Drug and disorder chart
Drug and disorder chart NROSCI 0081
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This 3 page Study Guide was uploaded by Anna Perry on Monday December 7, 2015. The Study Guide belongs to NROSCI 0081 at University of Pittsburgh taught by Fanselow,Erika in Fall 2015. Since its upload, it has received 24 views. For similar materials see DRUGS AND BEHAVIOR in Neuroscience at University of Pittsburgh.
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Date Created: 12/07/15
Drug Class Drug Binds to Pharmaco Pharmacodynamics Effects Side effects Kinetics Opioid Opioid receptors Do not easily Postsynaptic inhibition: Euphoria, pain Nausea, vomiting, (Metabotropic) cross BBB receptors open K+ relief, involved pupil constriction, (except H) channels (hyperpolarize) in reward, stress respiratory Distribute evenly Axoaxonic inhibition: response, depression, blood through body receptors close Ca2+ pleasure, pressure and channels (reduce NT breathing temperature fall release) Naloxone Opioid receptors Antagonist for opioid Reverses an (antagonist) receptors opioid overdose Inhalants Many receptors Rapidly Enhancement of GABA A Comparable to Strong depressant absorbed from receptors, inhibition of alcohol, affects, coma lungs into blood, NMDA glutamate anesthesia Crosses BBB receptors, inhibition of nicotinic acetylcholine receptors GHB GABA A Absorbed into Similar to GABA, Memory Decreased HR, receptors blood through GI metabolite of GABA impairment, coma, non (agonist) tract depressed convulsive Crosses BBB respiration seizures Anxiolytic Rohypnol CNS depressant Induces sleep Can cause anterograde amnesia Barbiturates GABA reA ptor Short acting: Decrease neuron Mood changes, Mental clouding, (different highly lipid excitability, increase sedation, induce loss of judgment, binding site) soluble duration of GABA sleep slowed reflexes, A Longacting: poor receptor channel staggering, lipid solubility opening, directly opens jumbled speech, GABA Aeceptor impaired thinking Benzos GABA receptor Time to effect on Decrease neuron Reduce sense of Less magnitude of A (different onset depends on excitability, increase worry and side effects than binding site) lipid solubility number of times GABA A physical barbiturates No binding site receptor channel opens, symptoms of on respiratory increases affinity for anxiety neurons GABA Antidepressant MOIs Inhibits Can take several Monoamines that are not Therapeutic Can be dangerous monoamine weeks to reach packaged into vesicles oxidase therapeutic effect are now not metabolized – more available Tricyclic Presynaptic NT Require several Inhibit reuptake of NT Therapeutic Small margin of proteins weeks to take safety effect Second Gen Presynaptic Inhibit reuptake of NT More selective Fewer – anxiety reuptake SSRIs and sexual transporter dysfunction Mood stabilizer Lithium Don’t know Not clear Reduce mania Low therapeutic and depression index symptoms Antipsychotic Selective D2 D2 receptors Block dopamine Reduces Sedation is mild dopamine receptors and inhibit positive Motor side effects receptors dopamine release symptoms Dopamine Dopamine Partial agonist of Reduces Few system receptors dopamine receptors, positive and stabilizers activate dopamine negative receptors in areas of symptoms brain where there isn’t enough Broad spectrum Multiple types Blocks many receptors, Reduces Fewer motor side of receptors in addition to 2 negative and effects, many other cognitive serious ones symptoms Symptomatic Cholinesterase Inhibits enzyme Decrease breakdown of More Can’t reverse Treatment AD inhibitors acytlcholine acetylcholine symptoms Type Disorder Prevalence Caused by Correlated with Symptoms Treatments Theories Anxiety GAD Can run in Increased size of Activation of Drugs that families, not a amygdala sympathetic auto enhance GABA strong More neuronal NS function influence activity in amygdala (anxiolytics) Reduction in GABA Panic Disorder Physiological Panic attacks, Anxiolytics reaction to sudden intense immediate fearfulness, danger in the activation of absence of SANS danger Phobias Irrational fear Behavioral desensitization Social anxiety Extreme fear Levels of neuronal Can restrict disorder of being activity in the activities evaluated or amygdala correlate criticized with symptom severity PTSD Traumatic Family history of Nightmares, events psychopathology flashbacks, outbursts OCD Recurring, Increased neuronal Compulsions: Uncontrolled persistent, activity in basal repetitive rituals movement troublesome ganglia disorder thoughts Affective Depression More Extreme Increased levels of Feeling down, Antidepressant Monoamine women negative mood stress hormones anhedonia, hypothesis (cortisol), low levels thoughts of of serotonin suicide, loss of metabolites appetite, insomnia Bipolar Same in Mania Anxiety disorders, Same as Mood stabilizers Monoamine women and alternating addiction depression, also hypothesis men with with mania depression Psychiatric Schizophrenia Same in Reduced Less brain tissue in Positive: Antipsychotics Dopamine women and dopamine in basal ganglia and hallucinations, imbalance men mesocortical hippocampus, delusions hypothesis neurons, enlarged ventricles, Negative: increased excessive loss of reduced speech, dopamine in synapses or failure social withdraw mesolimbic to lose enough. Cognitive: neurons, Disorganized impaired working inadequate neurons, neurons in memory and levels of PFC don’t show as executive glutamate in much activity functioning PFC Neuro Parkinson’s Dopamine Resting tremor, LDOPA, degenerative neurons in difficulty in MAOIs midbrain die starting moving, Dopamine and can’t cognitive receptor supply to BG symptoms agonists, Surgical interventions Alzheimer’s Accumulation Amyloid Plaques, loss in memory Cholinesterase of Abeta, Neurofibrillary function inhibitors alteration in tangles, loss of tau proteins cholinergenic neurons Huntington’s Trinucleotide Genetics Can’t suppress Only repeat unwanted symptomatic movements, repetitive thoughts and behaviors
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