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Neurohumoral
Transmission In Central
Nervous System
SUBMITTED TO - DR. AKASH JAIN
PREPARED BY - SONALI VERMA, RISHABH CHALOTRA,
SANCHIT DHANKHAR
M.PHARMACY IST SEM PHARMACOLOGY
1
Overview:-
 Neurohumoral Transmission
 Steps Involved in Neurohumoral Transmission
 Introduction.
 GABA.
 Glycine.
 Glutamate.
 Serotonin.
 Dopamine.
 Histamine.
2
Neurohumoral Transmission
 Neurohumoral transmission refers
to the transmission of nerve impulse
through synapse & Neuroeffector
junction by the release of humoral
(chemical) substance e.g. a
biogenic amine, an amino acid or a
peptide.
 Information is communicated from
Nerve to Nerve, from Nerve to
Effector Organ, by the process
called Neurohumoral Transmission
3
CNS- Central Nervous System
 It consist of Brain and Spinal Cord
4
Steps Involved in Neurohumoral Transmission
 Impulse Conduction.
 Neurotransmitter Release.
 Neurotransmitter Action on Post junction Membrane.
 Post junction Activity.
 Termination of Neurotransmitter Action.
5
Impulse Conduction
 Refer to Passage of an Impulse along nerve fibre.
 After receiving an information from a Peripheral Organ through Sensory
Nerve.
 CNS sends message or Impulse through efferent autonomic nerve.
 Impulse Conduct by generating Action Potential.
 Action Potential is self propagating & is conducted along Axonal Fibre.
Note: Resting Potential is - 70mv ( negative Inside Neuron)
Depolarization – Influx of Na+ Repolarization – Efflux of K+
Repolarization is Shorter than Depolarization.
6
Neurotransmitter Release
 Depolarisation leads to stimulation and
opening of voltage sensitive Ca+ Channel.
 Ca+ helps in fusion between Axoplasmic
Membrane and Synaptic Vesicle (Store
house of Neurotransmitter)
 Neurons release by Exocytosis.
7
Neurotransmitter Action on Post -
Junctional Membrane
 The Released Transmitter combines with
specific receptors on the post junctional
membrane
 Depending on its Nature induces an :-
1. Excitatory Post Synaptic Potential.
2. Inhibitory Post Synaptic Potential.
8
Post Junctional Activity
 Excitatory Post synaptic Potential generates a propagated post Junctional
Action Potential, which results :-
1. Nerve impulse in Neurons
2. Contraction in Muscles
3. Secretions in Glands
 An Inhibitory Post Synaptic Potential Stabilize Post junctional membranes
and Resist Depolarization stimuli.
9
Termination of Transmitted Action
 It is either Locally Degraded or Partly taken back into Pre
junctional Neuron by active Reuptake.
It Can also be explained easily by the following Diagram :-
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Gamma Aminobutyric Acid (GABA)
 Gaba is the main inhibitory Neurotransmitter in CNS, Synthesized in Brain.
 It acts by binding to specific receptor on both Pre and Post synaptic Membrane.
 Synapses using GABA are referred to as GABAergic synapses.
15
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GABA RECEPTOR
 It has pentameric structure.
 It has structural similarity & functional
similarity with ligand Gated ion
channels.
 Each GABA receptor subunit contains
two alpha subunit, two beta subunit &
one gamma subunit.
18
19
Glycine
 Simplest Amino acid, semi essential Amino acid.
 Major Inhibitory neurotransmitter in CNS also known as Inhibitory chloride
Channel Protein.
 They are Present in abundance in Spinal cord.
 Glycine receptor is a member of Nicotinic receptor superfamily.
 To prevent Tissue Injury.
 To enhance anti – oxidant Capacity.
 To promote protein synthesis and wound healing.
 Used in Spasticity
 For biosynthesis of Heme, Creatinine & Glutathione.
Function
20
Synthesis
 Serine + tetrahydrofolate → glycine +
N5,N10Methylene tetrahydrofolate + H2O
21
Receptor
 The Glycine receptor responsible for inhibition is a Cl- Channel.
 It is Ionotropic in Nature & is Pentamer made up of two subunits.
a) The ligand- Binding Alpha Subunit.
b) The Structural Beta Subunit.
22
Glutamate
 They are Excitatory Amino Acid.
 Principal excitatory neurotransmitter in CNS, stored in Neuronal cell membrane.
 Glutamate comes into the CNS mainly by glial cells and by Kreb’s Cycle.
 Responsible for neural communication, memory formation, learning and regulation.
 Glutamate Comes from glial cells in the neuron.
 In the neurons the glutamine is converted into glutamate with the help of
glutaminase enzyme
 Glutamate is stored in the synaptic vesicles.
 From synaptic vesicles glutamate release by the process of exocytosis which is Ca+
dependent.
Synthesis
23
24
25
Receptors
 Glutamate receptors are synaptic receptors located primarily on the membranes of
Neuronal cells.
 Glutamate (glutamic acid ) is abundant in the human body, but particularly in the
nervous system and especially prominent in the human brain where it is the body’s
most prominent neurotransmitter, the brain’s main excitatory neurotransmitter.
 Glutamate receptors are responsible for the glutamate – mediated postsynaptic
excitation of neural cells, and are important for neural communication, memory
formation, learning, and regulation.
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SEROTONIN
 The scientific name for serotonin is 5-hydroxytryptamine, or 5-HT
 It is a monoamine neurotransmitter.
 About 90% of is found/localized in the intestines: the rest in brain and platelets.
 The level of 5-HT in whole blood is in the range of 65–250 mg/ml
 It is popularly thought to be a contributor to feelings of well-being and happiness
it is a key mediator in the physiology of mood, vascular function and
gastrointestinal motility.
 This explains the number of therapeutic agents that act targeting the
serotonergic system such as: 5-HT3 antagonists, SSRIs and triptans
29
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ACTION AND FUNCTIONS OF
SEROTONIN
32
PERIPHERAL MEDIATED
PHYSIOLOGICAL FUNCTIONS OF 5-
HT RECEPTORS In periphery
 Peristalsis
 Vomiting
 Platelet aggregation and haemostasias
 Inflammatory mediator
 Sensitization of nociceptors (Pain Receptor)
 Microvascular control
33
Central effects of Serotonin receptor
 Neuronal inhibitions through decrease of cAMP
 Behavioral effects
 Sleep mood
 Feeding thermoregulatory
 Anxiety
 Cerebral vasoconstrictions
34
Serotonin pathways in the Brain
 Serotonin pathways that are located in the brainstem area “the Raphe nuclei”
these neurons control muscle activity, 5-HT receptors trigger vomiting.
 The serotonin neurons in frontal cortex, regulate cognition and memory.
 The serotonin neurons in the hippocampus regulate memory.
 The serotonin neurons in the other limbic areas regulate mood. (Basal
ganglia and cerebral cortex). SSRI’s work in this pathway.
35
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Drugs acting on 5-HT receptors 38
Drugs acting on serotonergic
neurotransmission
39
 MAO inhibitors ;-
Monoamine oxidase is a key enzyme for serotonin, dopamine and
norepinephrine inactivation. MAO inhibitors prevent inactivation of
monoamines within a neuron, causing excess neurotransmitter to diffuse into
the synaptic space. This class of agents is used in the treatment of depression
(phenelzine, tranylcypromine, selegiline) and Parkinson’s disease (selegiline).
Dietary restrictions (because of tyramine toxicity) limit their widespread use.
 Inhibitors of serotonin storage ;-
They interfere with the ability of synaptic vesicles to store monoamines;
displace serotonin, dopamine and norepinephrine from their storage in
presynaptic nerve terminals.
Agents that share this mechanism of action include amphetamine,
methylphenidate and modafinil
40
41
The Side Effects of Selective
Serotonin Reuptake Inhibitor’s
 Dry mouth
 Sweating
 Headaches
 Sedation
 Dizziness
 Nausea
 Somnolence (Sleepeness)
 Insomnia
 Diarrhea
42
Serotonin agonist 43
5-HT2 Antagonist
Ketanserin is a 5-HT2A/2C antagonist used for the treatment of hypertension. In addition to its serotonin
antagonism, it has affinity for alpha-1 receptors, which may contribute to its antihypertensive effect.
44
Serotonin Syndrome – What Happens When Your
Serotonin Levels Are Too High? 45
Tips for naturally boosting serotonin
1. Get morning sunlight, its more intense and this can boost your body’s production
melatonin.
2. Get plenty of exercise, researchers have found that exercise boost serotonin.
3. Reduce your stress (both physical and emotional), prolonged stress produce
adrenaline and cortisol which interfere with serotonin.
4. Eating foods that are high in protein because of high percentage of tryptophan.
5. Also food containing carbohydrates as they produce insulin which helps tryptophan go
into the brain
46
Dopamine
 Dopamine belongs to the family of catecholamines
 Hormones Epinephrine and Norepinephrine (other catecholamines) are
derived from Dopamine.
 Significant role in learning, goal-directed behavior, regulation of hormones,
motor control
47
48
Storage and Release 49
Metabolism 50
51
Physiological roles 52
Control of movement
 The largest Dopamine tract in the brain
which contains about 80% of brain’s
dopamine in the nigrostriatal system.
 Assisted in learning coordinated
movements.
53
54
Parkinson’s Disease
 Substantial loss of Dopamine in the striatum (70 – 80%)
 Loss of dopamine neurons in other systems also (Mesolimbic,
Mesocortical and Hypothalamic systems)
 Treatment strategy includes increasing dopamine levels by administering ;-
 Dopamine precursor : Levodopa (l-dopa)
 (b) Peripheral decarboxylase inhibitors : Carbidopa,.
 (c) Dopaminergic agonists: Bromocriptine, Ropinirole, Pramipexole
 (d) MAO-B inhibitor: Selegiline
 (e) COMT inhibitors: Entacapone, Tolcapone
 (f) Dopamine facilitator: Amantadine
55
56
Schizophrenia
 Defective dopamine neurotransmission – relative excess of central dopaminergic
activity
 An increase in DA function in the mesolimbic system and a decreased function in
the mesocortical DA systems
 Behavior similar to the behavioral effects of psychostimulants
 Antipsychotics such as chlorpromazine, bind to D 2 dopamine receptors and
reduced positive psychotic symptoms
57
58
59
Parmacological effects 60
Histamine
Introduction
 Histamine is a biogenic amine found in many tissues, including mast cells,
basophils, lymphocytes, neurons, and gastric enterochromaffin-like cells.
 It is an autacoid—that is, a molecule secreted locally to increase or decrease the
activity of nearby cells.
 Histamine is a major mediator of allergic and inflammatory processes.
 It also has significant roles in the regulation of gastric acid secretion,
neurotransmission, and immune modulation.
61
62
Storage and Release
 Histamine synthesis and storage can be divided into two “pools”:
 A slowly turning over pool
 A rapidly turning over pool
 The slowly turning over pool is located in mast cells and basophils.
 Histamine is stored in large granules in these inflammatory cells, and the
release of histamine involves complete degranulation of the cells.
 The rapidly turning over pool is located in gastric ECL (Enterochromaffin)
cells and in histaminergic CNS neurons.
 These cells synthesize and release histamine as required for gastric acid
secretion and neurotransmission, respectively.
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Thank You
69

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Neurohumoral transmission in central nervous system

  • 1. Neurohumoral Transmission In Central Nervous System SUBMITTED TO - DR. AKASH JAIN PREPARED BY - SONALI VERMA, RISHABH CHALOTRA, SANCHIT DHANKHAR M.PHARMACY IST SEM PHARMACOLOGY 1
  • 2. Overview:-  Neurohumoral Transmission  Steps Involved in Neurohumoral Transmission  Introduction.  GABA.  Glycine.  Glutamate.  Serotonin.  Dopamine.  Histamine. 2
  • 3. Neurohumoral Transmission  Neurohumoral transmission refers to the transmission of nerve impulse through synapse & Neuroeffector junction by the release of humoral (chemical) substance e.g. a biogenic amine, an amino acid or a peptide.  Information is communicated from Nerve to Nerve, from Nerve to Effector Organ, by the process called Neurohumoral Transmission 3
  • 4. CNS- Central Nervous System  It consist of Brain and Spinal Cord 4
  • 5. Steps Involved in Neurohumoral Transmission  Impulse Conduction.  Neurotransmitter Release.  Neurotransmitter Action on Post junction Membrane.  Post junction Activity.  Termination of Neurotransmitter Action. 5
  • 6. Impulse Conduction  Refer to Passage of an Impulse along nerve fibre.  After receiving an information from a Peripheral Organ through Sensory Nerve.  CNS sends message or Impulse through efferent autonomic nerve.  Impulse Conduct by generating Action Potential.  Action Potential is self propagating & is conducted along Axonal Fibre. Note: Resting Potential is - 70mv ( negative Inside Neuron) Depolarization – Influx of Na+ Repolarization – Efflux of K+ Repolarization is Shorter than Depolarization. 6
  • 7. Neurotransmitter Release  Depolarisation leads to stimulation and opening of voltage sensitive Ca+ Channel.  Ca+ helps in fusion between Axoplasmic Membrane and Synaptic Vesicle (Store house of Neurotransmitter)  Neurons release by Exocytosis. 7
  • 8. Neurotransmitter Action on Post - Junctional Membrane  The Released Transmitter combines with specific receptors on the post junctional membrane  Depending on its Nature induces an :- 1. Excitatory Post Synaptic Potential. 2. Inhibitory Post Synaptic Potential. 8
  • 9. Post Junctional Activity  Excitatory Post synaptic Potential generates a propagated post Junctional Action Potential, which results :- 1. Nerve impulse in Neurons 2. Contraction in Muscles 3. Secretions in Glands  An Inhibitory Post Synaptic Potential Stabilize Post junctional membranes and Resist Depolarization stimuli. 9
  • 10. Termination of Transmitted Action  It is either Locally Degraded or Partly taken back into Pre junctional Neuron by active Reuptake. It Can also be explained easily by the following Diagram :- 10
  • 11. 11
  • 12. 12
  • 13. 13
  • 14. 14
  • 15. Gamma Aminobutyric Acid (GABA)  Gaba is the main inhibitory Neurotransmitter in CNS, Synthesized in Brain.  It acts by binding to specific receptor on both Pre and Post synaptic Membrane.  Synapses using GABA are referred to as GABAergic synapses. 15
  • 16. 16
  • 17. 17
  • 18. GABA RECEPTOR  It has pentameric structure.  It has structural similarity & functional similarity with ligand Gated ion channels.  Each GABA receptor subunit contains two alpha subunit, two beta subunit & one gamma subunit. 18
  • 19. 19
  • 20. Glycine  Simplest Amino acid, semi essential Amino acid.  Major Inhibitory neurotransmitter in CNS also known as Inhibitory chloride Channel Protein.  They are Present in abundance in Spinal cord.  Glycine receptor is a member of Nicotinic receptor superfamily.  To prevent Tissue Injury.  To enhance anti – oxidant Capacity.  To promote protein synthesis and wound healing.  Used in Spasticity  For biosynthesis of Heme, Creatinine & Glutathione. Function 20
  • 21. Synthesis  Serine + tetrahydrofolate → glycine + N5,N10Methylene tetrahydrofolate + H2O 21
  • 22. Receptor  The Glycine receptor responsible for inhibition is a Cl- Channel.  It is Ionotropic in Nature & is Pentamer made up of two subunits. a) The ligand- Binding Alpha Subunit. b) The Structural Beta Subunit. 22
  • 23. Glutamate  They are Excitatory Amino Acid.  Principal excitatory neurotransmitter in CNS, stored in Neuronal cell membrane.  Glutamate comes into the CNS mainly by glial cells and by Kreb’s Cycle.  Responsible for neural communication, memory formation, learning and regulation.  Glutamate Comes from glial cells in the neuron.  In the neurons the glutamine is converted into glutamate with the help of glutaminase enzyme  Glutamate is stored in the synaptic vesicles.  From synaptic vesicles glutamate release by the process of exocytosis which is Ca+ dependent. Synthesis 23
  • 24. 24
  • 25. 25
  • 26. Receptors  Glutamate receptors are synaptic receptors located primarily on the membranes of Neuronal cells.  Glutamate (glutamic acid ) is abundant in the human body, but particularly in the nervous system and especially prominent in the human brain where it is the body’s most prominent neurotransmitter, the brain’s main excitatory neurotransmitter.  Glutamate receptors are responsible for the glutamate – mediated postsynaptic excitation of neural cells, and are important for neural communication, memory formation, learning, and regulation. 26
  • 27. 27
  • 28. 28
  • 29. SEROTONIN  The scientific name for serotonin is 5-hydroxytryptamine, or 5-HT  It is a monoamine neurotransmitter.  About 90% of is found/localized in the intestines: the rest in brain and platelets.  The level of 5-HT in whole blood is in the range of 65–250 mg/ml  It is popularly thought to be a contributor to feelings of well-being and happiness it is a key mediator in the physiology of mood, vascular function and gastrointestinal motility.  This explains the number of therapeutic agents that act targeting the serotonergic system such as: 5-HT3 antagonists, SSRIs and triptans 29
  • 30. 30
  • 31. 31
  • 32. ACTION AND FUNCTIONS OF SEROTONIN 32
  • 33. PERIPHERAL MEDIATED PHYSIOLOGICAL FUNCTIONS OF 5- HT RECEPTORS In periphery  Peristalsis  Vomiting  Platelet aggregation and haemostasias  Inflammatory mediator  Sensitization of nociceptors (Pain Receptor)  Microvascular control 33
  • 34. Central effects of Serotonin receptor  Neuronal inhibitions through decrease of cAMP  Behavioral effects  Sleep mood  Feeding thermoregulatory  Anxiety  Cerebral vasoconstrictions 34
  • 35. Serotonin pathways in the Brain  Serotonin pathways that are located in the brainstem area “the Raphe nuclei” these neurons control muscle activity, 5-HT receptors trigger vomiting.  The serotonin neurons in frontal cortex, regulate cognition and memory.  The serotonin neurons in the hippocampus regulate memory.  The serotonin neurons in the other limbic areas regulate mood. (Basal ganglia and cerebral cortex). SSRI’s work in this pathway. 35
  • 36. 36
  • 37. 37
  • 38. Drugs acting on 5-HT receptors 38
  • 39. Drugs acting on serotonergic neurotransmission 39
  • 40.  MAO inhibitors ;- Monoamine oxidase is a key enzyme for serotonin, dopamine and norepinephrine inactivation. MAO inhibitors prevent inactivation of monoamines within a neuron, causing excess neurotransmitter to diffuse into the synaptic space. This class of agents is used in the treatment of depression (phenelzine, tranylcypromine, selegiline) and Parkinson’s disease (selegiline). Dietary restrictions (because of tyramine toxicity) limit their widespread use.  Inhibitors of serotonin storage ;- They interfere with the ability of synaptic vesicles to store monoamines; displace serotonin, dopamine and norepinephrine from their storage in presynaptic nerve terminals. Agents that share this mechanism of action include amphetamine, methylphenidate and modafinil 40
  • 41. 41
  • 42. The Side Effects of Selective Serotonin Reuptake Inhibitor’s  Dry mouth  Sweating  Headaches  Sedation  Dizziness  Nausea  Somnolence (Sleepeness)  Insomnia  Diarrhea 42
  • 44. 5-HT2 Antagonist Ketanserin is a 5-HT2A/2C antagonist used for the treatment of hypertension. In addition to its serotonin antagonism, it has affinity for alpha-1 receptors, which may contribute to its antihypertensive effect. 44
  • 45. Serotonin Syndrome – What Happens When Your Serotonin Levels Are Too High? 45
  • 46. Tips for naturally boosting serotonin 1. Get morning sunlight, its more intense and this can boost your body’s production melatonin. 2. Get plenty of exercise, researchers have found that exercise boost serotonin. 3. Reduce your stress (both physical and emotional), prolonged stress produce adrenaline and cortisol which interfere with serotonin. 4. Eating foods that are high in protein because of high percentage of tryptophan. 5. Also food containing carbohydrates as they produce insulin which helps tryptophan go into the brain 46
  • 47. Dopamine  Dopamine belongs to the family of catecholamines  Hormones Epinephrine and Norepinephrine (other catecholamines) are derived from Dopamine.  Significant role in learning, goal-directed behavior, regulation of hormones, motor control 47
  • 48. 48
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  • 53. Control of movement  The largest Dopamine tract in the brain which contains about 80% of brain’s dopamine in the nigrostriatal system.  Assisted in learning coordinated movements. 53
  • 54. 54
  • 55. Parkinson’s Disease  Substantial loss of Dopamine in the striatum (70 – 80%)  Loss of dopamine neurons in other systems also (Mesolimbic, Mesocortical and Hypothalamic systems)  Treatment strategy includes increasing dopamine levels by administering ;-  Dopamine precursor : Levodopa (l-dopa)  (b) Peripheral decarboxylase inhibitors : Carbidopa,.  (c) Dopaminergic agonists: Bromocriptine, Ropinirole, Pramipexole  (d) MAO-B inhibitor: Selegiline  (e) COMT inhibitors: Entacapone, Tolcapone  (f) Dopamine facilitator: Amantadine 55
  • 56. 56
  • 57. Schizophrenia  Defective dopamine neurotransmission – relative excess of central dopaminergic activity  An increase in DA function in the mesolimbic system and a decreased function in the mesocortical DA systems  Behavior similar to the behavioral effects of psychostimulants  Antipsychotics such as chlorpromazine, bind to D 2 dopamine receptors and reduced positive psychotic symptoms 57
  • 58. 58
  • 59. 59
  • 61. Histamine Introduction  Histamine is a biogenic amine found in many tissues, including mast cells, basophils, lymphocytes, neurons, and gastric enterochromaffin-like cells.  It is an autacoid—that is, a molecule secreted locally to increase or decrease the activity of nearby cells.  Histamine is a major mediator of allergic and inflammatory processes.  It also has significant roles in the regulation of gastric acid secretion, neurotransmission, and immune modulation. 61
  • 62. 62
  • 63. Storage and Release  Histamine synthesis and storage can be divided into two “pools”:  A slowly turning over pool  A rapidly turning over pool  The slowly turning over pool is located in mast cells and basophils.  Histamine is stored in large granules in these inflammatory cells, and the release of histamine involves complete degranulation of the cells.  The rapidly turning over pool is located in gastric ECL (Enterochromaffin) cells and in histaminergic CNS neurons.  These cells synthesize and release histamine as required for gastric acid secretion and neurotransmission, respectively. 63
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Editor's Notes

  1. BH4 - Tetrahydrobiopterin