Nervous system 3 - Nov. 22nd Flashcards
Mastery
Difference between NT and neuropeptides
on a table just flip slide
Acetylcholine
receptors? system? agonist receptors? recycled? by what? Sarin? what disease?
Serotonin
from where? onset? muscle control? sensory mediation? what can it affect? block what with drug? what drug and medication
Acetylcholine (Ach)
Cholinergic receptors
* Parasympathetic system/muscle
* Muscarinic vs nicotinic receptors
(agonists)
* Broken down by acetylcholinesterase and recycled
⬧ Sarin – inhibits this enzyme, Ach stays out and we get sustained muscle contraction
* Alzheimer’s Disease. low Ach
From tryptophan / modulates (slow onset)
Excitatory on muscle control
Inhibitory on sensory mediation
Mood, anxiety, wakefulness
Block reuptake with Paxil (anti-depressant). block back into presynaptic cell
Also LSD
Catecholamines
what? types? affect what? receptors? broken down by what? — inhibitors increase what? drugs?
A type of neurohormone
Epinephrine / norepinephrine. Type of catecholamines
Affect consciousness, mood, attention, BP, HR
Adrenergic / noradrenergic receptors
Broken down by MAO
(monoamine oxidase)
MAO inhibitors increase epinephrine levels in synapse
longer epinephrine response. to increase mood
* Anti-depressant
***KNOW THIS
Parkinson’s Disease
decrease what? result?
***DONT NEED TO KNOW
Synaptic Drug Interactions
Alter what about an NT?
modify NT what at the receptor?
influence what?
replace what?
Decrease release of dopamine from basal nuclei
inhibit unwanted muscle actions
Tremors / muscle rigidity
cognitive behaviour
Possible drug actions
- Altering the synthesis, axonal transport,
storage, or release of a neurotransmitter
- Modifying neurotransmitter interaction with the postsynaptic receptor
- Influencing neurotransmitter reuptake or destruction
- Replacing a deficient neurotransmitter with a substitute transmitter
Drug Interactions
Agonists (eg.)
what is morpine?
Antagonists (eg. Atrophine)
Agonists – mimic NT when they bind
Eg. Morphine (opiates). A fake opiate
Antagonists- bind but don’t activate
receptor – blocks sites
don’t get the response
Eg. Atropine (Ach). Block Ach, muscle paralysis
Drugs that alter synaptic transmission
Cocaine
Strychnine
competes with what?
Cocaine
Blocks reuptake of neurotransmitter dopamine at presynaptic terminals. prolonged dopamine repsonse and euphoria.
Strychnine
Competes with inhibitory neurotransmitter GLYCINE at postsynaptic receptor site.
NOT ALLOWING INHIBITION OF THE MUSCLE
* convulsions
Examples of Bacterial toxins that alter synaptic transmission
Tetanus toxin
prevent release of? how? affecting?
Botulism
interferes with ? muscle —-?
Tetanus toxin
Prevents release of inhibitory neurotransmitter GABA, affecting skeletal muscles.
* (destroys SNARE proteins)
SO CAN’T INHIBIT MUSCLE CONTRACTIONS
Botulism
Interferes with SNARE proteins for excitatory NT
Muscle paralysis
DIAPHRAGM, CAN’T RELAX OR CONTRACT.
Batrachotoxin - Poison-dart frogs
threshold? how much? repolarizing? neurons can’t?
Paralysis? Spasm? Ach? nerve stimulation to muscles? on the heart? Failure?
Batrachotoxin - Poison-dart frogs
- Toxin causes the nerves to reach threshold easier
– more likely to get AP’s
- Batrachotoxin can lower threshold by 30-50 mV
* Can fire at resting membrane potential
- Neurons can’t repolarize
- blocking nerve signal transmission to the muscles
Effects of the neurotoxin
Initial muscle spasms (including the diaphragm)
* Paralysis in contracted state
- Eventual depletion of Ach stores
* block nerve stimulation of muscles
* Similar effects occur on the heart
* RESPIRATORY FAILURE OR CARIDAC
Black Mamba Snake Toxin-Dendrotoxin K
K gates? AP repolarization and length? NT release?
muscle contraction? Diaphragm? convulsions? Failure of what?
INJECTING KCL
K+ flow? [k]? close or far from threshold? AP?
in the brain - seizures? astrocytes? ppl who have seizures
- Dendrotoxin K - inhibit K+ gates
- Prevents AP repolarization
- Action potential is prolonged
- Neuron releases more neurotransmitter - burst of
signals - Muscle contraction (spasms) and tremors and ataxia
- Can’t relax the diaphragm
Victims of a mamba bite suffer from convulsions - eventually die of respiratory failure or cardiac
arrest
The concentration gradient of K+ across the cell
membrane is reduced. K+ is high inside the cell/
* Less K+ flows out of the cell through the “leak” current
channels
* Intracellular concentration rises
LESS k+ moving out the cell
* Membrane potential closer to threshold
Will depolarize the neuron
* more likely to undergo an action potential
In the brain
- likely to produce seizures
- Astrocytes usually “absorb” excess potassium
from the extracellular space by way of
potassium channels in their membranes
PEOPLE who have seizures don’t have those astrocytes
Curare
from where and put Where? receptors? action? muscle? paralysis? death by?
Tetrodotoxin (TTX)
from where? method of acquiring? inhibits? depolarization? sensation? paralysis? death by?
Box Jellyfish Toxin
name? cells? k+ gates(name)? [k] gradient? cardiovascular what? death in?
CURARE
cure A. cure Ach
- South and Central America. Paralyzing poison used on arrows
- Competes with Ach at nicotinic cholinergic receptors
- Inhibits action of Ach at the neuromuscular junction
- Causes muscle weakness/paralysis eventual death by asphyxiation
* Paralysis of the diaphragm
TTX
-Poison from Pufferfish
- Ingestion, inhalation, injection or open skin
- Inhibits voltage sensitive Na+ gates
- No depolarization possible
- Loss of sensation, paralysis of voluntary muscles (diaphragm), stopping breathing
Sea Wasp
- Toxin to kill 60 people
- Cells become porous
- Allowed potassium leakage
* Hyperkalemia
* Lose K+ gradient for neural cells
⬧ Cardiovascular collapse
⬧ death as quickly as within 2 to 5 minutes
General Anaesthetic - Sevoflurane
Which channels affected? ——polarization? threshold? AP?
inhalation ones target what? consciousness? CNS, muscle and heart?
Opens K+ leak channels that help maintain the resting membrane potential
This will HYPERPOLARIZE the membrane harder to reach threshold
* Less likely to send AP’s
- Inhalation anaesthetics prefer to target neurons
in the brainstem that control consciousness and
respiration (Reticular Activating System and sleep) - Reduces level of consciousness and respiratory rate
- Entire CNS is depressed – muscle action,
reduced heart rate
DDT
where? gates? firing of neurons? spasms and death? repolarize?
in humans
stimulates what? sperm? cancer? neural?
DDT
- In insects – acts to open Na+ gates
- Over-firing of action potentials lead to Spasms and death
- cant repolarize
- Over-use in humans
- Stimulates estrogens
- Lower sperm counts / miscarriages etc.
- Cancer-causing
- Neural degradation
Lidocaine – Local anesthetic
blocks channels where? AP? action on skin? other MN?
***heart beating in a weird way, inject Lidocaine? affects on threshold and what does it reduce
Lidocaine – Local anaesthetic
- Blocks voltage-sensitive Na+ channels in sensory neurons
- No action potentials
* Numbing
- Also blocks in cardiac motor neurons
- Raises threshold. LESS EXCITABLE
- Reduces arrhythmias
