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Pre-synaptic blockers:
1. Example: Hemicholinium: prevents ACh synthesis in cell body
Pre-synaptic blockers:
2. Block / interfere with release of Ach from motor nerve terminal. a). BOTULINUM TOXIN: in food contaminated by clostridium botulinum. Growth of the bacteria in improperly canned foods (Botulism = Latin word for sausage; in association with poorly preserved meet). b). Black Spider Venom
Pre-synaptic blockers:
Black Spider Venom: First increases, & then eliminates ACh release at NMJ. Venom protein attaches to presynaptic membrane to form a pore pore allows Na+ and Ca++ influx membrane depolarization total depletion of neurotransmitter.
A. COMPETITIVE BLOCKERS:
Compete with Ach to bind with Ach receptors on motor end plate no depolarization & no EPP muscle relaxes. Examples: NATURAL: D-tubocurarine. First used by South American Indians on the tips of their blowgunarrows. Once stuck into animal limb, the animal could no run. Curare-Form Drugs: (STNTHETIC) galamine, atracurium, mivacurium etc. SNAKE POISONS (cobra toxin): Alpha Bungaro toxin in snake venom.
Tubocurarine, found in curare of the South American plant Pareira, Chondrodendron tomentosum,
B. Non-competitive/DEPOLARIZING BLOCKERS:
Resemble Ach in action. They bind with receptors persistent depolarization. Only 1 nerve impulse is transmitted. (Initial twitching of muscles only).
Examples: SUXA-METHONIUM (Succinylcholine)*** DECA-METHONIUM, HEXA-METHONIUM.