Quiz 2 Exam 2 Flashcards
Neuro
What chemical was used in the first experiments that blocked the muscle response to nerve stimulation?
Curare (it was later found that curare blocked the Ach receptors so Ach could not bind)
What is retrograde neurotransmission?
This is when transmission goes in the opposite direction. NTs are released from the postsynaptic site and activate the presynaptic site.
What are the two broad categories of receptors located on the postsynaptic site?
Ionotropic (fast and ions) and Metabotropic (slow and G proteins 2nd messengers)
An action potential stimulates the release of ____________ into the cell which activates _______ channels. This then allows the secretory vesicles to bind to the presynaptic site and release the NTs into the cleft.
Na+
Ca2+
What is the neuromuscular junction?
These are the skeletal muscle neurons that are not apart of the ANS. They are activated by Acetylcholine (Ach) binding to nicotinic acetylcholine receptors and stimulate the release of Na+ which is part of muscle contraction.
Where is epinephrine made?
Adrenal glands
What are the 3 main groups of neurotransmitters?
- Biogenic Amines/ Catecholamines- dopamine, EPI, and NE
- Amino acids- glutamate and GABA
- Acetylcholine (Ach)
What is the amino acid precursor for catecholamines synthesis?
Tyrosine
What are the steps in converting tyrosine to dopamine, NE, and Epi?
Tyrosine ——-> DOPA via Tyrosine Hydroxylase
DOPA——–> Dopamine via Aromatic Amino Acid Decarboxylase (AADC)
Dopamine ——> NE via dopamine beta-hydroxylase (DBH)
NE travels in systemic circulation and reaches adrenals
NE ——-> Epi via PNMT
What is the rate limiting enzyme of catecholamine synthesis?
Tyrosine hydroxylase
What are two enzymes that metabolism catecholamines to their inactive versions?
Monoamine oxidase (MAO) and Catechol-O-methyltransferase (COMT)
What is the primary mechanism of inactivating catecholamines in the cleft?
Reuptake transporters. They remove catecholamines from the synapse and suck them back up into the presynaptic neuron.
What is the MOA of cocaine?
Cocaine blocks the reuptake of NE in the peripheral and dopamine in the reward pathway.
What is the MOA of amphetamines?
Amphetamines reverse the direction of the reuptake transporter therefore spitting more catecholamines out and not taking an back up. Overall, it increases the release of dopamine and NE.
What are presynaptic autoreceptors?
These are typically alpha2 and dopamine2 autoreceptors. There are feedback inhibitory receptors that sense how much NE or dopamine has been released and when it senses the limit, it tells the neuron to slow down and stop the release of the NTs.
What are the steps in the creation and breakdown of acetylcholine (Ach)?
Acetyl CoA + Choline ——-> Acetylcholine (Ach) via Choline Acetyltransferase (ChAT)
Acetylcholine (Ach)——–> Acetic acid + Choline via acetylcholinesterase (Ache)
What happens to choline after Ach is metabolizied?
It is taken back up into the presynaptic neuron.
What is myasthenia gravis?
Myasthenia gravis is an autoimmune disorder that results in the destruction of Nicotinic Acetylcholine Receptors in the neuromuscular junction. It is characterized by muscle weakness.
Curare (plant alkaloid) and a-bungarotoxin (snake venom) have what MOA?
These compounds block Ach receptors.
What is the MOA of botox/ botulinum toxins?
Botox destroys the presynaptic vesicles that hold Ach which leads to the inhibition of Ach release.
What is the MOA of black widow toxin?
Black widow toxin stimulates the release of Ach
What is the MOA of insecticides?
Insecticides inhibit Acetylcholinesterase leading to massive increases in Ach levels.
What is a disease state that uses acetylcholinesterase inhibitors to slow the progression of the disease?
Alzheimer’s
The effect of an alpha2 agonist would be to?
A. Inhibit release of NE
B. Inhibit reuptake of NE
C. Inhibit metabolism of NE
D. Increase the release of NE
A. Inhibit the release of NE
Alpha2 receptors are the autoreceptors that are the natural breaks for the release of NTs. Stimulating that receptor would inhibit the release of more NE.