Psych 3313 Week 5 Class Notes
Psych 3313 Week 5 Class Notes PSYCH 3313
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This 8 page Class Notes was uploaded by Casey Kaiser on Sunday September 25, 2016. The Class Notes belongs to PSYCH 3313 at Ohio State University taught by Dr. Supe in Fall 2016. Since its upload, it has received 15 views.
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Date Created: 09/25/16
Class Notes Week 5 Psych 3313 Psychopharmacology Neurochemicals Neurotransmitters o Released at directed synapses - it will have a target to act on in the immediate vicinity Neuromodulators and neurohormones o Neuromodulators can change the way certain things react o Neurohormones typically released into the blood The neurotransmitter classifications are important Acetylcholine (ACh) Role in the peripheral nervous system o Autonomic - both pre-ganglionic, parasympathetic post-ganglionic o Somatic - neuromuscular junction, main neurotransmitter at a neuronal junction Central Nervous System o Projections from basal forebrain to hippocampus and amygdala, septal area, brainstem Behaviors o Autonomic functions, movement, learning and memory Clinical conditions o Alzheimer's disease, myasthenia gravis, schizophrenia? How do we make and break down Ach Made with the combo of choline +acetate via enzyme choline acetyltransferase - typically called ChAT There are two main subtypes of receptors for Ach Nicotinic (ionotropic) Muscarinic (metabotropic) Degradation Reuptake or broken down by enzyme (AChE) Major releasing centers - Basal forebrain, smaller area but can project to the entire forebrain o Damage here in Alzheimer's Disease o Means that there is less acetylcholine being released, severe memory loss is a symptom of this disease Cholinergic nuclei to the pons and brainstem Nicotinic Ach Receptor Binds nicotine Blocked by curare o A plant based poison, our muscles cannot respond to messages and will not contract Ionotropic receptor o Quick, short time being active Located at neuro muscular junction, autonomic nervous system, and central nervous system Excitatory, this junction will open with the presence of acetylcholine and sodium will come in, causing muscles to contract Post-synaptic Muscarinic ACh Receptor Binds muscarine Blocked by atropine o Other variations of chemicals can be used o Atropine is used in eye exams Metabotropic receptor - GPCR Response is slower and prolonged, amplified Found on Myocardial and smooth muscles, in the heart, digestive system and central nervous system Mediates inhibition and excitation in target cells - it depends on the subtype that is involved Both pre and post synaptic, more common on post synaptic Small Molecule NTs: Monoamine Neurotransmitters Catecholamine's - dopamine, norepinephrine, epinephrine Synthesized from tyrosine Indolemines - Serotonin, melatonin Synthesized from tryptophan Histamine Catecholamine's Synthesis Start with tyrosine - found abundantly in the diet (enzymatic step involving Tyrosine Hydroxylase) Enzymatic step turns it into I-dopa Step into dopamine Step into norepinephrine Stop into epinephrine Rate limiting step - Tyrosine Hydroxylase, this step determines how much of the rest we can make L-dopa as potential treatment for Parkinson's Disease - increasing overall amount of dopamine available Dopamine (DA) Role in the peripheral nervous system o Neuromodulator for other NTs Role in central nervous system o Substantia Nigra releases dopamine to the basal ganglia o Ventral tegmental area projects to the hippocampus, amygdala, nucleus accumbens, and frontal lobe Behaviors o Movement control, reinforcement, planning Clinical conditions o Parkinson's disease, schizophrenia, drug abuse Synthesis - made with tyrosine hydroxylase Receptors D1, D5 - stimulatory, metabotropic G-protein coupled receptors D2, D3, D4 - inhibitory G-protein coupled receptors Degradation Enzymes Monoamine Oxidase (MAO), catechol-O-methyl transferase (COMT), and aldehyde dehydrogenase, act in sequence to break down dopamine Projection Areas in the Brain Ventral tegmental area - reward system Substantia Nigra - motor system Norepinephrine (NE) / Noradrenaline Role in peripheral nervous system o Autonomic - sympathetic post-ganglionic synapses Signal to increase heart rate, breathing, any fight or flight changes Role in central nervous system o Widespread projection from Pons (Locus Coeruleus), medulla, hypothalamus Behaviors o Arousal and vigilance (high attention), mood Clinical conditions o Depression, mania, PTSD Synthesis o Made from dopamine Receptors o Alpha and beta Alpha - Beta - blockers, can block certain symptoms of anxiety, quickened heart-rate, shaking, etc.. Degradation o Enzymes monoamine oxidase, catechol-O-methyl transferase, and aldehyde dehydrogenase, acting in sequence to break it down o Pretty much the same as dopamine Projections Locus Coeruleus - to pretty much the entire brain o Probably release more in times of stress Epinephrine/adrenaline Relatively minor role in brain, strong neurohumoral effect Adrenergic neurons Regulation of blood pressure, eating Serotonin (5HT) Role in the PNS o Enteric - digestive motility Role in CNS o Widespread projection from Pons (raphne Nucleus) to brain and spinal cord Behaviors o Sleep-wake cycles, appetite, mood, aggression, social rank Clinical conditions o Depression, OCD, alcoholism, pretty much any mood or anxiety disorder "Serotonin is involved in everything but responsible for nothing" Synthesis o Made from tryptophan Receptors o At least 15 types and sub-types o Most are metabotropic, can be excitatory or inhibitory Degradation o Reuptake - SSRIs block reuptake o Monamine Oxidase Projections o Raphe Nuclei Histamine Synthesized from histidine Projections from basal posterior hypothalamus, Mast cells Associated with wakefulness - like how Benadryl makes someone sleepy Amino Acids Neurotransmitters GABA o Main inhibitory nt in the brain o Mood - especially anxiety o Involved in seizures Glutamate o Main excitatory nt in the brain o Long-term memory o May be associated with neurotrauma like spinal cord damage Glutamate Synthesis and Removal Made from the Kreb's Cycle Isolation of the synapse with astrocytes o Astrocytes are critical in removing glutamate Glutamate Receptors Ionotropic o AMPA - most common, excitatory opens sodium channel o Kainate - opens sodium channel o NMDA -open sodium and calcium channel Metabotropic NMDA Glutamate receptor Glutamate is not enough to open the NMDA channel The channel is both ligand gated and voltage gated Potentially excitotoxic o Opens too much, lets too much in and can lead to cell death GABA synthesis and removal Generally inhibitory It is synthesized and derived from glutamate Glutamic Acid Decarboxylase (GAD) is the enzyme that synthesizes GABA Terminated by high-affinity uptake systems in Neurons and Glia Likely involved in epilepsy and anxiety disorders o Medicated for dogs to prevent seizures for them (typically larger dogs) GABA Receptors Synthesized from glutamate GABAa - ionotropic o Open and allow chloride to come in o It has many different molecular recognition sites, many different binding sites GABAb - metabotropic o Gates the potassium channel Glycine Role in the Central Nervous System o No major direct role In the brain, more in the spinal cord o Major inhibitory NT in the spinal cord o Excitatory co-activator at NMDA glutamate Behaviors o Sleep wake cycles Toxins o Strychnine - umbrella murder ATP and Adenosine Act in the CNS and connections between autonomic neurons and the vas deferens, bladder, heart, and gut ATP is associated with pain perception and sleep-waking cycles Adenosine inhibits the release of many neurotransmitters - how caffeine works, blocks these receptors Peptides Endorphins o Reduce pain and enhance reinforcement, feelings of well-being o Associated with the "runners high" o The morphine within Substance P o Transmitter in spinal cord neurons sensitive to pain Insulin and cholecystokinin o Digestive functions o Different amounts of these will influence food response Oxytocin and vasopressin o Neuromodulators and neurohormones o Associated with childbirth and love o Have a lot to do with relationships and social interactions Gaseous Neurotransmitters Diffuse through membranes and interact with intracellular receptors They work backwards - the signal goes from post-synaptic to pre-synaptic, retroactive Nitric Oxide o Found in CNS and PNS, smooth muscle o Relaxes smooth muscle cells and blood vessels o Can cause erection Carbon monoxide o Deadly o Can make you go crazy or kill you What is a drug? Any substance that alters the body or its functions We have a communal understanding that a drug is used as medicine, recreation, enhancement, or abuse but it can be anything They can be divided into - Agonist - "acts like" o Either going to mimic or enhance effects of NT o Activate receptor o Block reuptake or degradation - more of NT is available, larger effect Antagonist - "bad guy" o Blocks or decreases the effect of the NT o Competitive or non-competitiv o Blocks receptors without activating o Decreases the availability of Nt by reducing the effect Effects of agonists Affinity - how strongly the agonists binds to the receptor o NOT MAGNETISM but you can kind of think of it this way Potency - amount of the drug needed to make a response o More potent drug has more power Efficacy - how much of this agonist is going to produce its effect o Partial agonist will be similar to a NT but has some slightly different properties, so maybe the channel Is not open as long Dose Responsive Curves Logarithmic Curves The ED50 is the effective dose for 50% of the population o When looking at medication something that only works for 50% of the people is also not working for 50% When the option to take the medication comes with a lower or higher dose, typically people want to take the lower dose A lot of drugs will not effect one receptor, typically they will bind to other receptors as well, and that is how side effects come into play Therapeutic Index Effective dose over the toxic dose o The difference between where the effective dose and the toxic dose for 50% of the population is called the margin of safety The public typically wants a larger margin of safety We start low with a dosage, see what the response is and slowly raise it until we find the effects we want. If there are no responses they must be in the 50% who do not respond to a certain drug Sites of Drug Action Every step in the life of a NT is a step that a drug can be involved Anything presynapse is typically indirect Post-synaptic receptor effects You can change the affinity or potency You can change different qualities of the receptor not just block Drug interactions at Cholinergic Synapse **** Test self with the steps; synthesis, storage, release, breakdown, and action Drug interactions at the Dopamine Synapse Drug interactions at the Serotonergic Synapse Basic Principles of Drug Effects Administration of drugs o Method of administration leads to different effects of the nervous system o Don’t forget the blood-brain barrier Most drugs are used because they are good at surpassing the BBB Individual differences o Body type, weight, sex, and genetics o People will react to drugs differently Placebo effects o User expectations influence drug effects This can result in real biochemical and physiological effects in the brain\ If people think they are ingesting something and truly believe it, it can have the same effects on them as if they had actually consumed the substance Tolerance o Decreased response to a drug with repeated use o 3 types Metabolic - breakdown processes can change Liver enzymes Functional - receptors for NT can down regulate or up regulate changing the drug response Learned - Wenger Body may be more practiced later after more use even though it is impaired in the same way Withdrawal o Occurs when the substance use is discontinued, opposite effect can be caused by discontinued drug o Your body develops a response to a drug so when it is not there it wants that drug more Addiction o Characterized by compulsive need to re-administer a drug despite the harm o There are so many aspects to addiction from many different fields
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