G PROTEINS
guanine nucleotide-binding proteins, are a family of proteins that act as molecular switches inside
cells, and are involved in transmitting signals from a variety of stimuli outside a cell to its interior.
Pertussis toxin: permanently inhibits Gi suppression and PKA and PKC
catalyzing the ADP- modulation of host immune effected
ribosylation of a cysteine and inflammatory
residue on the carboxy responses.
terminal of α subunit of Gi and
Go.
Cholera toxin permanently activates Gs begins to transport lots of dehydration
water and sodium rapid loss of fluids and
stimulating the enzyme outwards. salts (electrolytes).
adenylate cyclase, which diarrhea
catalyses the production oc PKA and PKC
cyclic AMP from ATP. effected
ION CHANNELS
Tetrodotoxin (TTX) Sodium-channel It inhibits the firing of action responsible for the
antagonist potentials in neurons by binding rising phase of an
to the voltage-gated sodium action potential
sodium channel blocker. channels in nerve cell
membranes and blocking the rapid weakening and
passage of sodium ions into the paralysis of muscles,
neuron including those of
the respiratory tract,
NO DEPOLARIZATION which can lead to
respiratory arrest and
death.
Tetraethylammonium Potassium channel blocks autonomic ganglia, responsible for phase
(TEA) Antagonist calcium- and voltage- activated 3 repolarization.
potassium channels, and Therefore, blocking
nicotinic acetylcholine receptors these channels slows
channel blocker. (delays)
depolarized the resting repolarization, which
potential, prolonged the action leads to an increase
potential and increased the in action potential
amplitude and duration of the duration and an
ensuing passive depolarizing increase in the
after-potential (DAP) in a dose- effective refractory
dependent and reversible period (ERP)
manner.
CHOLINERGIC SYSTEM
, 2
▪ The term cholinergic refers to those receptors which respond to the transmitter acetylcholine and
are mostly parasympathetic.
▪ The cholinergic system regulates various aspects of brain function, including sensory processing
(1), attention (2), sleep (3), and arousal (4), by modulating neural activity via acetylcholine
receptors (5, 6)
▪ liberating, activated by, or involving acetylcholine cholinergic nerve fiber cholinergic
functions. 2 : resembling acetylcholine especially in physiologic action a cholinergic drug.
Acetylcholine Muscarinic Receptors Agonist Activate receptors
Nicotinic receptors Drop in BP(vasodilation
Mrec.)
Muscarine Muscarinic Receptors Agonist M2 on heart
Pos. charge Sweat syndrome,
Bradycardia
Nicotine Nicotinic receptor Agonist Autonomic ganglia (CNS)
No charge - stimulation then
block stimulation
tachycardia, sweat
Carbachol Muscarinic receptors Direct-acting Does not cross BBB
parasympathomimetic drug - Postoperative
Agonist atony of the
intestine and
bladder
- Glaucoma
Atropine Muscarinic receptors Competitive Antagonist Bradycardia
Poison antidote
Pilocarpine Muscarinic receptors (M2) Direct-acting Effect CNS
parasympathomimetic drug - No charge →
Agonist crosses BBB
- Glaucoma (eye
drops)
constriction
pupils →miosis
Pirenzepine Muscarinic receptors Antagonist Duodenal Ulcer
(M1) Inhibit gastric acid
secretion
Pralidoxime Cholinesterase Inhibitor Kick of inhibitory
substance on the
Reactivates cholinesterase that Cholinesterase (antidote
was irreversibly inhibited for irreversible inhibition)
Poisoning
Physostigmine Cholinesterase Indirect-acting parasympathetic Atropine Poisoning
drug
No charge Carbamylating inhibitors →
enzyme restored
inhibitor
Neostigmine Cholinesterase Indirect-acting parasympathetic - avoid overdosing
drug of muscarinic
Charge Carbamylating inhibitors → antagonist
enzyme restored - myasthenia gravis
Inhibitor - glaucoma
- decurarization
Botulinum Anywhere with Ach Block Acetylcholine release Muscle relaxants
toxin vesicles binding presynaptically to high-
affinity recognition sites on the
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