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Exam 5 - Lecture 5

Common Amino Acid Neurotransmitters Glutamate, Aspartate, and Glycine
Common Amino Acid Derivative Neurotransmitters GABA (from Glutamate), Serotonin (from Tryptophan), Histamine (from Histidine), Epinephrine (from Tyrosine), Norepinephrine (from Tyrosine), and Dopamine (from Tyrosine)
Neuroendocrine Cells Chromaffin Cells, EnteroChromaffin Cells (EC), EnteroChromaffin-Like Cells (ECL), Platelets, and Mast Cells, Basophils
What do Chromaffin Cells Release? Epinephrine and Norepinephrine from the Adrenal Medulla
What do EnteroChromaffin Cells Release? Serotonin from the Intestines
What do EnteroChromaffin-Like Cells Release? Histamine from the Stomach
What do Platelets Release? Serotonin
What do Mast Cells/Basophils Release? Histamine
Which two NTs essentially do most of the work in the CNS? Glutamate and GABA (the rest mostly act as neuromodulators)
Neurotransmitter Gestalt Dopamine → Histamine → ACh → Norephinephrine → Serotonin [Motivation → Anticipation → Acquisition → Escape → Cessation]
Dopamine is Which Action? Motivation
Histamine is Which Action? Anticipation
ACh is Which Action? Acquisition
Norephinephrine is Which Action? Escape
Serotonin is Which Action? Cessation
Dopamine Pathways: Mesocortical Pathway, Nigrostriatal Pathway, Tuberoinfundibular Pathway (as hormone)
Mesocortical Pathway is associated with: Attention, Memory, Motivation (desire or fear)
Nigrostriatal Pathway is associated with: Inhibitive control on posture and movement
Tuberoinfundibular Pathway is associated with: Decrease prolactin from anterior pituitary
Decreased activity of the Mesocortical Dopamine Pathway results in: ADD, Social anxiety (Negative Schizophrenia), and Depression of wanting (hunger libido)
Increased activity of the Mesocortical Dopamine Pathway results in: Hyperfocus/Hyperactivity Disorder (HD), Psychosis (Positive Schizophrenia), Mania of wanting (hunger, libido, shopping)
Decreased activity of Nigrostriatal Dopamine Pathway results in Restless Legs Syndrome, Parkinson’s Disease
Decreased activity of Tuberoinfundibular Dopamine Pathway results in Excess Prolactin → decreased Estrogen → Osteoporosis and infertility
Dopamine probably comes from where? Adrenal Medulla (Dopamine → Norepinephrine → Epinephrine)
Low does of IV administered Dopamine causes: [normal health?] Increased renal perfusion, diuresis (increases amount of liquid that goes through kidneys and increases urine output)
High doses of IV administered Dopamine causes: [acute stress?] Increased HR and SV → Increased BP, Systemic vasoconstriction → Increase BP, Renal vasoconstriction → Antidiuresis
When you are stressed, you may have increased Dopamine production in order to make more ________, but the Dopamine may get into circulation and cause unwanted effects Epinephrine
Amphetamine Mechanism Reverses transporters (BOTH transporters from synapse into neuron and those from neuron to vesicles) for Dopamine and Norepinephrine
Reversing Dopamine and Norepinephrine transporters causes: Efflux of Dopamine/NE from neuronal vesicles; Efflux into synapses via reuptake transporters; Increases Dopamine/NE levels in brain
Cocaine Mechanism Inhibits transporters for Dopamine and Norepinephrine
Inhibiting Dopamine and Norepinephrine transporters causes: Inhibition of reuptake transporter; increases Dopamine/NE levels in brain
Buproprion (Wellbutrin, Zyban) Mechanism Inhibits transporters for Dopamine only
Inhibiting Dopamine transporters causes: Inhibition of reuptake transporters; increases Dopamine levels in brain
Which drugs cause increased levels of Dopamine in the brain? Amphetamines, Cocaine, and Buproprion
Why is Buproprion less addictive than Cocaine? Buproprion is more specific to Dopamine and does not increase NE as much as Cocaine does. Neurons may also compensate against Buproprion by making more reuptake transporters, which is doesn’t do for Cocaine
Two Families of Dopamine Receptors D1-Like and D2-Like
D1-Like Dopamine Receptors Excitatory (D1, D5)
D2-Like Dopamine Receptors Inhibitory (D2, D3, D4)
D1-Like Agonism is responsible for: Movement, Wanting, Mood (excitatory)
D2-Like Autoreceptor Agonism is responsible for: Negative feedback control
D2-Like Heteroreceptor Agonism is responsible for: Inhibiting Prolactin release, allowing antagonistic muscle control
D2-Like Heteroreceptor Antagonism is responsible for: Increased Prolactin secretion, decreased motor control
Zyprexa (Olanzapine) works on which Dopamine receptors? Works on D2-Like Heteroreceptor as an Antagonist (inhibits Serotonin receptors also)
Peripheral Involvement of Histamine 1. Hyper-defense 2. Eating 3. Arousal
Histamine’s Role in Hyper-defense Histamine is released by WBCs in connective tissue; it causes WBC recruitment, itching, inflammation
Histamine’s Role in Eating Histamine is released by EnteroChromaffin-Like Cells (ECL Cells) in stomach; it causes the release of stomach acid
Histamine’s Role in Arousal Histamine causes vessel dilation in penis and causes erection
Types of Histamine Receptors: H1 (Excitatory), H2 (Excitatory), H3 (Inhibitory), H4
H1 Agonism results in: Wakefulness, Vessel dilation/permeability (to WBCs), Itching, Bronchoconstriction
H1 CNS Antagonism results in: Unsure, but possibly reduce neuronal excitation in cortex (Antihistamines are H1 Antagonists)
H1 Antagonists (in order of increasing drowsiness) Claritin (Loratadine), Zyrtec (Cetirizine), Benadryl (Diphenhydramine), Phenergan (Promethazine)
Ability of H1 Antagonists to enter the CNS is directly related to the amount of _________ it causes Sedation
Phenergan (Promethazine) H1 Antagonist; also antagonist to muscarinic M5 receptors: anti-emetic and anti-motion sickness
H2 Agonism results in: Release of HCl from parietal cells in stomach; erection
H2 PNS Antagonism results in: Decrease in release of HCl from stomach cells; possibly decreases ability to have erection?
H2 Antagonists Tagamet (Cimetidine), Zantac (Ranitidine)
H3 (Autoreceptor) Agonism results in: Inhibition of the release of Histamine (autoregulation)
H4 Agonism results in: Increased WBC chemotaxis (more WBCs move toward the Histamine)
Two Types of ACh Receptors in Brain Nicotinic (Excitatory) and Muscarinic (mostly Excitatory)
CNS Nicotinic Agonism results in: Behavioural arousal (stimulates Dopamine release; ex. cigarette addiction)
CNS Muscarinic Agonism results in: Short term memory formation (involved during “rest and digest” time)
Peripheral Involvement of ACh Nicotinic receptors have direct control of skeletal muscle movement & adrenal medulla secretions, and indirect control of ACh to Muscarinic receptors & NE/E to adrenergic recptors
Norephinephrine involvement in brain results in: Increased wakefulness, alertness (Decreased NE) and Learning, memory, attention (Decreased NE)
Decreased Norepinephrine in the brain affects wakefulness/alertness to cause: Lethargy, Narcolepsy, Depression
Decreased Norepinephrine in the brain affects memory/attention to cause: ADHD
Peripheral Norepinephrine is Secreted from: Adrenal Medulla
Peripheral Involvement of Norepinephrine Causes Increased: Mobilization of fuels from storage, Breathing, HR/SV/BP, Circulation to skeletal muscles, Sweating
Drugs that affect Norepinephrine transporters Amphetamies, Cocaine, Amitriptyline, Atomoxetine (Straterra)
Amitriptyline Mechanism [anti-depressant] Inhibits transporters of Norepinephrine and Serotonin
Inhibiting Norepinephrine and Serotonin Transporters causes: Inhibition of reuptake transporter; Increases NE/Serotonin levels in brain
Atomoxetine (Straterra) Mechanism [anti-ADHD] Inhibits Norephinephrine Transporters
Inhibitin Norepinephrine Transporters causes: Inhibition of reuptake transporters; Increases NE levels in brain
Types of Norepinephrine/Epinephrine Adrenergic Receptors Alpha and Beta: Alpha-1 (Excitatory), Alpha-2 (Inhibitory), Beta-1 (Excitatory), Beta-2, Beta-3
Agonism of Alpha-1 NE/E Receptor results in: Vasoconstriction (Sudafed PE [Phenylephrine] – decongestant)
Antagonism of Alpha-1 NE/E Receptor results in: Vasodilation (Minipress [Prazosin] – hypertension)
Agonism of Alpha-2 NE/E Receptor results in: Decreased NE release in brain and from adrenal gland (Catapress [clonidine] – hypertension)
Agonism of Beta-1 NE/E Receptor results in: Heart stimulation (Dobutamine – heart failure)
Antagonism of Beta-1 NE/E Receptor results in: Heart inhibition (Lopressor [Metoprolol] – hypertension)
Agonism of Beta-2 NE/E Receptor results in: Airway relaxation (Proventil [Albuterol] – asthma)
Agonism of Beta-3 NE/E Receptor results in: Lipolysis from fat cells (No drug for this receptor)
Which NE/E Receptor has no drug associated with it? Beta-3
Serotonin Release in CNS Associated with: Positive mood, Sensory input, Cessation of appetite, Cessation of arousal, Heart/Lung modulation
Two things that stimulate peripheral release of Serotonin Presence of GI irritants and Damage to blood vessels
Presence of GI Irritants Stimulates Serotonin release by EnteroChromaffin Cells in intestines which results in hyper-contraction of intestines, vomiting (dysregulation = Irritable Bowel Syndrome)
Damage to Blood Vessels Stimulates Serotonin release by Platelets which stimulates vasoconstriction (increases vascular tone) and stimulates fibroblast proliferation
Excess plasma Serotonin can result in: Fibrosis of heart valves
Reversal of Serotonin Transporters causes: Efflux of Serotonin from neuronal vesicles or circulating Platelets which increases Serotonin levels in brain and plasma (MDMA [Ecstasy] causes a positive mood; Fenfluramine causes a loss of appetite)
Inhibition of Serotonin Transporters causes: Increased levels of Serotonin in brain, but NOT in plasma (SSRIs increase Serotonin in brain – used for depression and OCD; Paxil [Paroxetine] – anti-depression)
Therapeutic Lag for SSRIs occurs because: The autoreceptors must first desensitize before the concentration of extracellular Serotonin in the synapses can become elevated enough to make a difference
Four of the Seven Families of Serotonin Receptors 5-HT1 (Inhibitory), 5-HT2 (Excitatory), 5-HT3 (Excitatory), 5-HT4 (Excitatory)
Subtypes of 5-HT1 5-HT1A and 5-HT1B/1D
Agonism of 5-HT1A causes: Decreased release of Glutamate (Buspirone) which causes less anxiety and Decreased release of Substance P which causes less pain
Effect of Buspirone on 5-HT1A Decreases release of Glutamate which reduces anxiety
Agonism of 5-HT1B/1D causes: Decreased release of Dopamine which allows Prolactin production and Vasoconstriction in CNS (Imitrex [Sumatriptan] – anti-migraines)
Subtypes of 5-HT2 5-HT2A and 5-HT2B
Agonism of 5-HT2A causes: Increased CNS excitation, Vasoconstriction of renal blood vessels, Stimulation of platelet aggregation
5-HT2A Agonists LSD, Mushrooms (hallucinogens)
5-HT2A Antagonists Zyprexa [Olanzapine] – anti-psychotic that inhibits Dopamine receptors also
Agonism of 5-HT2B causes: Increased proliferation of fibroblasts
Agonism of 5-HT3 causes: CNS – anxiety in receptors that are accessible to circulating Serotonin; PNS – stimulates vomiting via receptors on Vagus nerve in GI tract
Antagonism of 5-HT3 causes: Anti-emetic effects (stops vomiting)
5-HT3 Antagonists Zofran (Ondansetron)
Agonism of 5-HT4 causes: Stimulation of peristaltic contractions in GI tract
Created by: Cyndi1087