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Neurotransmitters PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Neurotransmitters”.

This medical PowerPoint presentation is about neurotransmitters, chemical messengers that transmit signals across synapses, the gaps between neurons. They are essential for communication within the nervous system and play a critical role in a variety of physiological and psychological processes, including mood, behavior, and cognitive function.

There are many different types of neurotransmitters, including acetylcholine, serotonin, dopamine, norepinephrine, glutamate, and gamma-aminobutyric acid (GABA), among others. Each neurotransmitter has a unique chemical structure and function, and can either excite or inhibit the activity of the neurons it interacts with.

Imbalances in neurotransmitter levels have been associated with a number of psychiatric and neurological disorders, including depression, anxiety, schizophrenia, Parkinsons disease, and Alzheimers disease. As a result, many medications used to treat these conditions work by altering neurotransmitter levels in the brain.

Tags : Neurotransmitters, synapses, neurons, cognitive function, acetylcholine, serotonin, dopamine, norepinephrine, glutamate, gamma-aminobutyric acid, Neurology, Neurology PowerPoint presentation

Published on : Jun 20, 2023 | Views : 1238 | Downloads : 7

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Slide 1-

Neurotransmitters In the 60's, people took acid to make the world weird. Now the world is weird and people take Prozac to make it normal.
Slide 2-

Processes Involved in Neurotransmission Precursors (getting the raw materials) Biosynthesis (making the NTs) Storage (vesicles - Golgi bodies) Transport (neurofilaments and microtubules) Docking Influx of Ca++ Vesicle movement Exocytosis— (fusion and release) Crossing synaptic gap Binding postsynaptic receptors Reuptake mechanisms to recover NTs Deactivation
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Categories of NTs Amino Acids Glutamate (Glu) GABA Biogenic Amines Quaternary Amines Acetylcholine (Ach) Monoamines Catecholamines Dopamine (DA) Norepinephrine (NE) Indolamines Serotonin (5-HT) Neuropeptides Opioid Peptides Enkephalins Endorphins Dynorphins Others (e.g. lipids, nucleosides)
Slide 5-

Receptors Genetically-coded proteins embedded in cell membrane Gating Ligand-gated - Stretch-gated Voltage-gated Effects Ionotropic Metabotropic Location Postsynaptic Presynaptic Heteroreceptor Autoreceptor ionotropic metabotropic
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Ionotropic Receptors Work very fast; important role in fast neurotransmission Each is made of several subunits (together form the complete receptor) At center of receptors is channel or pore to allow flow of neurotransmitter At rest - receptor channels is closed When neurotransmitter bind -- channel immediately opens When ligand leaves binding site -- channel quickly closes
Slide 7-

Metabotropic Receptors Work more slowly than ionotropic receptors Though it takes longer for postsynapic cell to respond, response is somewhat longer-lasting Comprise a single protein subunit, winding back-and-forth through cell membrane seven times (transmembrane domains) They do not possess a channel or pore
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Theory of Drug Action Emil Fischer’s ‘Lock and Key’ Hypothesis (1890) Every ‘lock’ has its own ‘key’ If the ‘key’ is not precise, the ‘lock’ does not open The ‘drug’ is the key that has to fit the target specifically and productively
Slide 10-

Theory of Drug Action Corollary of ‘Lock & Key’ Hypothesis Does not explain why some ‘keys’ open doors partially? …… e.g., partial agonists or antagonists
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Theory of Drug Action Daniel Koshland’s ‘Induced-Fit’ Hypothesis (1958) At least two steps …… step 1 is initial binding and step 2 is a change in structure of the receptor (and/or drug) Receptor is flexible! …… can wrap around the drug
Slide 12-

Common Neurotransmitters Involved in Dependence Probable functional dysregulation: Dopamine (DA) Serotonin (SER) Acetylcholine (ACh) Endorphins (END) Gamma-aminobutyric acid (GABA) Glutamate (GLU)
Slide 13-

Drugs Associated with Neurotransmitters Why do people have “drugs of choice”? • Dopamine - amphetamines, cocaine, ETOH • Serotonin - LSD, ETOH • Endorphins - opioids, ETOH • GABA - benzodiazepines, ETOH • Glutamate –ETOH • Acetylcholine - nicotine, ETOH Anandamide – Marijuana
Slide 14-

Amino Acid NTs High concentration in brain (micromolar) Circuits Cortico-cortical Sensory-motor Point-to-point communication Consistently excitatory or inhibitory Mainly ionotropic receptors but do have metabotropic receptors Fast acting, short duration (1-5 ms) Examples: Glutamate, Aspartate, GABA, Glycine
Slide 15-

GABA and Glutamate . Because they are structurally very similar, various drugs affect the presence of GLU and GABA in the synaptic gap and increase or decrease action potentials.
Slide 16-

Glutamate Principal excitatory NT Biosynthesized as byproduct of cell metabolism Removed by reuptake Elevated levels  neurotoxic 4 receptor types NMDA AMPA Kainate mGluR - Metabotropic
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NMDA Binding Sites 4 outside cell Glutamate Glycine Obligatory co-agonist Inhibitory NT at its “own” receptor Zinc (inverse agonist) Polyamine (indirect agonist) 2 inside cell Magnesium (inverse agonist) PCP (inverse agonist) “The specific subunit composition of each receptor determines its overall pharmacological properties”
Slide 18-

GABA (Gamma Aminobutyric Acid) Principal Inhibitory NT Biosynthesis: Removed by reuptake 2 receptor types GABAA GABAC (ionotropic; Cl- channel) GABAB (metabotropic; K+ channel)
Slide 19-

GABAa Binding Sites GABA Benzodiazepine (indirect agonist) Probably also site for alcohol Endogenous inverse agonist binds here Barbiturate (indirect agonist) Steroid (indirect agonist) Picrotoxin (inverse agonist) Phosphate groups attach to the receptor inside the cell and regulate receptor sensitivity (via phosphorylation) to agents such as alcohol
Slide 20-

GABAergic Drugs Ro15-4513, a GABAa antagonist (indirect for GABA, direct for alcohol) reverses alcohol intoxication Agonists (anti-anxiety) Benzodiazepines Barbiturates Ethyl alcohol (ETOH) Antagonists Picrotoxin Inverse agonist Ro 15-4513
Slide 21-

Biogenic Amines Medium concentration in brain (nanomolar) Circuits Single-source divergent projections Mainly midbrain to cortex Modulatory functions Excitatory or inhibitory as a function of receptor More metabotropic receptors than ionotropic, but plenty of both Slow acting, long duration (10-1000 ms) Examples: Acetylcholine, Epinephrine, Norepinephrine, Dopamine, Serotonin
Slide 22-

Acetylcholine Mostly excitatory effects Removal 2 receptor types Nicotinic (ionotropic) Muscarinic (metabotropic) Synthesis
Slide 23-

Major ACh Pathways Dorsolateral Pons  mid/hindbrain [REM sleep] Basal Forebrain  cortex [Learning (esp. perceptual), Attention] Medial Septum  Hippocampus [Memory]
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Monoamines Catecholamines Dopamine - DA Dopaminergic Norepinephrine - NE Noradrenergic Epinephrine - E Adrenergic ~ Indolamines Serotonin - 5-HT Serotonergic
Slide 26-

Monoamines (DA, NE, 5-HT) Modulatory (can have both excitatory and inhibitory effects- varies by receptor) Recycled by reuptake transporter Excess NT in terminal broken down by monoamine oxidase (MAOA/B) catechol-O-methyltranferase - COMT Axonal varicosities (bead-like swellings) with both targeted and diffuse release
Slide 27-

Dopamine Rewarding/motivating effects Biosynthesis: Dopamine reuptake transporter (DAT) 5 receptor types (D1–D5, all metabotropic) D1 (postsynaptic) D2 (pre autoreceptors and postsynaptic) Autoreceptors are release-regulating homeostatic mechanisms
Slide 28-

Major DA Pathways Nigrostriatral (Substantia Nigra  Striatum) [Motor movement] Mesolimbic (VTA  limbic system) [Reinforcement and Addiction] Mesocortical (VTA  prefrontal cortex) [Working memory and planning] Tuberoinfundibular tract (hypothalamus  pituitary) [neuroendocrine regulation]
Slide 29-

Norepinephrine Generally excitatory behavioral effects Biosynthesis: Many receptor types (metabotropic) 1, 1-2 (postsynaptic, excitatory) 2 (autoreceptor, inhibitory)
Slide 30-

Major NE Pathway Locus Coeruleus  throughout brain [vigilance and attentiveness]
Slide 31-

Serotonin Varying excitatory and inhibitory behavioral effects Biosynthesis: At least 14 receptor types, all metabotropic and postsynaptic except: 5-HT1A,B,D (autoreceptors) – found in CNS 5-HT3 (inhibitory, ionotropic) – found in the intestines
Slide 32-

Major 5-HT Pathways Dorsal Raphe Nuclei  cortex, striatum Medial Raphe Nuclei  cortex, hippocampus Roles in: Mood Eating Sleep and dreaming Arousal Pain Aggression
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MAOIs Iproniazid Reuptake blockers Tricyclic antidepressants Imipramine Desipramine - SSRIs Cocaine & Amphetamine ~ Indirect Monoamine Agonists
Slide 35-

Neuropeptides Low concentration in brain (picomolar) Large vesicles Co-localized with other transmitters Circuits Interneuronal Modulatory functions Mostly inhibitory Virtually all metabotropic Slow acting, long duration (10-1000 ms) Examples: Enkephalins, Endorphins, Oxytocin, Vasopressin, Opioids
Slide 36-

Opioids -endorphin made from proopiomelanocortin (POMC) produced in pituitary gland, hypothalamus, brain stem Enkephalin made from proenkephalin (PENK) produced throughout brain and spinal cord Dynorphin made from prodynorphin (PDYN) produced throughout brain and spinal cord
Slide 37-

Opioids Receptors Receptor High affinity ligands mu -endorphin, enkephalins delta enkephalins kappa dynorphins Opioids act at all opioid receptors, but with different affinities Distributed throughout brain and spinal cord, especially in limbic areas Some overlap but quite distinct localizations
Slide 38-

Opioid Receptors (cont.) Metabotropic, with either moderately fast indirect action on ion channels long-term action via changes in gene expression Most analgesic effects from mu receptor action Some analgesic effects from delta Many negative side effects from kappa
Slide 39-

Endorphins Morphine and heroin are agonists that bind to receptor sites, thereby increasing endorphin activity
Slide 40-

An Evolutionary Perspective Nesse and Berridge, 1997 An electrochemical brain Neurotransmitters have retained function for millions of years and are found in many species - from invertebrates to humans Maximization of Darwinian fitness Evolution created many chemically-mediated adaptive and self-regulatory mechanisms to control emotion and behavior Mismatch between ancient chemical mechanisms and modern environments “The problem is rooted in the fundamental design of the human nervous system”
Slide 41-

Darwinian Fitness DA and opioids are part of chemically-mediated incentive mechanisms that act as signals (motivation/reward) for a fitness benefit you “like” something (opioids) or you “want” something (dopamine) Furthermore, DA plays a role in drawing attention/highlighting significant or surprising stimuli Mechanisms for greater control? As a means to prioritize likes? for anticipatory processing? facilitates learning? These functions become susceptible to disruption and addiction from external chemical signals
Slide 42-

Mismatch Technological inventions such as the hypodermic needle, synthetic psychoactive drugs, video games, snacks etc are evolutionarily novel features that create specific ecological pressures They can be inherently pathogenic because they bypass the adaptive mechanisms and act directly on neurotransmitter systems positive emotions are signals to approach drugs that artificially induce positive emotions give a false signal of a fitness benefit under some circumstances this could be beneficial (increase empathy) negative emotions are signals to avoid drugs that block negative emotions can impair useful defenses is there utility to anxiety? jealousy? low mood and depression (decrease the tendency for behaviors that are dangerous or useless? embarrassment and guilt (regulating the individual’s hierarchical role in a group?
Slide 43-

Drug Effects External drugs hijack these evolved incentive mechanisms and most likely impair adaptation When exposed to drugs the wanting system motivates persistent pursuit of drugs that no longer give pleasure – a core feature of addiction. Drugs produce sensitization of incentive mechanisms