NCSU PHY 503 - TBL#2 Toxins Diagram | Quizlet

TERM

Dendrotoxin

DEFINITION

Blocks the presynaptic potassium (K⁺) channels which inhibit depolarization of the presynaptic membrane, thereby prolonging the duration of the action potential and facilitating the release of transmitter in response to the entry of calcium (Ca⁺⁺) into the nerve terminal

TERM

𝛚 - Conotoxin

DEFINITION

Blocks N-type (voltage-gates Ca⁺⁺ channels in the active zone of the neuromuscular junction) Ca⁺⁺ current in a virtually irreversible fashion. Exposure to 𝛚-conotoxin inhibits the release of neurotransmitter by preventing calcium from entering the presynaptic nerve terminal which prevents vesicle fusion

TERM

Tetanus Toxin

DEFINITION

Tetanus (Lockjaw) a general increase in muscle tension and muscle rigidity (starting with muscles for mastication) tetanus toxin have the greatest effect on inhibition of synaptic transmission by inhibitory neurons (stopping the stop signal) in the spinal cord, neurons that would normally inhibit muscle contraction, tetanus toxin cleaves synaptobrevin an integral membrane protein of synaptic vesicle membrane, preventing ACh release from inhibitory neurons thus only activation signals are being used.

TERM

Botulinum Toxin

DEFINITION

Weakness and paralysis of skeletal muscles as well as by a variety of symptoms that are related to inhibition of cholinergic nerve endings in the autonomic nervous system. Activation signals are not being transmitted to the muscles, because botulinum effects vesicle fusion, interrupting synaptobrevin (Botulinum B, D, F, G) SNAP-25 (Botulinum A/E) or syntaxin (Botulinum C1). ACh is not being released therefore no muscle contraction.

Carbamycholine

Are resistant to hydrolysis by muscle AChE, which prolongs activation of AChR channels.

Succinylcholine

Is resistant to hydrolysis by muscle AChE (but not resistant to plasma/liver esterases) which prolongs activation of AChRs. Succinylcholine is used to produce sustained muscle relaxation, "flaccid paralysis" which is used in some surgeries in which it is important to prevent excitation and contraction of skeletal muscles. Succinylcholine prolongs the opening of AChR channels and thereby depolarized the muscle membrane in the vicinity of the end plate, results in initial repetitive excitation and tremors followed by relaxation secondary to inactivation of Na⁺ channels in the end plate. This effect prevents the spread of muscle action potentials beyond the end plate.

TERM

d - Tubocurarine

DEFINITION

Is a competitive inhibitor of ACh binding to 2 activation sites on the 𝛂 - subunits of the AChR this leads to flaccid paralysis of the skeletal muscle from inhibition of the nicotinic AChR. Curare doesn't cause depolarization. d-Tubocurarine can be reversed by an increase in concentration of the natural agonist ACh by binding competition. A large increase in local ACh concentration can be produced indirectly by an inhibition of AChE such as neostigmine

Pancuronium

A drug that is useful for the production of neuromuscular blockade in surgery, and it is a more potent selective competitive antagonist of the muscle nicotinic AChR than d-Tubocuraine

TERM

𝛂 - Bungarotoxin (𝛂-Bgt)

DEFINITION

Binds virtually irreversibly to nicotinic AChR of the skeletal muscle. 𝛂-Bgt obstructs the agonist binding site and prevents activation of the receptor by ACh

𝛋 - Bungarotoxin (𝛋-Bgt)

This toxin has little effect on nicotinic AChR channels at the neuromuscular junction but it does inhibit AChR channels in the neuronal tissue.

TERM

Physostigmine and Neostigmine

DEFINITION

anti-AChE drugs that used to treat myasthenia gravis. Inhibitors of acetylcholinesterase prolongs and magnifies the end-plate potential. Physostigmine and neostigmine produce a carbamoylated form of AChE that is inactive the slow hydrolysis of the carbamoylated enzyme relieves esterase inhibition.

TERM

Diisopropylfluorophosphate (DFP)

DEFINITION

Is a organphosphorus compound, a synthetic AChE inhibitor, A irreversible inhibitor, DFP reacts with the serine residue of AChE and form a essentially irreversible covalent modification of the enzyme. DFP is among the most potent and lethal of toxic chemicals, due to excessive enhancement of cholinergic neurotransmission mediation by both muscarinic and nicotinic receptors. results in flaccid paralysis of the respiratory muscle (stimulation followed by depolarization blockade).