Neurotransmitters and Neurochemistry – Flashcards
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            What are the criteria needed to be a NT?
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        1. Present in presynaptic axon terminals 2. Synthesized by enzymes in neuron 3. Released in significant quantities when AP reaches terminal 4. Specific receptors on postsynaptic neuron recognize the substance 5. Postsynaptic cell can be changed by experimental application of substance 6. Blocking release of substance prevents synaptic activity from affecting postsynaptic cell
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            Amines
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        Acetylcholine, norepinephrine, epinephrine, dopamine, serotonin, melatonin
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            Dopaminergic Pathways (amine)
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        (dopamine) Mesostriatal: motor control, affected by Parkinson's Disease  Mesolimbic: reward reinforcement, addiction, affected by schizophrenia
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            Cholinergic Pathways (amine)
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        (acetylcholine) learning and memory, affected by Alzheimer's disease nicotinic receptors --> muscle contraction
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            Serotonergic Pathways (amine)
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        (serotonin) Sleep states, mood, sexual behavior, anxiety 5-HT receptors --> nausea
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            Noradrenergic Pathways (amine)
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        (norepinephrine) mood, arousal, sexual behavior
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            Amino Acids
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        GABA, glutamate, glycine, histamine
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            GABA
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        inhibitory NT
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            Glutamate
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        excitatory NT, most abundant
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            Neuropeptides
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        opioid peptides, oxytocin, substance P, hypothalamic releasing hormones, etc. feeding, social/sexual behavior
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            Substance P
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        pain sensation
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            Soluble Gases
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        nitric oxide, carbon monoxide learning/memory, erection, hair growth
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            Pharmacological and Recreational Drugs
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        1. Can be targeted to specific receptor subtypes 2. Diffuse widely (do not seek out receptor molecules) 3. Binding usually temporary
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            Competitive Ligands
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        agonists, antagonists, inverse agonists same binding site
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            Agonists
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        mimics effect of NT exogenous  helpful for people who don't have enough NT
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            Antagonists
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        bind and do not allow the NTs to flow through exogenous prevents normal action (binds and doesn't activate)
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            Inverse Agonist
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        has the reverse effect of the NT exogenous
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            Noncompetitive Ligands
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        activate receptor or prevent receptor from activation by NT neuromodulator
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            Affinity
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        it will stay attached to the receptor site
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            Efficacy
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        it will activate for longer (less drug needed to bind to a receptor)
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            How can the different stages of Neural conduction be affected?
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        presynaptic events and postsynaptic events
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            Presynaptic Events
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        transmitter production, transmitter release, transmitter clearance
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            Transmitter Production
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        1. Block NT synthesis of enzymes 2. Block axonal transport 3. Interfere with storage of NT in vesicles
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            Transmitter Release
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        1. Block Na+ channels (no Na coming through no AP) 2. Block Ca channels (need so vesicles can fuse and release NT) 3. Block release of specific NTs 4. Affect autoreceptor signals (release more or less)
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            Transmitter Clearance
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        1. Block transporter proteins (prevents reuptake) 2. Inhibit degradation (leave more NT in the synapse)
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            Postsynaptic Events
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        transmitter receptors, cellular processes
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            Transmitter Receptors
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        1. Block receptors (antagonists) 2. Activate receptors (agonists)
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            Cellular Processes
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        1. Activation of second messengers or genes 2. Production of proteins 3. Down-regulation/up-regulation of receptor density
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            Down-Regulation
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        decreases the number of receptors available  less opportunity for NT to bind --> more drug to make more NT to increase likelihood that the NT will bind
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            Up-Regulation
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        increases the number of receptors available more opportunity for NT to bind --> if not enough NT present, you make more receptors to increase the likelihood that the NTs can bind (generally a good thing)
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            Nicotine
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        receptors located in the ventral tegmentum and nucleus acumbens  release dopamine nicotine has high affinity and efficacy for dopamine direct agonist
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            Meth
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        affects dopamine transporters (reuptake) mimics dopamine --> taken back up into the transporter --> enters vesicles --> reverse transporters --> makes more dopamine in the synapse --> more dopamine affects postsynaptic neuron makes so much dopamine that you can't make anymore for awhile after that
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            THC
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        cannabinoid receptors int he substantia nigra, hippocampus, cerebellar cortex anandamide is the endogenous NT --> causes GABA to come out --> inhibits next NT from coming out --> which then keeps releasing dopamine disinhibition agonist high dose --> impaired creativity low dose --> doesn't affect creativity