Psych455 Neurochemistry

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neurochemistry
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focuses on the basic chemical composition and processes of the nervous system
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neuropharmacology
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the study of compounds that selectively affect the nervous system
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Frog Heart Experiment
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Otto Loewi (1921), role of the vagus nerve and the neurotransmitter acetylcholine (Ach) in slowing heart rate
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Acetylcholine
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first neurotransmitter discovered in the PNS and CNS activates skeletal muscles in the somatic nervous system and may excite or inhibit internal organs in the autonomic nervous system
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Epinephrine (EP/Adrenaline)
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chemical messenger that acts as a hormone to mobilize the body for fight or flight during times of stress and as a neurotransmitter in the central nervous system
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Norepinephrine (NE/Noradrenaline)
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neurotransmitter found in the brain and in the parasympathetic division of the autonomic nervous system
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Ligands
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fit receptors exactly and activate or block them Endogenous ligands and Exogenous ligands
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Endogenous Ligands
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neurotransmitters (chemical released by a neuron onto a target with an excitatory or inhibitory effect) and hormones – outside the CNS, many of these chemicals circulate in the blood stream as hormones
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Exogenous ligands
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drugs and toxins from outside the body
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Electron Microscope
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1950s: invention of electron microscopy allowed view of synaptic structure for the first time – projects a beam of electrons through a very thin slice of tissue – varying structure of the tissue scatters the beam onto a reflective surface where it leaves an image, or shadow, of the tissue – much better resolution than the light microscope
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Synaptic Vesicle
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organelle consisting of a membrane structure that encloses a quantum of neurotransmitter
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Quantum
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quantity, equivalent to the contents of a single synaptic vesicle, that produces a just observable change in postsynaptic electric potential
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Synaptic Cleft
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gap that separates the presynaptic membrane from the postsynaptic membrane
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Chemical Synapse
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Junction where messenger molecules are released when stimulated by an action potential
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Presynaptic Membrane
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membrane on the transmitter, output side of a synapse
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Postsynaptic Membrane
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membrane on the transmitter, input side of a synapse
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Storage Granule
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membranous compartment that holds several vesicles containing a neurotransmitter
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Chemical Synapses
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majority in mammals are chemical, some are electrical – allow for more flexibility to neuron to neuron communication (inhibitory and excitatory) than electrical
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Electrical Synapse (Gap Junction)
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fused presynaptic and postsynaptic membrane that allows action potential to pass directly from one neuron to the next – faster than chemical
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Neurotransmission in 4 Steps
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1. Synthesized and stored in the axon terminal 2. Transported to the presynaptic membrane and released in response to an action potential 3. Able to activate the receptors on the target- cell membrane located on the postsynaptic membrane 4. Inactivated, or it will continue to work indefinitely
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Step 1: Synthesis and Storage
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neurotransmitters derived in two general ways: 1) synthesized in the axon terminal: building blocks from food are pumped into cell via transporters (protein molecules embedded within the cell membrane) 2) synthesized in the cell body: according to instructions contained in DNA, transported on microtubules to axon terminal
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Step 2: Neurotransmitter Release
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at the terminal, action potential opens voltage-sensitive calcium channels – Ca enters terminal and binds to the protein calmodulin forming a complex – complex causes some vesicles to empty their contents into the synapse (exocytosis) and others to get ready to empty their contents
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Exocytosis
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mediated by specialized proteins – SNAREs serve as tethers
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SNAREs
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v-SNAREs: attach to vesicles t-SNAREs: attach to the presynaptic membrane
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Synaptotagmin
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protein attached to the vesicle, activated by Ca, triggering the fusion of the vesicle with the presynaptic membrane, thus releasing neurotransmitter
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Step 3: Receptor-Site Activation
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after being released, the neurotransmitter diffuses across the synapse and activates receptors on the postsynaptic membrane – transmitter-activated receptors: protein embedded in the membrane of a cell that has a binding sit for a specific neurotransmitter -neurotransmitter may 1) depolarize the postsynaptic membrane, causes excitatory action on the presynaptic neuron 2) hyper polarize the postsynaptic membrane, causing inhibitory action on the postsynaptic neuron 3) initiate other chemical reactions that modulate either the excitatory or inhibitory effect/ influence other functions of the receiving neuron
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Autoreceptors
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“self receptor” on the presynaptic membrane that responds to the transmitter that the neuron releases
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Inotropic Receptor
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embedded membrane protein with two parts 1) a binding sit for a neurotransmitter 2) a pore that regulates ion flow to directly and rapidly change membrane voltage – ligand-gated ion channels
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Metabotropic Receptor
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embedded membrane protein with a binding site for a neurotransmitter but no pore – liked to a G protein that can affect other receptors or act with second messengers to affect other cellular processes – G-protein coupled receptor
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G Protein
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belongs to a family of guanyl-nucleootide binding proteins coupled to metabotropic receptors that when activated, bind to other proteins
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second messenger
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chemical that carries a message to initiate a biochemical process activated by a neurotransmitter (first messenger) ex: alter ion flow in a membrane channel, formation of new ion channels, production of new proteins
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Up-regulation/Down-regulation
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number of receptors in cells can vary (daily in adulthood, during development, with drug use) up: increase in the number of receptors down: decrease in the number of receptors
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autoreceptors
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some neurotransmitter molecules do not cross the cleft, bind to auto receptors that inform the presynaptic cell about the net concentration of neurotransmitter in the cleft
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Step 4: Deactivation of the Neurotransmitter
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accomplished 4 ways 1) diffusion away from synaptic cleft 2) degradation by enzymes in the synaptic cleft 3) reuptake into the presynaptic neuron for subsequent reuse 4) taken up by neighboring glial cells – not mutually exclusive, a given neurotransmitter can be deactivated in multiple ways
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Type I Synapses: Excitatory
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typically located on dendrites, round vesicles, dense material on membranes, wide cleft, large active zone
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Type II Synapses: Inhibitory
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typically located on cell body, flat vesicles, sparse material on membrane, narrow cleft, small activation zone
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varieties of neurotransmitters
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more than 50 kinds identified some inhibitory at one location, and excitatory at another more than 1 neurotransmitter may be active at a single synapse no simple one to one relationship between 1 neurotransmitter and 1 behavior
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Criteria for identifying neurotransmitters
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1. The chemical must be synthesized in the neuron or otherwise be present in it 2. When the neuron is active, the chemical must be released and produce a response in a target 3. The same response must be obtained when the chemical is experimentally placed on the target 4. A mechanism must exist for removing the chemical from its site of action after its work is done
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Classes of Neurotransmitters
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1. Amino acid transmitters 2. Amine transmitters 3. Peptide transmitter 4. Transmitter gases 1 and 2 small-molecule transmitters
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Small-molecule transmitters
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class of quick acting neurotransmitters synthesized from dietary nutrients and packaged read for use in axon terminals ex) acetylcholine (ACh) Amines: Dopamine (DA), Norepinephrine (NE), Epinephrine (EP), Serotonin (5-HT) Amino Acids: Glutamate (Glu), GABA, Glycine, histamine
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Acetylcholine Synthesis
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Choline, Acetate enzymes: acetyl coenzyme A, ChAT break down of acetylcholine: AChE
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Sequential Synthesis of Three Amines
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Catecholamines (Dopamine, Noradrenaline, Adrenaline)
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Rate-Limiting Factor
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tyrosine hydroxylase restricts the rate at which all he catecholamines can be synthesized
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Serotonin
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L-Tryptohan (tryptohan hydroxylase) 5-HTP degraded by Monoamine oxidase (MAO)
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Amino Acid Transmitters
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Glutamate: main excitatory transmitter GABA: main inhibitory transmitter
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Glutamate
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cannot pass blood-brain barrier, synthesized within the cell using glutamine released by glial cells glial cells take up released glutamate and transform to glutamine
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GABA
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synthesized in brain from glutamate receptors divided into classes: GABAa: inoptropic, producing fast inhibitory effects GABAb: metabotropic, slow inhibitory effects GABAc: ionotropic with a chloride channel
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Neuropeptide
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multifunctional chain of amino acids that act as a neurotransmitter synthesized from mRNA on instructions from the cell’s DNA do not bind to ion channels, do not have direct effects on the protein coupled receptors ex) opioids, neurohypophyseals, secretins, insulins, gastrins, somatostatins, corticosteroids
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Transmitter Gases
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synthezied in cell, as needed easily crosses cell membrane support metabolic processes ex) nitric oxide (NO) vasodilation, Carbon Monoxide (CO)
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Activating System
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pathway that coordinates activity through a single neurotransmitter
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Somatic Nervous System and Cholinergic Neurons
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neuron that uses acetylcholine (ACh) as its main neurotransmitter excites skeletal muscles to cause contractions – nicotinic ACh receptor: ionotropic receptor (responsive to nicotine)
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Autonomic Nervous System and Cholinergic Neurons
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cholinergic neurons from the CNS control both divisions (sympathetic and parasympathetic) Both NE and ACh have excitatory and inhibitory effects on some organs, depending on the receptors present
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5 Activating Systems in Central Nervous System
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1) Cholinergic 2) Dopaminergic (x2) 3) Noradrenergic 4) Serotonergic
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Cholinergic System
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ACh produced in nuclei in midbrain and basal forebrain Nicotinic ACh Receptor: inotropic receptor, responsive to nicotine Muscarinic ACh Receptor: metabotropic receptor, responsive to muscarine – involved in attention and member – maintaining neuronal excitability: helps maintain waking electroencephalographic pattern
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Cholinergic System: Alzheimer’s Disease
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degenerative brain disorder that first appears as progressive memory loss and later develops into generalized dementia – linked to decreased ACh synthesis – treatment: acetylcholinesterase inhibitors: increase amount of ACh remaining in synapse
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Dopaminergic System
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two pathways: mesostriatal: originates in substantia nigra, projects to stratym (caudate, putamen), maintaining normal motor behavior mesolimbocortical: originates in ventral tegmentum, projects to nucleus accumbens, basal forebrain, frontal cortex, reward motivation, addiction
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Dopaminergic System: Diseases with Nigrostriatal
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Parkinson’s Disease a degenerative disorder characterized by motor symptoms such as rigidity, slowness of movement, tremor, and abnormal gait loss of DA producing neurons in substantial nigra treatment with L-dopa
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Dopaminergic System: Diseases with Mesolimbic
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Increased DA: Schizophrenia behavioral disorder characterized by delusions, hallucinations, disorganized speech, blunted emotion, agitation or immobility and a host of other symptoms positive symptoms (hallucinations) linked to over activation of DA2 receptors schizophrenia-like psychosis can be induced by drugs that increase DA (cocaine, amphetamines) Decreased DA: ADHD treatment with DA stimulants (ritalin) reduces hyperactivity
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Noradgrenergic System
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originates in locus, coeruleus, projects throughout cortex (particularly to limbic system: amygdala, hippocampus, cingulate gyrus)
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Noradrenergic System: Diseases
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Decreased NE: Major Depression mood disorder characterized by prolonged feelings of worthlessness and guilt, the disruption of normal eating habits, sleep disturbances, a general slowing of behavior, and frequent thoughts of suicide Increased NE: Mania elevated mood, arousal, basically the opposite of depression – some anti-depressants that affect multiple transmitter systems (NE, DA, 5-HT) can trigger manic episodes in individuals with undiagnosed bipolar disorder
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Serotonergic System
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originate in raphe nuclei, project throughout the brain maintaining wakefulness learning
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Serotonergic System: Diseases
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Increase 5-HT: OCD behavioral disorder characterized by compulsively repeated acts (hand washing) and repetitive, often unpleasant thoughts (obsessions) Decreased 5-HT: Depression – abnormalities in brainstem 5-HT neurons linked to sleep apnea and SIDS
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Psychopharmacology
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study of how drugs affect the nervous system and behavior
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drugs
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chemical compounds administer to produce a desired change in the body
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Psychoactive Drug
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substance that acts to alter mood, thought, or behavior used to manage neuropsychological illness
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Routes of Drug Administration
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oral administration is safest/easiest/most common/most complex (more barriers that drug must cross to have desired effect) other methods: inhalation or injection: faster results fewer barriers if drug is injected directly into brain
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Blood Brain Barrier
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body presents a number of barriers to the internal movements of drugs: cell membranes, capillary walls, placenta BBB prevents most substances (drugs) from entering the brain via the bloodstream
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Endothelial cells
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in brain capillaries, surrounded by the end feet of astrocytes attached to the capillary wall, covering about 80% of it glial cells provide a rout for the exchange of food and waster between capillaries and the brain’s extracellular fluid and from there to other cells in capillaries: tightly joined, easy for substances to move into and out of the bloodstream in brain: tightly joined and the presence of astrocytes help keep most substances out
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Routes of Drug Administration: Size of Molecules
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small/uncharged molecules: fat soluble, can freely cross the BBB large/charged molecules: actively transported across BBB – hard to develop drugs that follow these properties, 98% of all drugs that may affect brain function cannot cross the blood-brain barrier
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Barrier-free brain sites
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pineal gland: entry of chemicals that affect day night cycles pituitary gland: entry of chemicals that influence pituitary hormones area postrema: entry of toxic substances that induce vomitting
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How the Body Eliminates Drugs
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drugs are broken down in the kidneys, liver (catabolizing drugs so they are more easily excreted from the body), and intenstines – excreted in urine, feces, sweat, breast milk, and exhaled air – some substances that cannot be removed may build-up in the body and become toxic
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Drug Action at Synapses
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most drugs exert their effects by influencing chemical reactions at synapses
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Agonist
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Substance that enhances the effectiveness of a neurotransmitter
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Antagonist
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Substance that blocks/decreases the effectiveness of a neurotransmitter
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Seven Major Stages of Synaptic Transmission
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where drugs can alter chemical processes: 1. Synthesis: of neurotransmitter in cell body, axon, or terminal 2. Storage: of neurotransmitter in granules or vesicles 3. Release: of transmitter from presynaptic terminal 4. Receptor interaction: in postsynaptic membrane 5. Inactivation: of excess neurotransmitter at the synapse 6. Reuptake: into the presynaptic terminal 7. Degradation: of excess neurotransmitter
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Ligands can be…
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1. Agonists: mimic effects of another transmitter 2. Antagonists: bind receptor without activating it 3. Inverse agonists: bind to receptor and initiates opposite effect of usual transmitter 4. Competitive ligands: bind tot he same part of receptor molecule as endogenous ligands 5. Noncompetitive ligands (neuromodulators): bind to modulatory sites that are not part of the receptor complex that normally binds the transmitter
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Binding affinity
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degree of chemical attraction between a ligand and a receptor – a drug with a high affinity for its receptor will be effective at very low doses – neurotransmitters are low-affinity ligands, allowing them to rapidly dissociate from receptors
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Efficacy (intrinsic activity)
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ability of a bound ligand to activate the receptor – agonists: high efficacy – antagonists: low efficacy partial agonists: produce a medium response regardless of dose
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Dose-response curve (DRC)
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graph of the relationship between drug doses and the effects – tool to understand Pharmacodynamics – dose at which the drug shows half of its maximal effect is termed the effective dose 50% (ED50) – potency of two drugs can be compared by their ED50 values: comparable effects at lower doses more potent
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Pharmacodynamics
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the functional relationship between drugs and their targets
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Principles of Psychopharmacology
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-efficacy can be compared by evaluation maximal responses – a drug of only moderate efficacy is termed a partial agonist (or antagonist) – DRCs can be non monotonic: indicating the point at which the drug is starting to have effects at lower-affinity receptors
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Therapeutic Index
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separation between the effective dose and a toxic one – toxic dose: TD50, 50% of animals show symptoms of toxicity – lethal dose: LD50, 50% of animals die – wider therapeutic index= safer
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Tolerance
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decrease in response to a drug with the passage of time – larger dose is required to maintain the drug’s initial effect
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metabolic tolerance
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– organ systems become more effective at eliminating the drug – increase in number of enzymes used to break down substance
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functional tolerance
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-target tissue show altered sensitivity to the drug – activities of the brain cells adjust to minimize effects of the substance
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down-regulate vs. up-regulate
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changes in numbers of receptors can alter sensitivity in the direction opposite to the drug’s effects – down-regulate: response to agonist drug- fewer receptors available – up-regulate: in response to an antagonist
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Blood Alcohol
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12-20 days of alcohol consumption, blood alcohol and the signs of intoxication do not correspond to each other
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cross- tolerance
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response to a novel drug is reduced because of tolerance developed in response to a related drug – suggests that the two drugs affect a common nervous system target
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withdrawal symptoms
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may be caused by drug tolerance
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sensitization
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occurs when drug effects become stronger with repeated treatment
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Classification of Psychoactive Drugs
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1. Anti anxiety Agents and Sedative Hypnotics 2. Antipsychotic Agents 3. Antidepressants and mood stabilizers 4. Opioid Analgesics 5. Psychotropics
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Group 1: Anti anxiety agents and sedative hypnotics
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anxiolytics (tranquilizers) depressants: reduce nervous system activity – excitation of GABAa Receptor, hyper polarizes the neuron – 2 sides of GABAa receptor: sedative-hypnotic side (alcohol and barbiturates) and anti anxiety side (benzodiazepines)
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Group 1: Benzodiazepines
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minor tranquilizers, anti anxiety agents often used for temporary purposes (coping with stress due to a death in the family)
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Group 1: Barbiturates
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produces sedation and sleep can also produce general anesthesia, coma, and death mostly replaced by benzodiazepines
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Group 1: Sedative Hypnotics
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dissociative anesthetics group of sedative-hypnotics developed as anesthetics produce altered states and hallucinations ex) GHB, flunitrazepam, ketamine, ‘date rape’ drugs
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Group 1: Alcohol
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similar neurochemical effects as barbiturates – activates GABAa receptors and increases inhibitory effects – contributes to social disinhibition and – stimulates dopamine pathways, causing euphoric effects – chronic use: liver damage and vitamin B1 deficiency
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Group 2: Antipsychotic Agents
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psychosis: applied to behavioral disorders such as schizophrenia – have improved functioning of schizophrenia patients and reduced number housed in institutions
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Group 2: 1st Generational, Chlorpromazine and haloperidol
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major tranquilizer (neuroleptic) blocks the D2 dopamine receptor reduces positive symptoms of schizo (delusions and hallucinations) produce symptoms reminiscent of Parkinson’s disease – immediate effect of reducing motor activity – after short use, reduction in symptoms of schizo – negative side effect: Dyskinesia (impaired control of movement)
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Group 2: Dopamine Hypothesis of Schizo
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proposal that schizo symptoms are due to excess activity of the neurotransmitter dopamine – antipsychotic drugs block D2 receptors – amphetamine promotes release of dopamine and can also produce symptoms similar to schizo
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Group 2: 2nd Generation, Clozapine
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weakly block D2 receptors but also block serotonin 5-HT2 receptors – reduce negative symptoms (such as social withdrawal and blunted emotional responses) of schizo – affect motivation and reduce agitation but may result in weight gain
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Group 2: Phencyclidine (PCP) and Ketamine (Special K)
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produce schizo like symptoms (hallucinations and out of body experiences) – exert par of their action by blocking glutamate receptors, suggesting the involvement of excitatory glutamate synapses in schizo
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Group 3: Antidepressants
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– Major Depression: mood disorder characterized by prolonged feelings or worthlessness and guilt, disruption of normal eating habits, sleep disturbances, general slowing of behavior, frequent thoughts of suicide
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Group 3: Classes of Antidepressants
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1. Monoamine Oxidase (MAO) Inhibitors – block the enzyme MAO from degrading neurotransmitters such as dopamine, noradrenaline, and serotonin 2. Tricyclic Antidepressants – first-generation antidepressants with a chemical structure characterized by three rings that block serotonin reuptake transporter proteins 3. Second-Generation Antidepressants – action is similar to 1st gen, more selective inits action on the serotonin reuptake transporter proteins (atypical antidepressants) – Selective Serotonin Reuptake Inhibitors (SSRIs) – block the reuptake of serotonin into the presynaptic terminal
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Group 3: Prozac (SSRI)
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antidepressants affect synapses quickly, anti depressive actions take weeks to develop – Prozac enhances neurogenesis in hippocampus
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Group 3: Mood Stabilizers
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used to treat bipolar disorder – mites the intensity of one pole of the disorder, thus making the other pole less likely to recur
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Group 4: Opioid Analgesics
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Opioid: compound that binds to a group of brain receptors, sensitive to morphine 2 natural sources: – opium: used for thousands of years to produce euphoria, analgesia, sleep, and relief from diarrhea and coughing – brain: peptides in the body that have opioid-like effects are collectively called endorphins (endogenous morphines)
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Group 4: Where Endorphins are found
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in brain and spinal cord – natural (morphine) and synthetic (heroin, oxymorphone, methadone, oxycodone, fentanyl) opioids mimic endorphins – prescribed for clinical use in pain management – potently addictive, abuse of prescription opioids more common
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Group 4: Endorphins
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peptide hormone that acts as a neurotransmitter and may be associated with feelings of pain or pleasure 3 classes: endomorphins, enkephalins (meaning in the head) and dynorphins
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Group 4: Opioid Analgesic/ Opiates
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opioid analgesic: drug with sleep-inducing (narcotic) and pain-relieving (analgesic) properties opiates: derived from opium (extract of the seeds of the opium poppy) – codeine also derived from plant, used in cough medicine
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Group 4: Morphine/ Heroin
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most closely mimics the endomorphins and binds most selectively to the mu receptors synthetic opioid: heroin, opiate drug synthesized from morphine, more fat soluble and penetrates the BBB faster than morphine, therefore it produces very rapid pain relief
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Group 4: Synthetic Opioids
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prescribed for clinical use in pain management hydromorphone, levorphanol, oxymorphone, methadone, meperidine, oxycodone, fentanyl – competitive inhibitors can be used to treat opioid addiction after the person has recovered from withdrawal symptoms (Nalorphine, Naloxone)
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Group 4: Opioid Ingestion
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wide-ranging physiological changes: relaxation, sleep, euphoria, constipation, respiratory depression, decreased blood pressure, pupil constriction, hypothermia
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Group 5: Psychotropics
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behavioral stimulants affect motor activity and mood psychedelic and hallucinogenic stimulants affect perception and produce hallucinations general stimulants mainly affect moods
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Group 5: Behavioral Stimulants
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increase motor behavior and elevate a person’s mood and level of alternates – rapid administration of behavioral stimulants is most likely to be associated with addiction
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Group 5: Cocaine
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obtained from leaves of coca plant – blocks dopamine reuptake – powder snorted/injected – derivates such as novocaine are used as local anesthetics: reduce cell;s permeability to Na thereby reducing nerve conduction
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Group 5: Amphetamine
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dopamine agonist: blocks dopamine reuptake transporter, leaving more dopamine available in the synaptic cleft, stimulates release of dopamine from presynaptic membrane – both mechanisms increase the amount of dopamine to stimulate dopamine receptors – uses: initially asthma treatment, study aid, improvement of alternates and productivity, weight-loss aid
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Group 5: methamphetamine (amphetamine derivative)
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relatively inexpensive, potentially devastating – neurotoxic, causes brain damage with prolonged use, damages both DA and 5HT neurons
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Group 5: General Stimulants
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drugs that cause a general increase in the metabolic activity of cells -caffeine: inhibits enzyme that normally breaks down the second messenger cyclic AMP, increase in cAMP, increase in glucose, makes more energy, higher rates of cellular activity – blocks effect of adenosine (endogenous neuromodulator that normally inhibits catecholamine release)
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Group 5: Psychedelics
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alter sensory perception and cognitive processes, can produce hallucinations 5 types: Acetylcholine (atropine, nicotine), Norepinephrine (mescaline), Serotonin (LSD, psilocybin, ecstacy), Anandamide (THC), Glutamate (PCP, Ketamine)
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Group 5: Psychedelics, Hallucinogens
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alter sensory perception and price peculiar experiences – LSD (acid), mescaline (peyote), psilocybin (shrooms) visual effects – diverse neural actions, including those on the noradrenergic (mescaline) serotnergic (mescaline, psilocybin and LSD), Ach (muscarine), and opiate (salvia) systems Clinical uses: OCD, anxiety, depression, PTSD
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Group 5: Psychedelics, Acetylcholine Psychedelics
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block (atropine) or facilitate (nicotine) transmission at ACh synapses
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Group 5: Nicotine (from tobacco)
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increases heart rate, blood pressure, hydrochloric acid secretion, and bowel activity – acts as an agonist on nicotinic ACh receptors in the body and brain – rewarding effects are mediated by receptors in the body and brain – nicotine in one cigarette can occupy 88% of the brains nicotinic receptors
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Group 5: Norepinephrine psychedelics
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mescaline produces pronounced psychi alterations, including a sense of spatial boundlessness and visual hallucinations
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Group 5: Serotonin psychedelics
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LSD and psilocybin stimulate some serotonin receptors – ecstasy elevates serotonin concentrations by blocking reuptake and stimulating release – chronic use can cause depression, memory disturbances and alters the structure and function of serotonergic neurons
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Group 5: Anandamide psychedelics (Marijuana)
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endocannabinoid: alters memory formation, stimulates appetite, reduces pain sensitivity, protects from excitotoxic brain damage, lowers blood pressure, combats nausea, lowers eye pressure from glaucoma
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Group 5: Endocannabinoids
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homologs of marijuana produced in the brain: act as retrograde messengers and may influence neurotransmitter release from the presynaptic neuron
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Group 5: Marijuana and THC
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derived from Cannabis sativa (THC): relaxation, mood alteration, stimulation, hallucination, paranoia – two kinds of receptors (both metabotropic) 1 Cb1 receptor: CNS, mediates rewarding properties of cannaboids, concentrated in substantial nigra, hippocampus, cerebellar cortex, cerebral cortex 2 CB2 receptor: prominent in the immune system
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Group 5: Glutamate psychedelics
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PCP and Special K can produce hallucinations and out-of-body experiences Exert part of their action by blocking glutamate NMDA receptors involved in learning
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Drugs and Brain Damage
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many substances can be neurotoxins – glutamate-like substances kill neurons (Ca+ into cell gives a suicide gene to kill cell), high doses can cause neuronal death
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Drugs associated with brain damage
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Amphetamines (ecstasy, meth) Cocaine (blocks cerebral blood flow) PCP (blocks NMDA receptors)
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Alcohol and Damage
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chronic use associated with damage to the thalamus and limbic system – not directly caused by alcohol, it interferes with absorption of B1 vitamin in intestines, plays a vital role in maintaining cell membrane
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Drugs not associated with long-lasting brain damage
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LSD, Opiates, Marijuana – marijuana contains 400 chemicals, cannot determine whether a psychotic attack is related to THC or another chemical
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Substance Abuse
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use of a drug for the psychological and behavioral changes that it produces aside from its therapeutic effects
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Addiction (substance dependence)
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desire for a drug manifested by frequent use of the drug, leading to the development of physical dependence in addition to abuse – often associated with tolerance and unpleasant, sometimes dangerous, withdrawal symptoms upon cessation of drug use – complex interaction of neurobiological, psychological, social and environmental factors
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Physical Dependence
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tolerance, withdrawal
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Withdrawal Symptoms
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physical and psychological behaviors displayed by an addict when drug use ends ex) muscles aches and cramps, anxiety attacks, sweating, nausea, convulsions, death time- course: withdrawal symptoms from alcohol and morphine start within several hours of last dose and intensify over several days before subsiding
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Psychomotor Activation
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increased behavioral and cognitive activity at certain levels of consumption, the drug user feels energetic and in control occurs with many drugs
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Important role of Dopamine in Drug Abuse
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abused drugs are agonists, cause the release of dopamine or prolong its availability in the synapse dopamine antagonists (block the effect of dopamine) not abused substances
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Addiction and Dependence
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addictive drugs can influence gene regulation addictive drugs can selectively turn off genes related to voluntary control and turn on genes related to behaviors susceptible to addiction changes are relatively permanent and can be passed along, perhaps through the next few generations
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Why everyone does not abuse drugs
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most people who use drugs recreationally never become addicted – genetics: no gene related to alcoholism, any satisfactory explanation of drug abuse will require genetic/ learning components – personality: unusual risk taking may be trait common to drug abusers – neurobiological, psychological, social and environmental factors involved

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