CSF goes down the middle of our spinal cord —> going through that cerebrospinal canal —> exits out the bottom —> starts to surround your brain
- Initially getting created in your lateral ventricles —> flows to the third ventricle —> flows to the fourth. —> down the super of spinal canal —> can see how it goes around your brain and spinal cord to help protect it
- If we have excess CSF —> it will drain through things called arachnoid granulations
- eventually it will actually become part of your blood —> excess CSF will go into special veins called sinuses —> go into your jugular vein —> back to your heart
- Should never have a big feeling with regards to —> have this continuous making of CSF —> just goes in one big loop || if we have excess —> should get drained into your blood supply + part of your nutrients
- Occasionally the flow of CSF is interrupted
28
Q
CSF Process
A
- Some type of obstruction in that flow from ventricles down through to surrounding the person’s brain —> usually happens earlier on in life, bones haven’t finished growing and fusing —> especially during childhood —> if we have a blockage in this passageway of CSF —> brain and the bone, the skull —> will grow around it —> big enlargement happening
- The brain grows around it —> sometimes it can’t withstand that type of pressure —> will have intracranial pressure occur (pressure on the brain)
- In some circumstances —> if left untreated —> will result in brain damage
- Actual shunt —> surgery, if it’s discovered sooner rather than later
- Get the excess fluid on out —> make it become part of your normal abdominal fluid (the peritoneal fluid) —> have a lot of fluid there anyway, to protect all those visceral organs —> just becomes part of the normal fluid intake
29
Q
Meninges
A
- cushioning for your brain
- a PAD for your brain || PAD —> helps us out with regards to naming conventions of the three meningeal layer
- Closest to your bone is called Dura mater (hard mother)
- connective tissue —> super, super thick —> help to be padding + acting as seat belts for your brain —> it will attach to your skull in particular locations
- Once you come to a stop, a red light —> helping to seat belt your brain into your skull so you don’t move quite as far
- super thick
- connective tissue —> super, super thick —> help to be padding + acting as seat belts for your brain —> it will attach to your skull in particular locations
30
Q
Arachnoid Matter
A
- Depiction of the spinal cord and showing the arachnoid matter
- arachnoid matter —> spider —> webbing
31
Q
Pia Matter
A
- Layer closest to your brain is called the pia mater (soft mother)
- glistens
- All connective tissue —> very strong
- helps to make that padding —> can withstand some aspects of protection in that way
32
Q
Blood Brain Barrier
A
- two types of blood vessels called capillaries —> smallest blood vessels in your body that help you out with gas exchange
- Left —> usually see throughout your body || right —> what we see in the brain
- No gaps in the one in the capillaries that we find in our brain —> along with the presence of one of our favourite Glia(astrocytes) —> surrounding blood vessels —> together helping to make a really good barrier to anything that’s super, super small like viruses and bacteria
- They’re missing any type of gaps in their capillaries + astrocytes of surrounding them another type of boundary —> viruses and bacteria should not be able to come from your blood into your brain tissue
- If things do pass on through —> because this is such like tight junctions between the cells —> it gets stuck there, can’t get back out
- What can pass?
- Very small things like oxygen and carbon dioxide can pass
- water has to have some help
- glucose —> your brain is mostly all about —> needs special transporters to get on by the blood brain barrier
- Very, very good body guard against most types of things —> including things that we actually need like sugar
33
Q
occipital lobe
A
- helping us out with vision —> receives visual information
- coding is predominantly being taken place over here
- if your occipital lobe were to get damaged —> no longer be able to code visual information technically —> would not be able to see || even if your eyes are fine and dandy —> because you don’t have the brain or the appropriate part of your brain to code the information —> you can’t see
34
Q
Temporal lobe
A
- super close to your ears —> helping us out with coding auditory information
- super helpful for learning and memory —> bc the hippocampus is deep in there
- primarily known for audition (fancy word for our state of hearing or sense of hearing) + higher visual processing
- After visual information goes to your occipital lobe —> goes to the temporal lobe for a little bit more finessing
- When stuff goes wrong —> temporal lobe seizures —> imagining seizures are like motor movements —> actually inappropriate electrical storm
- If your part of the brain has action potentials happening when it shouldn’t —> in your temporal lobe —> Van Gogh had inappropriate activity in his temporal lobe —> heard stuff —> cut off his ear
- Because of that seizures happening in his temporal lobe —> brush strokes and his paintings are very vivid —> temporal lobe also involved in higher visual processing —> believed that’s what he actually perceived —> his world of experience was actually like that —> schizophrenia
- Auditory hallucinations believed to be stemming from this circumstance of temporal lobe seizures
35
Q
Parietal lobe
A
- Part that is just behind your central sulcus, or posterior, or dorsal to your central sulcus —> primary somatosensory cortex
- known for sensations of your body in spatial awareness
- if it’s damaged —> actually have problems with figuring out where your body is in space and time —> something as simple as putting your clothes on can be to do bc you don’t know where your joints are
36
Q
Frontal lobe
A
- just in front of that central sulcus —> primary motor cortex
- Involved in motor planning, emotional regulation
37
Q
Grey Matter vs White Matter
A
- Gray matter is the superficial structures around
- predominantly soma + dendrites —> all the superficial stuff is going to be the soma of your brain
- White matter —> actually seen before —> myelin
- Axons part of neuron —> white matter all about moving information because it’s in the axons
- All those axons talking between the cerebral hemispheres, talking between the brain and the spinal cord or talking between gyri
