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Dr. RAGHU PRASADA M S
MBBS,MD
ASSISTANT PROFESSOR
DEPT. OF PHARMACOLOGY
SSIMS & RC.
1
2
Classes of CNS Transmitters
Neurotransmitter % of
Synapses
Function Primary Receptor
Class
Monoamines
Catecholamines: DA, NE,
EPI
Indoleamines: serotonin
(5-HT)
2-5 Slow change in
excitability (secs)
GPCRs
Acetylcholine (ACh) 5-10 Slow change in
excitability (secs)
GPCRs
Amino acids
Inhibitory: GABA, glycine
Excitatory: Glutamate,
aspartate
15-20
75-80
Rapid inhibition
(msecs)
Rapid excitation
(msecs)
Ion channels
Ion channels
Neurotransmitter Cell Bodies Terminals
Norepinephrine
(NE)
Locus coeruleus
Lateral tegmental
area
Very widespread: cerebral cortex,
thalamus, cerebellum, brainstem
nuclei, spinal cord
Basal forebrain, thalamus,
hypothalamus, brainstem, spinal
cord
Epinephrine (EPI) Small, discrete
nuclei in medulla
Thalamus, brainstem, spinal cord
Dopamine (DA) Substantia nigra
(pars compacta)
Ventral tegmental
area
Arcuate nucleus
Striatum
Limbic forebrain, cerebral cortex
Median eminence
Serotonin (5-HT) Raphe nuclei
(median and dorsal),
pons, medulla
Very widespread: cerebral cortex,
thalamus, cerebellum, brainstem
nuclei, spinal cord
Localization of Monoamines in the Brain
The blood-brain barrier (BBB) is a membrane that
controls the passage of substances from the blood into
the central nervous system.
It is a physical barrier between the local blood vessels
and most parts of the central nervous system itself,
and stops many substances from travelling across it.
The BBB is permeable to alcohol, and some heavy
metals can cross the blood-brain barrier as well.
The BBB can be broken down by:
Hypertension (high blood pressure): high blood
pressure opens the BBB
Development: the BBB is not fully formed at birth.
Hyperosmolitity: a high concentration of a substance in
the blood can open the BBB.
Microwaves: exposure to microwaves can open the
BBB.
Radiation: exposure to radiation can open the BBB.
Infection: exposure to infectious agents can open the
BBB.
Trauma, Ischemia, Inflammation, Pressure: injury to
the brain can open the BBB.
Catecholamine synthesisSynthesis of catecholamines
Peptides
Examples: substance P, somatostatin, leu-enkephalin, met-
enkephalin, vasoactive intestinal polypeptide (VIP), bombesin
Peptide synthesized in rough endoplasmic reticulum
Packaged in Golgi apparatus
Transported down axon to presynaptic ending of the axon
terminal secretory vesicles transported down axon by
orthograde axonal transport
Small molecule transmitters (amino acids and amines)
Examples of amino acid neurotransmitters: gamma-
amino butyric acid (GABA), glutamate (Glu), glycine (Gly)
Examples of amine neurotransmitters: acetylcholine
(ACh), dopamine (DA), epinephrine, histamine,
norepinephrine (NE), serotonin (5-HT)
Occurs in axon terminal
Precursor molecule is transformed by synthetic enzyme
into neurotransmitter molecule
Neurotransmitter molecules are gathered by transporter
molecules and packaged in synaptic vesicles
 Sympathetic nerves take up amines and release them as
neurotransmitters
 Axonal uptake or Uptake I is a high efficiency system, more
specific for NA
 By norepinephrine transporter (NET)
 Located in neuronal membrane
 Inhibited by Cocaine, TCAD, Amphetamines
 Vesicular uptake-
 By vesicular monoamine transporter (VMAT-2)
 Also capture DA for synthesis of NA
 Inhibited by Reserpine
 Extraneuronal uptake is less specific for NA
 Located in smooth muscle/ cardiac muscle
 By extraneuronal amine transporter
 Inhibited by steroids/ phenoxybenzamine
 No Physiological or Pharmacological importance
NE can be transported back into the pre-synaptic neuron
(reuptake). Enzymes involved in metabolism are
Mono Amine Oxidase (MAO)
Intracellular bound to mitochondrial membrane
Present in NA terminals and liver/ intestine
Catechol-o-methyl-transferase (COMT)
Neuronal and non-neuronal tissue
Acts on catecholamines and byproducts
End product of EPI metabolism  VMA-vanilyl mandelic acid
End product of DOPA metabolism  HVA-homovallinic acid
NE can activate the presynaptic receptors (α-2 for negative
feedback), 5HT  MAO  5HIAA
Amphetamines and cocaine block the reuptake of catecholamines,
thereby prolonging their synaptic action
Selectivity for the targeted pathway
Receptor subtypes
Allosteric sites on receptors
Presynaptic and postsynaptic actions
Partial/inverse agonist (activity dependent)
Plasticity reveals adaptive changes in drug response
Pharmacokinetic: drug metabolism
Pharmacodynamic: cellular
Acetylcholine is the transmitter used by motor neurons of
the spinal cord
Released at all vertebrate neuro-muscular junctions
Present in autonomic & parasympathetic neurons
Cholinergic fibres All somatic motar neurons
All preganglionic fibres and Post ganglionic
parasympathetic fibres
Exception-post ganglionic sympathetic fibres to apocrine
glands
DOPAMINE RECEPTORS
There are at least 5 subtypes of receptors:
D1 and D5: mostly involved in postsynaptic
inhibition.
D2, D3, and D4: involved in both pre-and
postsynaptic inhibition.
D2: the predominant subtype in the brain:
regulates mood, emotional stability in the limbic
system and movement control in the basal ganglia.
The nigrostriatal pathway (substantia nigra to striatum)
extrapyramidal motor control coordination of
voluntary movement
Mesolimbic- mesocortical (ventral tegmental to
n.accumbens, hippocampus, and cortex)emotion
Cognition, behavior
Tuberoinfundibular- (arcuate nucleus of hypothalamus to
median eminence then anterior pituitary)
prolactin release, pituitary system (endocrine)
The medulla oblongata (vomit)
Medullary - periventricular pathway ( eating behavior)
Behavioral – depression, anxiety, decreased
motivation, personality changes,
Sensory – non-specific pains,, restless legs and other
sleep problems
Autonomic – constipation, bladder dysfunction,
impotence, low blood pressure
Muhammad
Ali
The synthesis pathway continues from dopamine:
Dopamine beta-hydroxylase (DBH) makes dopamine
into norepinephrine
If the neuron is noradrenergic, the pathway stops here,
Or If the neuron is adrenergic the pathway can
continues Phentolamine N-methyl transferase
(PNMT) makes norepinephrine into epinephrine
Arousal, Mood, Blood pressure control
In the CNS, norepinephrine is used by neurons of
the locus coruleus, a nucleus of the brainstem with
complex modulatory functions
In the peripheral nervous system, norepinephrine is
the transmitter of the sympathetic nervous system
Norepinephrine can then be converted to
epinephrine
Sleep, Mood, Sexual function and Appetite
LSD- 5HT2 agonist – Visual hallucinations
5-HT has a modulatory effect on dopaminergic
neurones
Glutamate hypothesis
Phencyclidine, ketamine
Glutamate-NMDA antagonists –can produce psychotic
symptoms
Depression is due to deficiency of nor-epinephrine &
serotonin
Normally action of released NE & serotonin is terminated by
active reuptake into the nerve terminal from the synapse via
specific transporters.
TCAs block the amine transporters (uptake pumps) for nor-
epinephrine (NET) & serotonin (SERT) in brain.
Facilitation of NE & serotonin transmission ---- improves
symptoms of depression .
Memory (ChEI in Alzheimers disease)
Basal forebrain to cortex/hippocampus (A)
Extrapyramidal motor responses (benztropine for
Parkinsonian symptoms)
Striatum (B)
Vestibular control (scopolamine patch for motion sickness)
Nigrostriatal pathway
extrapyramidal motor responses
Interneurons throughout the brain
inhibit excitability, stabilize membrane potential, prevent
repetitive firing
Metabotropic GABA B receptors
These receptors are GPCRS
Largely presynaptic, inhibit transmitter release
Most important role is in the spinal cord
Baclofen, an agonist at this receptor, is a muscle relaxant
There are two GABA binding sites per receptor.
Benzodiazepines and the newer hypnotic drugs bind
to allosteric sites on the receptor to potentiate GABA
mediated channel opening.
Babiturates act at a distinct allosteric site to also
potentiate GABA inhibition.
These drugs act as CNS depressants
Picrotoxin blocks the GABA-gated chloride channel
 GABA –Gamma Amino Butyric Acid is a major
inhibitory neurotransmitter in CNS
 Benzodiazepines potentiate GABA ergic inhibition at
all levels of neuroxis—spinal cord, hypothalamus,
hippocampus, substantia nigra, cerebellar cortex and
cerebral cortex
 Pentameric structure 5 subunits
 Macromolecular complex of ion channel
Loss of GABA-ergic transmission contributes to
excessive excitability and impulse spread in epilepsy.
Picrotoxin and bicuculline ( GABA receptor blocker)
inhibit GABAA receptor function and are convulsants.
BDZs and barbiturates increase GABAA receptor
function and are anticonvulsants.
Drugs that block GABA reuptake (GAT) and metabolism
( GABA-T) to increase available GABA are
anticonvulsants
Major role is in the spinal cord
Glycine receptor is an ionotropic chloride channel
analagous to the GABAA receptor.
Strychnine, a competitive antagonist of glycine,
removes spinal inhibition to skeletal muscle and
induces a violent motor response.
Neurotransmitter at 75-80% of CNS synapses
Synthesized within the brain from
Glucose (via KREBS cycle/α-ketoglutarate)
Glutamine (from glial cells)
Actions terminated by uptake through excitatory
amino acid transporters (EAATs) in neurons and
astrocytes
Blocked at resting membrane potential (coincidence
detector)
Requires glycine binding
Permeable to Ca++ as well as Na
NMDA receptors involvement in disease
- seizure disorders
- learning and memory
- neuronal cell death
NMDA receptor as a
coincidence
detector :
requirement for
membrane
depolarization
36
NMDA receptor is Ca++ permeable
It is the GluR2 subunit that makes most AMPA
receptors Ca++ impermeable
The GluR2 subunit contains one amino acid
substitution : arginine (R) versus glutamine (Q) in all
other GluRs
Transmitter Anatomy Receptor Subtypes and
Preferred Agonists
Receptor
Antagonists
Mechanisms
Acetylcholine Cell bodies at all levels; long
and short connections
Muscarinic (M1): muscarine Pirenzepine,
atropine
Excitatory: in K+ conductance; IP3,
DAG
Muscarinic (M2): muscarine,
bethanechol
Atropine,
methoctramine
Inhibitory: K+ conductance; cAMP
Motoneuron-Renshaw cell
synapse
Nicotinic: nicotine Dihydro--
erythroidine, -
bungarotoxin
Excitatory: cation conductance
Dopamine Cell bodies at all levels;
short, medium, and long
connections
D1 Phenothiazines Inhibitory (?): cAMP
D2: bromocriptine Phenothiazines,
butyrophenones
Inhibitory (presynaptic): Ca2+;
Inhibitory (postsynaptic): in K+
conductance, cAMP
GABA Supraspinal and spinal
interneurons involved in pre-
and postsynaptic inhibition
GABAA: muscimol Bicuculline,
picrotoxin
Inhibitory: Cl–conductance
GABAB: baclofen 2-OH saclofen Inhibitory (presynaptic): Ca2+
conductance; Inhibitory
(postsynaptic): K+ conductance
Transmitter Anatomy Receptor Subtypes and
Preferred Agonists
Receptor Antagonists Mechanisms
Glutamate Relay neurons at
all levels and some
interneurons
N-Methyl-D-aspartate
(NMDA): NMDA
2-Amino-5-
phosphonovalerate,
dizocilpine
Excitatory: cation conductance,
particularly Ca2+
AMPA: AMPA CNQX Excitatory: cation conductance
Kainate: kainic acid, domoic
acid
Metabotropic: ACPD,
quisqualate
MCPG Inhibitory (presynaptic): Ca2+
conductance cAMP; Excitatory:
K+ conductance, IP3, DAG
Glycine Spinal
interneurons and
some brain stem
interneurons
Taurine, -alanine Strychnine Inhibitory: Cl–conductance
5-
Hydroxytryptam
ine (serotonin)
Cell bodies in
midbrain and pons
project to all levels
5-HT1A: LSD Metergoline,
spiperone
Inhibitory: K+ conductance,
cAMP
5-HT2A: LSD Ketanserin Excitatory: K+ conductance, IP3,
DAG
5-HT3: 2-methyl-5-HT Ondansetron Excitatory: cation conductance
Transmitter Anatomy Receptor Subtypes and
Preferred Agonists
Receptor
Antagonists
Mechanisms
Norepinephrin
e
Cell bodies in pons
and brain stem
project to all levels
1: phenylephrine Prazosin Excitatory: K+
conductance, IP3, DAG
2: clonidine Yohimbine Inhibitory (presynaptic):
Ca2+ conductance;
Inhibitory: K+
conductance, cAMP
1: isoproterenol,
dobutamine
Atenolol,
practolol
Excitatory: K+
conductance, cAMP
2: Salbutamol Butoxamine Inhibitory: may involve
in electrogenic sodium
pump; cAMP
Histamine Cells in ventral
posterior
hypothalamus
H1: 2(m-fluorophenyl)-
histamine
Mepyramine Excitatory: K+
conductance, IP3, DAG
H2: dimaprit Ranitidine Excitatory: K+
conductance, cAMP
H3: R--methyl-histamine Thioperamide Inhibitory autoreceptors
Transmitter Anatomy Receptor Subtypes and
Preferred Agonists
Receptor Antagonists Mechanisms
Opioid peptides Cell bodies at all levels;
long and short
connections
Mu: bendorphin Naloxone Inhibitory
(presynaptic): Ca2+
conductance, cAMP
Delta: enkephalin Naloxone Inhibitory
(postsynaptic): K+
conductance, cAMP
Kappa: dynorphin Naloxone
Tachykinins Primary sensory
neurons, cell bodies at
all levels; long and
short connections
NK1: Substance P
methylester, aprepitant
Aprepitant Excitatory: K+
conductance, IP3, DAG
NK2
NK3
Endocannabinoids Widely distributed CB1: Anandamide, 2-
arachidonyglycerol
Rimonabant Inhibitory
(presynaptic): Ca2+
conductance, cAMP
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Class intro to cns

  • 1. Dr. RAGHU PRASADA M S MBBS,MD ASSISTANT PROFESSOR DEPT. OF PHARMACOLOGY SSIMS & RC. 1
  • 2. 2 Classes of CNS Transmitters Neurotransmitter % of Synapses Function Primary Receptor Class Monoamines Catecholamines: DA, NE, EPI Indoleamines: serotonin (5-HT) 2-5 Slow change in excitability (secs) GPCRs Acetylcholine (ACh) 5-10 Slow change in excitability (secs) GPCRs Amino acids Inhibitory: GABA, glycine Excitatory: Glutamate, aspartate 15-20 75-80 Rapid inhibition (msecs) Rapid excitation (msecs) Ion channels Ion channels
  • 3. Neurotransmitter Cell Bodies Terminals Norepinephrine (NE) Locus coeruleus Lateral tegmental area Very widespread: cerebral cortex, thalamus, cerebellum, brainstem nuclei, spinal cord Basal forebrain, thalamus, hypothalamus, brainstem, spinal cord Epinephrine (EPI) Small, discrete nuclei in medulla Thalamus, brainstem, spinal cord Dopamine (DA) Substantia nigra (pars compacta) Ventral tegmental area Arcuate nucleus Striatum Limbic forebrain, cerebral cortex Median eminence Serotonin (5-HT) Raphe nuclei (median and dorsal), pons, medulla Very widespread: cerebral cortex, thalamus, cerebellum, brainstem nuclei, spinal cord Localization of Monoamines in the Brain
  • 4. The blood-brain barrier (BBB) is a membrane that controls the passage of substances from the blood into the central nervous system. It is a physical barrier between the local blood vessels and most parts of the central nervous system itself, and stops many substances from travelling across it. The BBB is permeable to alcohol, and some heavy metals can cross the blood-brain barrier as well.
  • 5.
  • 6. The BBB can be broken down by: Hypertension (high blood pressure): high blood pressure opens the BBB Development: the BBB is not fully formed at birth. Hyperosmolitity: a high concentration of a substance in the blood can open the BBB. Microwaves: exposure to microwaves can open the BBB. Radiation: exposure to radiation can open the BBB. Infection: exposure to infectious agents can open the BBB. Trauma, Ischemia, Inflammation, Pressure: injury to the brain can open the BBB.
  • 7.
  • 9.
  • 10. Peptides Examples: substance P, somatostatin, leu-enkephalin, met- enkephalin, vasoactive intestinal polypeptide (VIP), bombesin Peptide synthesized in rough endoplasmic reticulum Packaged in Golgi apparatus Transported down axon to presynaptic ending of the axon terminal secretory vesicles transported down axon by orthograde axonal transport
  • 11. Small molecule transmitters (amino acids and amines) Examples of amino acid neurotransmitters: gamma- amino butyric acid (GABA), glutamate (Glu), glycine (Gly) Examples of amine neurotransmitters: acetylcholine (ACh), dopamine (DA), epinephrine, histamine, norepinephrine (NE), serotonin (5-HT) Occurs in axon terminal Precursor molecule is transformed by synthetic enzyme into neurotransmitter molecule Neurotransmitter molecules are gathered by transporter molecules and packaged in synaptic vesicles
  • 12.  Sympathetic nerves take up amines and release them as neurotransmitters  Axonal uptake or Uptake I is a high efficiency system, more specific for NA  By norepinephrine transporter (NET)  Located in neuronal membrane  Inhibited by Cocaine, TCAD, Amphetamines  Vesicular uptake-  By vesicular monoamine transporter (VMAT-2)  Also capture DA for synthesis of NA  Inhibited by Reserpine  Extraneuronal uptake is less specific for NA  Located in smooth muscle/ cardiac muscle  By extraneuronal amine transporter  Inhibited by steroids/ phenoxybenzamine  No Physiological or Pharmacological importance
  • 13. NE can be transported back into the pre-synaptic neuron (reuptake). Enzymes involved in metabolism are Mono Amine Oxidase (MAO) Intracellular bound to mitochondrial membrane Present in NA terminals and liver/ intestine Catechol-o-methyl-transferase (COMT) Neuronal and non-neuronal tissue Acts on catecholamines and byproducts End product of EPI metabolism  VMA-vanilyl mandelic acid End product of DOPA metabolism  HVA-homovallinic acid NE can activate the presynaptic receptors (α-2 for negative feedback), 5HT  MAO  5HIAA Amphetamines and cocaine block the reuptake of catecholamines, thereby prolonging their synaptic action
  • 14.
  • 15. Selectivity for the targeted pathway Receptor subtypes Allosteric sites on receptors Presynaptic and postsynaptic actions Partial/inverse agonist (activity dependent) Plasticity reveals adaptive changes in drug response Pharmacokinetic: drug metabolism Pharmacodynamic: cellular
  • 16. Acetylcholine is the transmitter used by motor neurons of the spinal cord Released at all vertebrate neuro-muscular junctions Present in autonomic & parasympathetic neurons Cholinergic fibres All somatic motar neurons All preganglionic fibres and Post ganglionic parasympathetic fibres Exception-post ganglionic sympathetic fibres to apocrine glands
  • 17.
  • 18. DOPAMINE RECEPTORS There are at least 5 subtypes of receptors: D1 and D5: mostly involved in postsynaptic inhibition. D2, D3, and D4: involved in both pre-and postsynaptic inhibition. D2: the predominant subtype in the brain: regulates mood, emotional stability in the limbic system and movement control in the basal ganglia.
  • 19.
  • 20. The nigrostriatal pathway (substantia nigra to striatum) extrapyramidal motor control coordination of voluntary movement Mesolimbic- mesocortical (ventral tegmental to n.accumbens, hippocampus, and cortex)emotion Cognition, behavior Tuberoinfundibular- (arcuate nucleus of hypothalamus to median eminence then anterior pituitary) prolactin release, pituitary system (endocrine) The medulla oblongata (vomit) Medullary - periventricular pathway ( eating behavior)
  • 21. Behavioral – depression, anxiety, decreased motivation, personality changes, Sensory – non-specific pains,, restless legs and other sleep problems Autonomic – constipation, bladder dysfunction, impotence, low blood pressure Muhammad Ali
  • 22. The synthesis pathway continues from dopamine: Dopamine beta-hydroxylase (DBH) makes dopamine into norepinephrine If the neuron is noradrenergic, the pathway stops here, Or If the neuron is adrenergic the pathway can continues Phentolamine N-methyl transferase (PNMT) makes norepinephrine into epinephrine
  • 23. Arousal, Mood, Blood pressure control In the CNS, norepinephrine is used by neurons of the locus coruleus, a nucleus of the brainstem with complex modulatory functions In the peripheral nervous system, norepinephrine is the transmitter of the sympathetic nervous system Norepinephrine can then be converted to epinephrine
  • 24. Sleep, Mood, Sexual function and Appetite LSD- 5HT2 agonist – Visual hallucinations 5-HT has a modulatory effect on dopaminergic neurones Glutamate hypothesis Phencyclidine, ketamine Glutamate-NMDA antagonists –can produce psychotic symptoms
  • 25. Depression is due to deficiency of nor-epinephrine & serotonin Normally action of released NE & serotonin is terminated by active reuptake into the nerve terminal from the synapse via specific transporters. TCAs block the amine transporters (uptake pumps) for nor- epinephrine (NET) & serotonin (SERT) in brain. Facilitation of NE & serotonin transmission ---- improves symptoms of depression .
  • 26. Memory (ChEI in Alzheimers disease) Basal forebrain to cortex/hippocampus (A) Extrapyramidal motor responses (benztropine for Parkinsonian symptoms) Striatum (B) Vestibular control (scopolamine patch for motion sickness)
  • 27. Nigrostriatal pathway extrapyramidal motor responses Interneurons throughout the brain inhibit excitability, stabilize membrane potential, prevent repetitive firing Metabotropic GABA B receptors These receptors are GPCRS Largely presynaptic, inhibit transmitter release Most important role is in the spinal cord Baclofen, an agonist at this receptor, is a muscle relaxant
  • 28. There are two GABA binding sites per receptor. Benzodiazepines and the newer hypnotic drugs bind to allosteric sites on the receptor to potentiate GABA mediated channel opening. Babiturates act at a distinct allosteric site to also potentiate GABA inhibition. These drugs act as CNS depressants Picrotoxin blocks the GABA-gated chloride channel
  • 29.  GABA –Gamma Amino Butyric Acid is a major inhibitory neurotransmitter in CNS  Benzodiazepines potentiate GABA ergic inhibition at all levels of neuroxis—spinal cord, hypothalamus, hippocampus, substantia nigra, cerebellar cortex and cerebral cortex  Pentameric structure 5 subunits  Macromolecular complex of ion channel
  • 30.
  • 31. Loss of GABA-ergic transmission contributes to excessive excitability and impulse spread in epilepsy. Picrotoxin and bicuculline ( GABA receptor blocker) inhibit GABAA receptor function and are convulsants. BDZs and barbiturates increase GABAA receptor function and are anticonvulsants. Drugs that block GABA reuptake (GAT) and metabolism ( GABA-T) to increase available GABA are anticonvulsants
  • 32. Major role is in the spinal cord Glycine receptor is an ionotropic chloride channel analagous to the GABAA receptor. Strychnine, a competitive antagonist of glycine, removes spinal inhibition to skeletal muscle and induces a violent motor response.
  • 33. Neurotransmitter at 75-80% of CNS synapses Synthesized within the brain from Glucose (via KREBS cycle/α-ketoglutarate) Glutamine (from glial cells) Actions terminated by uptake through excitatory amino acid transporters (EAATs) in neurons and astrocytes
  • 34. Blocked at resting membrane potential (coincidence detector) Requires glycine binding Permeable to Ca++ as well as Na NMDA receptors involvement in disease - seizure disorders - learning and memory - neuronal cell death
  • 35. NMDA receptor as a coincidence detector : requirement for membrane depolarization
  • 36. 36 NMDA receptor is Ca++ permeable
  • 37. It is the GluR2 subunit that makes most AMPA receptors Ca++ impermeable The GluR2 subunit contains one amino acid substitution : arginine (R) versus glutamine (Q) in all other GluRs
  • 38. Transmitter Anatomy Receptor Subtypes and Preferred Agonists Receptor Antagonists Mechanisms Acetylcholine Cell bodies at all levels; long and short connections Muscarinic (M1): muscarine Pirenzepine, atropine Excitatory: in K+ conductance; IP3, DAG Muscarinic (M2): muscarine, bethanechol Atropine, methoctramine Inhibitory: K+ conductance; cAMP Motoneuron-Renshaw cell synapse Nicotinic: nicotine Dihydro-- erythroidine, - bungarotoxin Excitatory: cation conductance Dopamine Cell bodies at all levels; short, medium, and long connections D1 Phenothiazines Inhibitory (?): cAMP D2: bromocriptine Phenothiazines, butyrophenones Inhibitory (presynaptic): Ca2+; Inhibitory (postsynaptic): in K+ conductance, cAMP GABA Supraspinal and spinal interneurons involved in pre- and postsynaptic inhibition GABAA: muscimol Bicuculline, picrotoxin Inhibitory: Cl–conductance GABAB: baclofen 2-OH saclofen Inhibitory (presynaptic): Ca2+ conductance; Inhibitory (postsynaptic): K+ conductance
  • 39. Transmitter Anatomy Receptor Subtypes and Preferred Agonists Receptor Antagonists Mechanisms Glutamate Relay neurons at all levels and some interneurons N-Methyl-D-aspartate (NMDA): NMDA 2-Amino-5- phosphonovalerate, dizocilpine Excitatory: cation conductance, particularly Ca2+ AMPA: AMPA CNQX Excitatory: cation conductance Kainate: kainic acid, domoic acid Metabotropic: ACPD, quisqualate MCPG Inhibitory (presynaptic): Ca2+ conductance cAMP; Excitatory: K+ conductance, IP3, DAG Glycine Spinal interneurons and some brain stem interneurons Taurine, -alanine Strychnine Inhibitory: Cl–conductance 5- Hydroxytryptam ine (serotonin) Cell bodies in midbrain and pons project to all levels 5-HT1A: LSD Metergoline, spiperone Inhibitory: K+ conductance, cAMP 5-HT2A: LSD Ketanserin Excitatory: K+ conductance, IP3, DAG 5-HT3: 2-methyl-5-HT Ondansetron Excitatory: cation conductance
  • 40. Transmitter Anatomy Receptor Subtypes and Preferred Agonists Receptor Antagonists Mechanisms Norepinephrin e Cell bodies in pons and brain stem project to all levels 1: phenylephrine Prazosin Excitatory: K+ conductance, IP3, DAG 2: clonidine Yohimbine Inhibitory (presynaptic): Ca2+ conductance; Inhibitory: K+ conductance, cAMP 1: isoproterenol, dobutamine Atenolol, practolol Excitatory: K+ conductance, cAMP 2: Salbutamol Butoxamine Inhibitory: may involve in electrogenic sodium pump; cAMP Histamine Cells in ventral posterior hypothalamus H1: 2(m-fluorophenyl)- histamine Mepyramine Excitatory: K+ conductance, IP3, DAG H2: dimaprit Ranitidine Excitatory: K+ conductance, cAMP H3: R--methyl-histamine Thioperamide Inhibitory autoreceptors
  • 41. Transmitter Anatomy Receptor Subtypes and Preferred Agonists Receptor Antagonists Mechanisms Opioid peptides Cell bodies at all levels; long and short connections Mu: bendorphin Naloxone Inhibitory (presynaptic): Ca2+ conductance, cAMP Delta: enkephalin Naloxone Inhibitory (postsynaptic): K+ conductance, cAMP Kappa: dynorphin Naloxone Tachykinins Primary sensory neurons, cell bodies at all levels; long and short connections NK1: Substance P methylester, aprepitant Aprepitant Excitatory: K+ conductance, IP3, DAG NK2 NK3 Endocannabinoids Widely distributed CB1: Anandamide, 2- arachidonyglycerol Rimonabant Inhibitory (presynaptic): Ca2+ conductance, cAMP