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Neurotransmission
Submitted By-
Shruti Rajeev Gautam
(M.Pharma 1 𝑠𝑡
year )
Guide-
Prof J.V.Vyas
Vidya Bharati College of Pharmacy, Amravati.
2019-2020
INDEX
 Introduction
 Evidence for Neurohumoral
Transmission
 Step involved in neurotransmitter
 Adrenaline
 Acetylcholine
Introduction
 Neurotransmission (Latin: transmissio "passage,
crossing" from transmittere "send, let through"), is the
process by which signaling molecules called
neurotransmitters are released by the axon terminal of a
neuron ,(presynaptic neuron ) and bind to and react with
the receptors on the dendrites of another neuron
(postsynaptic neuron )
Evidence for Neurohumoral Transmission
 The concept of chemical neurotransmission was developed
primarily to explain observations relating to the transmission of
impulses from postganglionic autonomic fibers to effector cells.
 Evidence supporting this concept includes the following:
 Demonstration of the presence of a physiologically active
compound and its biosynthetic enzymes at appropriate sites;
 Recovery of the compound from the perfusate of an innervated
structure during periods of nerve stimulation but not (or in greatly
reduced amounts) in the absence of stimulation;
 Demonstration that the compound is capable of producing responses
identical to responses to nerve stimulation; and
 Demonstration that the responses to nerve stimulation and to the
administered compound are modified in the same manner by
various drugs, usually competitive antagonists
Step involved in neurohumoral
transmission
 Initiation of action potential & axonal
conduction
 Arrival of an action potential at the nerve
terminal resulting in the release
transmitter
 Event at the synaptic cleft & post junction
site
 Termination of the effect of released
transmitter
Initiation of action potential & axonal conduction
 At rest the interior of typical mammalian axon is 70mv
negative to the exterior
 This is due to high intracellular concentration of 𝐾+
and low
𝑁𝑎+
& 𝐶𝑙−
level
 These ionic gradient are maintained by an energy dependent
active transport pump
 In response to depolarization to threshold level there is rapid
increase in the permeability of the neuronal membrane to Na
& the whole membrane is rapidly depolarized
 There is a delayed opening of 𝐾+
channel resulting in
outflow of the 𝐾+
& repolarization of the membrane
 During this process ion current are produced which
depolarize adjacent region of the neural membrane & hence
actin potential is propagated
Arrival of an action potential at the nerve terminal
resulting in the release transmitter
 Classical neurotransmitter are synthesized in the nerve
terminal and stored within synaptic vessel
 Arrival of an action potential in the nerve terminal result
in the of 𝐶𝑎+
which promotes the fusion of synaptic
vesicle with adjacent axoplasmic membrane
 The content of the vesicle are discharged into the
synaptic cleft
 Adjacent section of membrane are pinched off to form
new vesicle
 Neuropeptide are synthesized in the perikaryon of the
neuron and must be transported to the nerve terminal
before they can be released
Event at the synaptic cleft & post junction
site
 The released neurotransmitter diffuse cross the synaptic
cleft interact with postjunctional receptor and produce
postjunctional effect
 The postjunctional effect may be excitatory post
synaptic potential with the entry of 𝐶𝑎+
or inhibitory
postsynaptic potential with the influx of 𝐶𝑙− or outflow
of 𝐾+ leading to hyperpolarization
Termination of the effect of released
transmitter
 At the cholinergic sites termination occur by metabolic
inactivation by an exceedinly efficient enzyme
acetlycholinesterase(AChE)
 At the aderenocptic site the major mechanism of
inactivation of the transmitter is by the enzyme mono
amine oxidase (MAO)or catechol-o-methyl transferase
(COMT) principally the termination of transmitter
activity is due to reuptake into nerve terminal
Adrenaline
 Norepinephrine (NE) is the neurotransmitter released
from all the postganglionic sympathetic nerve ending
where as epinephrine is released by the adrenal medulla
 Cathecholamine synthesis stop with formation of
dopamine in the dopaminergic neuron in the central
nervous system
 Symapthomimetic drug can be broadly classified as
catecholamine & non catecholamine
Adrenoceptors
 The adrenergic receptors or adrenoceptors are a class of
G protein-coupled receptors that are targets of many
catecholamines like norepinephrine (noradrenaline) and
epinephrine (adrenaline) produced by the body,
 The α adrenoceptors are of two type 𝛼1and 𝛼2 located at
different site in adrenergic system
 β adrenoceptors are of three type namely 𝛽1 ,𝛽2 and 𝛽3
each with specific action and location at different sites
 Dopamine receptor have predominate distribution in
CNS as well in the renal vasculature
Structural Feature
 All adrenergic receptor are G-protein coupled receptor
that linked to heterotrimeric G protein
 Structurally these are similarities in the region for ligand
binding and modulator by intracellular protein kinase
 The coding region of each of three β adrenergic receptor
gene & the three α2 adrenergic receptor gene is
contained in single exon
 Each of the three α1adrenergic receptor gene has a
single large intron separating region that encode the
body of the receptor from those that encode the seventh
trans membrane domain carboxyl terminus
 Each major receptor type show preference for particular
class of g protein that is
1) α1 to 𝐺 𝑞
2) α2 to 𝐺𝑖
3) β to 𝐺𝑠
α receptor mediated action
 Stimulation of receptor activates the 𝐺 𝑞 −
𝐼𝑃3/DAG Pathway and result in the activation PKC
and other 𝐶𝑎2+ and CaM kinase with sequelae
depending on cell differentiation
 The 𝐺 𝑞subfamily of G protein couple α receptor to
phospholipase C
 𝐼𝑃3promotes the release of 𝐶𝑎2+
from the
intracellular stores increasing the intracellular
concentration of𝐶𝑎2+ activating different calcium
dependent protein kinase
 𝐼𝑃3is dephosphorylated to form free inositol
 DAG activates protein kinase C that modulates the
activity of many signaling pathway
 α receptor inhibit adenyl cyclase activity and cause
decrease of intracellular cAMP level
 The inhibitory activity of cAMP is mediated by𝐺1 type
of G protein
Receptor G protein
coupling
Site of action Dominant effect
α1𝐴
𝐺α 𝑞
(α11 /α14 /α16 )
Heart , lung,
liver, smooth
muscle , blood
vessel
Dominate
receptor for
contraction of the
vascular smooth
muscle
α1𝐵
𝐺α 𝑞
( α11/α14/ α16)
Kidney , liver,
spleen, brain
steam
Most abundant
subtype in heart
α1𝐷
𝐺α 𝑞
(α11/α14/α16 )
Platelet, aorta ,
coronary artery,
Dominant
receptor for
vasoconstriction
in aorta
α2𝐴
𝐺𝛼 𝑞
(𝛼11/α14 /α16 )
Platelet, synaptic
neuron ,
pancreas , cns
vessel
Dominant
inhibitory
receptor on
sympathetic
neuron
𝛽 receptor mediated action
 Activation of the three 𝛽 receptor 𝛽1,𝛽2,𝛽2,
result in activation of adenyl cyclase and
enhanced conversion of ATP to cAMP
 This is brougth about by coupling with 𝐺𝑠
protein
 Cyclic AMP is the major second messenger of 𝛽
receptor activation
 In the liver the increased formation of cAMP is
responsible for activation of glycogen
phosphorylase breaking the glycogen stores and
causing glycogenolysis
 The accumulation of cAMP in the heart
causes 𝐶𝑎2+
flux leading to increase heart
rate & contractility
 𝛽 adrenoreceptor may activate voltage
sensitive 𝐶𝑎2+
channel in the heart via G
mediated enhancement independent of
change in cAMP
Receptor G protein
coupling
Site of action Dominant effect
𝛽1 𝐺𝛼 𝑠 Heart, kidney,
skeletal muscle,
spinal cord
Dominant mediator
of positive
inotropic and
chronotropic effect
in heart
𝛽2 𝐺𝛼 𝑠 Heart , kidney,
lung, skeletal
muscle
Smooth muscle
relaxztion
𝛽3 𝐺𝛼 𝑠 Adipose tissue, GI
tract , heart
Metabolic effect
Dopamine receptor mediated
action
 The 𝐷1 receptor is associated with
stimulation of adenylcyclase and smooth
muscle relaxant effect of 𝐷1 receptor is by
virtue of accumulation of cAMP
 𝐷2 receptor have been found to inhibit
adenylcyclase activity with opening of 𝑘+
channel and decrease 𝐶𝑎2+
influx
Acetylcholine
 Acetylcholine is the principal neurotransmitter of the
cholinergic system and is released at the following site
1) At all preganglionic nerve terminal of sympathetic and
parasympathetic division of autonomic nervous system
2) At all postganglionic nerve terminal of the
parasympathetic nerve terminal
3) At the autonomic ganglia both sympathetic and
parasympathetic
4) At the adrenal medulla which later facilitates the
released of adrenaline from the chromaffin cell
5) At the neuromuscular junction
Synthesis ,storage, and release acetylcholine
 Acetylcholine (ACh) is synthesized in the cytoplasm
from acetylCoA and choline through the catalytic action
of the enzyme choline acetyltransferase(ChAT)
 acetylCoA is synthesized in mitochondria which are
present in large number in the nerve terminal
 Choline is transported from the extracellular fluid into
the neuron terminal by a sodium dependent membrane
carrier
 After synthesis Ach is transported from cytoplasm into
the storage vesicles where it is stored along with ATP
and peptides
 Release of transmitter (ACh) is dependent upon
extracellular calcium and occur when action potential
(AP) reaches the terminal and trigger the influx of 𝐶𝑎2+
ion
 The increased intracellular𝐶𝑎2+
destabilizes the storage
vesicle and causes the release of Ach
 The released Ach act on the postsynaptic sites to
produce either muscarinic or nicotinic action depending
upon the receptor subtype on which it act
 The released Ach is acted upon by an enzyme known as
acetlycholinesterase
 The drug affecting the synthesis ,storage ,and release of
Ach are
1) Hemicholinium causes blockade of choline uptake
from the extracellular fluid into the cytoplasm
2) Vesamicol block the transport mechanism blocking the
shift of the synthesized Ach in the cytoplasm into the
storage vesicle
3) Black widow spider venom block the release of Ach
from axonal terminal
4) Botulinum toxic prevent the release of Ach from
storage vesicle
Mechanism of cholinoreceptor
 All muscarinic receptor appear to be of the G protein
coupled type
 Muscarinic agonist binding activates the 𝐼𝑃3 and DAG
cascade with a possible role of DAG in the opening of
smooth muscle calcium channel and 𝐼𝑃3 releasing
calcium from endoplasmic reticulum and sarcoplasmic
reticulum
 Muscarinic agonist also increase cellular cGMP
concentration
 Activation of muscarinic receptor also increases
potassium flux across cardiac cell membrane and
decrease it in ganglion and smooth muscle cell
 This effect is mediated by the binding of the
activated G protein directly to the channel
 Muscarinic agonist can attenuate the
activation of adenylcyclase and consequent
increase in cAMP level brought about by
cathecholamine
 The primary effect of the nicotinic receptor
activation is depolarization of the nerve cell
or neuromuscular and plate membrane
allowing flux of 𝑁𝑎+
and 𝑘+
ion in their
respective direction
 Muscarine
 Nicotine
Receptor subtype Location
𝑀1 CNS neurons ,sympathetic
postganglionic neurons
𝑀2 Myocardium, smooth muscle
𝑀3 Exocrine gland, smooth muscle
𝑁 𝑛 Postganglionic neuron
𝑁 𝑚 Skeletal muscle neuromuscular end
plates
Pharmacological response
 Eye: muscarinic agonist when used locally cause
contraction of the smooth muscle of sphincter papillae
resulting in meiosis and contraction of the ciliary muscle
resulting in spam of accommodation
 Cardiovascular system :muscarinic agonist cause
reduction and an eventual fall in blood pressure they act
directly on the 𝑀3 receptor present in the smooth muscle
of the vasculation as well as the endothelium of the
blood vessel liberating endothelium derived relaxing
factor which actually nitric oxide (NO)
 The following event take place in direct action of
muscarinic stimulant
1) An increase in a potassium current in atrial muscle
cells and cell of SA and AV nodes
2) A decrease in the slow inward calcium current
3) A decrease in the diastolic depolarization current
 Respiratory system : muscarinic agonist constrict the
smooth muscle of the bronchial tree , increase airway
resistance and produce bronchospasm
 Gastrointestinal tract :muscarinic agonist stimulate the
GIT tract causing increased peristaltic and secretory
activities
Anticholinesterase
 An anticholinergic agent is a substance that blocks the
action of the neurotransmitter acetylcholine at synapses
in the central and the peripheral nervous system. These
agents inhibit parasympathetic nerve impulses by
selectively blocking the binding of the neurotransmitter
acetylcholine to its receptor in nerve cells.
 Classification according to chemical composition
 Simple alcohols with quaternary ammonium group :
edrophonium
 Carbamic acid ester of alcohol with quaternary or
tertiary ammonium group carbamates : neostigmine,
physostigmine , rivastigmine,
 Organic phosphorous compound : organophosphate ,
ecothiophate , diisopropyfluorophosphate( DFP),
malathion,
Pharmacological response
 Eyes: anticholinesterase cause miosis and consequent
change in the intraocular pessure
 GIT tract : neostiamine and other drug have similar
effect as other cholinomimetic
 Urinary system: these drug cause contraction of the
smooth muscle of the bladder and ureter
 Bronchioles : anticholinesterase cause constriction of
the bronchioles with increased in airway
Reference
 Conceptual pharmacology : P
Jagadish Prasad
 Rang and Dale's
Pharmacology:James Ritter, Rod J.
Flower, G. Henderson, David J.
MacEwan, Yoon Kong Loke, H. P.
Rang
 Basic & Clinical Pharmacology:
Katzung and Bertram

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Neurotransmission

  • 1. Neurotransmission Submitted By- Shruti Rajeev Gautam (M.Pharma 1 𝑠𝑡 year ) Guide- Prof J.V.Vyas Vidya Bharati College of Pharmacy, Amravati. 2019-2020
  • 2. INDEX  Introduction  Evidence for Neurohumoral Transmission  Step involved in neurotransmitter  Adrenaline  Acetylcholine
  • 3. Introduction  Neurotransmission (Latin: transmissio "passage, crossing" from transmittere "send, let through"), is the process by which signaling molecules called neurotransmitters are released by the axon terminal of a neuron ,(presynaptic neuron ) and bind to and react with the receptors on the dendrites of another neuron (postsynaptic neuron )
  • 4. Evidence for Neurohumoral Transmission  The concept of chemical neurotransmission was developed primarily to explain observations relating to the transmission of impulses from postganglionic autonomic fibers to effector cells.  Evidence supporting this concept includes the following:  Demonstration of the presence of a physiologically active compound and its biosynthetic enzymes at appropriate sites;  Recovery of the compound from the perfusate of an innervated structure during periods of nerve stimulation but not (or in greatly reduced amounts) in the absence of stimulation;  Demonstration that the compound is capable of producing responses identical to responses to nerve stimulation; and  Demonstration that the responses to nerve stimulation and to the administered compound are modified in the same manner by various drugs, usually competitive antagonists
  • 5. Step involved in neurohumoral transmission  Initiation of action potential & axonal conduction  Arrival of an action potential at the nerve terminal resulting in the release transmitter  Event at the synaptic cleft & post junction site  Termination of the effect of released transmitter
  • 6. Initiation of action potential & axonal conduction  At rest the interior of typical mammalian axon is 70mv negative to the exterior  This is due to high intracellular concentration of 𝐾+ and low 𝑁𝑎+ & 𝐶𝑙− level  These ionic gradient are maintained by an energy dependent active transport pump  In response to depolarization to threshold level there is rapid increase in the permeability of the neuronal membrane to Na & the whole membrane is rapidly depolarized  There is a delayed opening of 𝐾+ channel resulting in outflow of the 𝐾+ & repolarization of the membrane  During this process ion current are produced which depolarize adjacent region of the neural membrane & hence actin potential is propagated
  • 7.
  • 8. Arrival of an action potential at the nerve terminal resulting in the release transmitter  Classical neurotransmitter are synthesized in the nerve terminal and stored within synaptic vessel  Arrival of an action potential in the nerve terminal result in the of 𝐶𝑎+ which promotes the fusion of synaptic vesicle with adjacent axoplasmic membrane  The content of the vesicle are discharged into the synaptic cleft  Adjacent section of membrane are pinched off to form new vesicle  Neuropeptide are synthesized in the perikaryon of the neuron and must be transported to the nerve terminal before they can be released
  • 9. Event at the synaptic cleft & post junction site  The released neurotransmitter diffuse cross the synaptic cleft interact with postjunctional receptor and produce postjunctional effect  The postjunctional effect may be excitatory post synaptic potential with the entry of 𝐶𝑎+ or inhibitory postsynaptic potential with the influx of 𝐶𝑙− or outflow of 𝐾+ leading to hyperpolarization
  • 10. Termination of the effect of released transmitter  At the cholinergic sites termination occur by metabolic inactivation by an exceedinly efficient enzyme acetlycholinesterase(AChE)  At the aderenocptic site the major mechanism of inactivation of the transmitter is by the enzyme mono amine oxidase (MAO)or catechol-o-methyl transferase (COMT) principally the termination of transmitter activity is due to reuptake into nerve terminal
  • 11. Adrenaline  Norepinephrine (NE) is the neurotransmitter released from all the postganglionic sympathetic nerve ending where as epinephrine is released by the adrenal medulla  Cathecholamine synthesis stop with formation of dopamine in the dopaminergic neuron in the central nervous system  Symapthomimetic drug can be broadly classified as catecholamine & non catecholamine
  • 12.
  • 13. Adrenoceptors  The adrenergic receptors or adrenoceptors are a class of G protein-coupled receptors that are targets of many catecholamines like norepinephrine (noradrenaline) and epinephrine (adrenaline) produced by the body,  The α adrenoceptors are of two type 𝛼1and 𝛼2 located at different site in adrenergic system  β adrenoceptors are of three type namely 𝛽1 ,𝛽2 and 𝛽3 each with specific action and location at different sites  Dopamine receptor have predominate distribution in CNS as well in the renal vasculature
  • 14. Structural Feature  All adrenergic receptor are G-protein coupled receptor that linked to heterotrimeric G protein  Structurally these are similarities in the region for ligand binding and modulator by intracellular protein kinase  The coding region of each of three β adrenergic receptor gene & the three α2 adrenergic receptor gene is contained in single exon  Each of the three α1adrenergic receptor gene has a single large intron separating region that encode the body of the receptor from those that encode the seventh trans membrane domain carboxyl terminus
  • 15.  Each major receptor type show preference for particular class of g protein that is 1) α1 to 𝐺 𝑞 2) α2 to 𝐺𝑖 3) β to 𝐺𝑠
  • 16.
  • 17. α receptor mediated action  Stimulation of receptor activates the 𝐺 𝑞 − 𝐼𝑃3/DAG Pathway and result in the activation PKC and other 𝐶𝑎2+ and CaM kinase with sequelae depending on cell differentiation  The 𝐺 𝑞subfamily of G protein couple α receptor to phospholipase C  𝐼𝑃3promotes the release of 𝐶𝑎2+ from the intracellular stores increasing the intracellular concentration of𝐶𝑎2+ activating different calcium dependent protein kinase
  • 18.  𝐼𝑃3is dephosphorylated to form free inositol  DAG activates protein kinase C that modulates the activity of many signaling pathway  α receptor inhibit adenyl cyclase activity and cause decrease of intracellular cAMP level  The inhibitory activity of cAMP is mediated by𝐺1 type of G protein
  • 19. Receptor G protein coupling Site of action Dominant effect α1𝐴 𝐺α 𝑞 (α11 /α14 /α16 ) Heart , lung, liver, smooth muscle , blood vessel Dominate receptor for contraction of the vascular smooth muscle α1𝐵 𝐺α 𝑞 ( α11/α14/ α16) Kidney , liver, spleen, brain steam Most abundant subtype in heart α1𝐷 𝐺α 𝑞 (α11/α14/α16 ) Platelet, aorta , coronary artery, Dominant receptor for vasoconstriction in aorta α2𝐴 𝐺𝛼 𝑞 (𝛼11/α14 /α16 ) Platelet, synaptic neuron , pancreas , cns vessel Dominant inhibitory receptor on sympathetic neuron
  • 20. 𝛽 receptor mediated action  Activation of the three 𝛽 receptor 𝛽1,𝛽2,𝛽2, result in activation of adenyl cyclase and enhanced conversion of ATP to cAMP  This is brougth about by coupling with 𝐺𝑠 protein  Cyclic AMP is the major second messenger of 𝛽 receptor activation  In the liver the increased formation of cAMP is responsible for activation of glycogen phosphorylase breaking the glycogen stores and causing glycogenolysis
  • 21.  The accumulation of cAMP in the heart causes 𝐶𝑎2+ flux leading to increase heart rate & contractility  𝛽 adrenoreceptor may activate voltage sensitive 𝐶𝑎2+ channel in the heart via G mediated enhancement independent of change in cAMP
  • 22. Receptor G protein coupling Site of action Dominant effect 𝛽1 𝐺𝛼 𝑠 Heart, kidney, skeletal muscle, spinal cord Dominant mediator of positive inotropic and chronotropic effect in heart 𝛽2 𝐺𝛼 𝑠 Heart , kidney, lung, skeletal muscle Smooth muscle relaxztion 𝛽3 𝐺𝛼 𝑠 Adipose tissue, GI tract , heart Metabolic effect
  • 23. Dopamine receptor mediated action  The 𝐷1 receptor is associated with stimulation of adenylcyclase and smooth muscle relaxant effect of 𝐷1 receptor is by virtue of accumulation of cAMP  𝐷2 receptor have been found to inhibit adenylcyclase activity with opening of 𝑘+ channel and decrease 𝐶𝑎2+ influx
  • 24. Acetylcholine  Acetylcholine is the principal neurotransmitter of the cholinergic system and is released at the following site 1) At all preganglionic nerve terminal of sympathetic and parasympathetic division of autonomic nervous system 2) At all postganglionic nerve terminal of the parasympathetic nerve terminal 3) At the autonomic ganglia both sympathetic and parasympathetic 4) At the adrenal medulla which later facilitates the released of adrenaline from the chromaffin cell 5) At the neuromuscular junction
  • 25. Synthesis ,storage, and release acetylcholine  Acetylcholine (ACh) is synthesized in the cytoplasm from acetylCoA and choline through the catalytic action of the enzyme choline acetyltransferase(ChAT)  acetylCoA is synthesized in mitochondria which are present in large number in the nerve terminal  Choline is transported from the extracellular fluid into the neuron terminal by a sodium dependent membrane carrier  After synthesis Ach is transported from cytoplasm into the storage vesicles where it is stored along with ATP and peptides
  • 26.  Release of transmitter (ACh) is dependent upon extracellular calcium and occur when action potential (AP) reaches the terminal and trigger the influx of 𝐶𝑎2+ ion  The increased intracellular𝐶𝑎2+ destabilizes the storage vesicle and causes the release of Ach  The released Ach act on the postsynaptic sites to produce either muscarinic or nicotinic action depending upon the receptor subtype on which it act  The released Ach is acted upon by an enzyme known as acetlycholinesterase
  • 27.
  • 28.  The drug affecting the synthesis ,storage ,and release of Ach are 1) Hemicholinium causes blockade of choline uptake from the extracellular fluid into the cytoplasm 2) Vesamicol block the transport mechanism blocking the shift of the synthesized Ach in the cytoplasm into the storage vesicle 3) Black widow spider venom block the release of Ach from axonal terminal 4) Botulinum toxic prevent the release of Ach from storage vesicle
  • 29. Mechanism of cholinoreceptor  All muscarinic receptor appear to be of the G protein coupled type  Muscarinic agonist binding activates the 𝐼𝑃3 and DAG cascade with a possible role of DAG in the opening of smooth muscle calcium channel and 𝐼𝑃3 releasing calcium from endoplasmic reticulum and sarcoplasmic reticulum  Muscarinic agonist also increase cellular cGMP concentration  Activation of muscarinic receptor also increases potassium flux across cardiac cell membrane and decrease it in ganglion and smooth muscle cell
  • 30.  This effect is mediated by the binding of the activated G protein directly to the channel  Muscarinic agonist can attenuate the activation of adenylcyclase and consequent increase in cAMP level brought about by cathecholamine  The primary effect of the nicotinic receptor activation is depolarization of the nerve cell or neuromuscular and plate membrane allowing flux of 𝑁𝑎+ and 𝑘+ ion in their respective direction
  • 32. Receptor subtype Location 𝑀1 CNS neurons ,sympathetic postganglionic neurons 𝑀2 Myocardium, smooth muscle 𝑀3 Exocrine gland, smooth muscle 𝑁 𝑛 Postganglionic neuron 𝑁 𝑚 Skeletal muscle neuromuscular end plates
  • 33. Pharmacological response  Eye: muscarinic agonist when used locally cause contraction of the smooth muscle of sphincter papillae resulting in meiosis and contraction of the ciliary muscle resulting in spam of accommodation  Cardiovascular system :muscarinic agonist cause reduction and an eventual fall in blood pressure they act directly on the 𝑀3 receptor present in the smooth muscle of the vasculation as well as the endothelium of the blood vessel liberating endothelium derived relaxing factor which actually nitric oxide (NO)
  • 34.  The following event take place in direct action of muscarinic stimulant 1) An increase in a potassium current in atrial muscle cells and cell of SA and AV nodes 2) A decrease in the slow inward calcium current 3) A decrease in the diastolic depolarization current  Respiratory system : muscarinic agonist constrict the smooth muscle of the bronchial tree , increase airway resistance and produce bronchospasm  Gastrointestinal tract :muscarinic agonist stimulate the GIT tract causing increased peristaltic and secretory activities
  • 35. Anticholinesterase  An anticholinergic agent is a substance that blocks the action of the neurotransmitter acetylcholine at synapses in the central and the peripheral nervous system. These agents inhibit parasympathetic nerve impulses by selectively blocking the binding of the neurotransmitter acetylcholine to its receptor in nerve cells.
  • 36.  Classification according to chemical composition  Simple alcohols with quaternary ammonium group : edrophonium  Carbamic acid ester of alcohol with quaternary or tertiary ammonium group carbamates : neostigmine, physostigmine , rivastigmine,  Organic phosphorous compound : organophosphate , ecothiophate , diisopropyfluorophosphate( DFP), malathion,
  • 37. Pharmacological response  Eyes: anticholinesterase cause miosis and consequent change in the intraocular pessure  GIT tract : neostiamine and other drug have similar effect as other cholinomimetic  Urinary system: these drug cause contraction of the smooth muscle of the bladder and ureter  Bronchioles : anticholinesterase cause constriction of the bronchioles with increased in airway
  • 38. Reference  Conceptual pharmacology : P Jagadish Prasad  Rang and Dale's Pharmacology:James Ritter, Rod J. Flower, G. Henderson, David J. MacEwan, Yoon Kong Loke, H. P. Rang  Basic & Clinical Pharmacology: Katzung and Bertram