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Stahl's Essential Psychopharmacology Online
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Stahl's Essential Psychopharmacology

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  • AAADC (aromatic amino acid decarboxylase), ,
  • AAB-001,
  • “able stabilizers”, ,
  • ABT089,
  • abuse,
  • acamprosate,
  • actions, in ventral tegmental area (VTA),
  • for alcohol dependency,
  • in combos for bipolar disorder,
  • icon,
  • ACC-001,
  • acetyl coenzyme A (AcCoA), as acetylcholine precursor,
  • acetylcholine (ACh), ,
  • in arousal pathways, ,
  • and arousal spectrum, ,
  • and blocked dopamine receptors,
  • overactivity,
  • production, ,
  • projections, ,
  • via basal forebrain,
  • psychotropic drugs and, , , ,
  • reciprocal relationship with dopamine,
  • and reward, ,
  • termination of action,
  • for treating nicotine dependence,
  • vesicular transporter for,
  • acetylcholine-linked mechanisms,
  • acetylcholine neurotransmitter,
  • as psychotropic drug target, ,
  • acetylcholine receptors, TCA and,
  • acetylcholine transporters, ,
  • acetylcholinesterase (AChE), , , ,
  • donepezil to inhibit,
  • galantamine to inhibit,
  • rivastigmine to inhibit,
  • ACh. See acetylcholine (ACh)
  • ACP 103,
  • ACP-104, ,
  • ACR16,
  • ACTH (adrenocorticotropic hormone), ,
  • actin, ,
  • action potential, , ,
  • control over firing,
  • encoding of,
  • ionic components of,
  • activity-dependent nociception,
  • acute pain,
  • neuropathic pain,
  • activity-dependent spine formation, by estradiol,
  • acute pain, , ,
  • vs. chronic,
  • acute stress reaction,
  • Adapin. See doxepin (Sinequan, Adapin)
  • adaptive states,
  • adatanserin,
  • addiction, , . See also substance abuse
  • nicotine and, ,
  • overvalued reward in,
  • adenosine, ,
  • adenylate cyclase, binding to G protein,
  • ADHD. See attention deficit hyperactivity disorder (ADHD)
  • adhesion molecules,
  • and neuronal migration,
  • adipose tissue, insulin resistance in, ,
  • adolescence
  • aggressiveness in,
  • antidepressants for,
  • brain restructuring in, , ,
  • mania in,
  • removal of synaptic connections, ,
  • risperidone for treating psychotic disorders,
  • adrenocorticotropic hormone (ACTH), ,
  • affective blunting,
  • affective disorders, . See also mood disorders
  • stress-induced, novel treatments,
  • affective flattening, as SSRI side effect,
  • affective spectrum disorders, ,
  • norepinephrine and,
  • pain in,
  • “affective storms”, in children,
  • affective symptoms
  • dorsal vs. ventral regulation,
  • mesolimbic dopamine pathway role in,
  • multiple disorders impacting,
  • pharmacy, ,
  • in schizophrenia, shared with other disorders,
  • afferent neurons, peripheral, neuropathic pain and,
  • age. See also adolescence children elderly
  • synapse formation by,
  • aggressive symptom pharmacy, ,
  • aggressiveness, ,
  • in dementia patients,
  • multiple disorders impacting,
  • in schizophrenic patients,
  • Agilect/Azilect (rasaligine),
  • for Parkinson’s disease,
  • aging. See also elderly
  • erectile dysfunction and,
  • hippocampus sensitivity to, ,
  • normal,
  • and synapse loss,
  • agitation,
  • benzodiazepines for,
  • in dementia patients,
  • agnosia,
  • agomelatine (Valdoxan), , ,
  • icon,
  • agonists
  • absence of, ,
  • actions on ion channel,
  • antagonist acting in presence of,
  • and G protein-linked receptor, ,
  • impact on ligand-gated ion channels,
  • spectrum,
  • and receptor conformation,
  • agoraphobia, in children,
  • agranulocytosis, clozapine and,
  • akathisia
  • from aripiprazole,
  • nigrostrial pathway dopamine deficiencies and,
  • from paroxetine withdrawal,
  • from SSRIs,
  • alanine-serine-cysteine transporter (ASC-T), glial,
  • alcohol
  • actions
  • on reward circuits,
  • in ventral tegmental area (VTA),
  • consumption, vs. sleepiness,
  • dependency/abuse
  • by ADHD patients,
  • social anxiety and,
  • treatment, ,
  • GABA-A receptor binding to,
  • heavy drinking
  • vs. reduced-risk,
  • will power to reduce,
  • icon,
  • probability of dependence,
  • reduced-risk drinking,
  • and reward,
  • alcoholics, smoking by,
  • aldehyde dehydrogenase,
  • alertness,
  • loss
  • bupropion for,
  • as SSRI side effect,
  • allodynia, , , ,
  • allosteric modulation, , ,
  • alogia, ,
  • alpha 1 adrenergic receptors
  • atypical antipsychotic agents and,
  • and sedation,
  • TCA and, ,
  • alpha 1 antagonist, for posttraumatic stress disorder,
  • alpha-1 receptor, antagonism,
  • alpha 1 selective hypnotics,
  • alpha-1 unit, ,
  • alpha-2 adrenergic receptors, atypical antipsychotic agents and,
  • alpha 2 antagonists,
  • icon,
  • and norepinephrine,
  • and serotonin,
  • as serotonin norepinephrine disinhibitors, ,
  • alpha 2 delta ligands, ,
  • for anxiety disorders,
  • binding of,
  • for chronic pain,
  • in dorsal horn,
  • for fibromyalgia,
  • and pain gate,
  • potential therapeutic effects,
  • alpha-2 delta protein,
  • gabapentin and pregabalin binding to,
  • alpha-2 delta unit,
  • alpha 2 receptors
  • on axon terminal,
  • blockade of,
  • somatodendritic, ,
  • alpha 2A agonists,
  • mechanism of action,
  • alpha-4 beta-2 nicotinic acetylcholine receptor,
  • alpha 4 beta 2 nicotinic receptors, ,
  • reinforcement and,
  • alpha-7-nicotinic cholinergic agonists,
  • alpha 7 nicotinic cholinergic receptors,
  • alpha amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, ,
  • synapses with,
  • alpha APP,
  • alpha heliz,
  • alpha-L-glutamyl transferace,
  • alpha pore
  • of voltage-sensitive calcium channels,
  • of voltage-sensitive sodium channels,
  • anticonvulsant binding,
  • alpha secretase,
  • alpha subunit, ,
  • alprazolam (Xanax),
  • and CYP 450 3A4,
  • and sedation,
  • alprostadil,
  • ALS (amyotrophic lateral sclerosis)
  • excitotoxicity and,
  • riluzole for,
  • Alzheimer’s disease, ,
  • amyloid cascade hypothesis,
  • Aβ42 oligomer interference with synaptic function, ,
  • Aβ42 production,
  • inflammation from plaque formation,
  • neuronal dysfunction and loss,
  • tangle formation,
  • amyloid plaques in,
  • Apo-E protein and, ,
  • cholinergic deficiency,
  • cholinesterase inhibitors
  • best responders, ,
  • donepezil, ,
  • galantamine,
  • palliative responders,
  • rivastigmine, ,
  • tacrine,
  • treatment outcomes,
  • usual responders,
  • clinical features,
  • cognitive symptoms,
  • excitotoxicity and, , ,
  • expected exponential increase,
  • familial cases early onset,
  • folate for depression,
  • glutamate hypothesis of cognitive deficiency, ,
  • identifying at presymptomatic/prodromal stage,
  • neurofibrillary tangles in,
  • problems with studies of,
  • symptom pattern onset,
  • symptomatic treatments in development,
  • symptoms shared with schizophrenia, , ,
  • treatment, ,
  • untreated time course,
  • amantadine,
  • for bipolar disorder,
  • icon,
  • mechanism of action
  • on GABA, glutamate, sigma, and dopamine,
  • VSSCs, synaptic vesicles, and carbonic anhydrase,
  • possible actions in bipolar disorder,
  • putative clinical actions,
  • amenorrhea, ,
  • American College of Rheumatology, criteria for fibromyalgia,
  • American Psychiatric Association,
  • amibegron,
  • amines,
  • d-amino acid oxidase (DAO),
  • amino acid transporters,
  • inhibitory,
  • amino acids,
  • to close VSSC,
  • for ligand-gated ion channels,
  • regulation of calcium channels,
  • in voltage-gated ion channels,
  • amisulpride, ,
  • and cardiometabolic risk,
  • clinical actions of,
  • and diabetes,
  • for negative symptoms in schizophrenia,
  • pharmacological icon,
  • and QTc prolongation,
  • amitriptyline (Elavil, Endep, Tryptizol, Loroxyl), , ,
  • amnesia,
  • amotivational syndrome,
  • amoxapine (Asendin), ,
  • AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole-priopionic acid) glutamate receptors, ,
  • glutamate at,
  • and synaptogenesis,
  • AMPA-kines,
  • amphetamines, , , ,
  • action
  • in ADHD,
  • MAO inhibitors with,
  • and dopamine displacement,
  • and dopamine release,
  • dopamine transporter (DAT) and, , ,
  • icon,
  • with MAOIs, and hypertension,
  • pharmacological actions,
  • VMAT transport fo,
  • for wakefulness, ,
  • amygdala,
  • activation,
  • by VMPFC,
  • and anxiety/fear,
  • and avoidance,
  • beta-3 receptors in,
  • connection with locus coeruleus,
  • and depressed mood,
  • and emotional learning,
  • and fear neurobiology,
  • and fearful faces,
  • impact on suicidal ideation,
  • information processing
  • and depressed mood,
  • serotonin and,
  • manic episode symptoms linked to,
  • noradrenergic receptor simulation in,
  • overactive circuits,
  • regulating anxiety in,
  • response to emotional input,
  • and schizophrenia symptoms,
  • serotonin and fear processing by,
  • amylin,
  • amyloid, and glutamate steady leak,
  • amyloid cascade hypothesis for Alzheimer’s disease, ,
  • neuronal dysfunction and loss,
  • amyloid plaques,
  • in Alzheimer’s disease,
  • and glutamate excitotoxicity,
  • and glutamate release,
  • treatment development to act on,
  • amyloid precursor protein (APP),
  • processing into Aβ peptides
  • processing into soluble peptides,
  • amyotrophic lateral sclerosis (ALS)
  • excitotoxicity and,
  • riluzole for,
  • Anafranil. See clomipramine (Anafranil)
  • analgesics,
  • probability of dependence,
  • anandamide, , ,
  • anatomic G protein-linked receptors,
  • anatomically addressed nervous system,
  • neurodevelopment in,
  • “angel dust”,
  • anhedonia, ,
  • anorexia, fluoxetine for,
  • antagonists, ,
  • acting alone,
  • acting in presence of inverse agonist,
  • acting in presence of partial agonist,
  • action in presence of agonists,
  • vs. inverse agonist,
  • inverse agonist action reversed by,
  • for ligand-gated ion channels,
  • vs. partial agonists,
  • presynaptic,
  • anterior cingulate cortex (ACC), ,
  • anterograde motor,
  • localization of,
  • anterograde transport,
  • fast,
  • antiaptotic receptors (TrkA),
  • anticholinergic agents
  • D2 antagonism and,
  • side effects,
  • anticholinergic effects, from diphenhydramine (Benadryl),
  • anticonvulsants, ,
  • carbamazepine (Equetro),
  • as mood stabilizers,
  • gabapentin,
  • lamotrigine, ,
  • levetiracetam,
  • oxcarbazepine/eslicarbazepine,
  • pregabalin,
  • riluzole,
  • topiramate,
  • zonisamide,
  • sodium channels as action site,
  • valproic acid, . See also specific agents
  • antidepressant “poop out”,
  • antidepressants. See also heroic combos serotonin norepinephrine reuptake inhibitors (SNRIs)
  • allosteric site for binding,
  • bipolar depression response to,
  • brain MAO-A inhibition for efficacy,
  • in clinical practice,
  • cost-based algorithm, ,
  • evidence-based algorithm,
  • evidence-based selections,
  • reduced positive affect vs. increased negative affect,
  • selection process,
  • symptom-based algorithm,
  • symptom-based selection, ,
  • clinical trials,
  • combinations for major depressive disorder,
  • combinations for unipolar depression,
  • continuation,
  • CYP450 2D6 impact on plasma levels,
  • delay in relief from depression,
  • in development,
  • targeting neurokinins,
  • targeting novel sites of action,
  • effectiveness in clinical practice,
  • enhancement of serotonin and/or norepinephrine,
  • general principles, ,
  • impact on mixed states of depression and mania,
  • increase in monoamines,
  • interaction with MAOIs,
  • interference with slow-wave sleep,
  • “intramolecular polypharmacy” of,
  • manic or hypmanic episode on,
  • L-5-methyltetrahydrofolate (MTHF) and,
  • monoamine oxidase inhibitors (MAOIs), ,
  • monoamine transporters as targets,
  • and neurogenesis in hippocampus,
  • norepinephrine and dopamine reuptake inhibitors (NDRIs), , , . See also norepinephrine dopamine reuptake inhibitors (NDRIs)
  • over life cycle, ,
  • pharmacokinetics,
  • prior responses to, and bipolar diagnosis,
  • putative mechanisms,
  • response rates,
  • risks of use or avoidance during pregnancy,
  • risks to fetus,
  • role in bipolar disorder,
  • serotonin norepinephrine reuptake inhibitors (SNRIs), . See also serotonin norepinephrine reuptake inhibitors (SNRIs)
  • sites on transporter for,
  • suicidality in adolescent females,
  • symptoms persisting after treatment with,
  • time course of effects,
  • trimonoaminergic modulators (TMMs) and,
  • triple-action combo,
  • two mechanisms vs. one, ,
  • antihistamines,
  • sedation by,
  • side effects of,
  • antipsychotic agents
  • as antidepressants,
  • atypical,
  • administration frequency,
  • cardiometabolic risk and,
  • cardiometabolic risk management,
  • hit-and-run receptor binding properties,
  • hypothetical action over time,
  • to improve schizophrenia symptoms,
  • pharmacological properties,
  • and prolactin,
  • properties, ,
  • and weight gain risk,
  • avoiding sedation and enhancing long-term outcome,
  • benzodiazepines to lead in or top off,
  • best practices for monitoring and managing,
  • cardiometabolic risk and, ,
  • combining two,
  • conventional,
  • vs. atypical,
  • D2 binding of,
  • D2-receptor antagonist,
  • hypothetical action over time,
  • muscarinic cholinergic blocking properties, ,
  • pharmacological properties, ,
  • and prolactin,
  • risk and benefits of long-term,
  • in use,
  • as D2 dopamine receptor blockers,
  • first-generation,
  • high doses,
  • links between binding properties and clinical actions,
  • low-potency, and dissociation,
  • “off-label” uses,
  • patient toleration of,
  • pharmacokinetics, ,
  • pharmacological properties, ,
  • prescribing information,
  • prophylactic,
  • receptor interactions for,
  • sedation as short-term tool,
  • side effects and compliance,
  • switching, ,
  • process to avoid,
  • from sedating to nonsedating,
  • antisocial personality disorder,
  • anxiety
  • 5HT1A partial agonist actions in,
  • amygdala and,
  • GABA and, ,
  • gabapentin for,
  • linking symptoms to circuits,
  • memories and,
  • noradrenergic hyperactivity in, ,
  • blocking,
  • pregabalin for,
  • reduced,
  • serotonin, stress and, ,
  • anxiety disorders
  • 5HT1A receptors and,
  • alpha 2 delta ligands for,
  • amygdala and fear neurobiology,
  • brain component regulating,
  • in children,
  • comorbid with fibromyalgia,
  • CSTC loops and worry neurobiology,
  • diabolical learning hypothesis and,
  • drug treatment action at ionotrophic receptors,
  • fear conditioning, vs. fear extinction, ,
  • fear extinction,
  • fluvoxamine for,
  • GABA-A allosteric modulatory sites, hypothetical shift in set point,
  • GABA and, , ,
  • generalized anxiety disorder (GAD),
  • pharmacy,
  • treatment,
  • inability to extinguish maladaptive fear responses,
  • linking symptoms to circuits,
  • MAO inhibitors for,
  • NET inhibition and,
  • noradrenergic hyperactivity in,
  • blocking,
  • obsessive compulsive disorder,
  • pharmacy,
  • treatment,
  • overlap with depression,
  • pain linked to, ,
  • painful somatic symptoms in,
  • panic disorder,
  • pharmacy,
  • treatment,
  • paroxetine for patients with,
  • phenotype,
  • posttraumatic stress disorder,
  • pharmacy,
  • treatment,
  • preemptive or prophylactic treatments,
  • with beta blockers,
  • prevalence of,
  • quetiapine for,
  • serotonin for regulating in amygdala,
  • serotonin projections regulation of, ,
  • social anxiety disorder,
  • pharmacy,
  • treatment,
  • stress progression to, treatment,
  • symptom dimensions, ,
  • symptom overlap in subtypes,
  • symptom overlap with depression,
  • treating insomnia in,
  • venlafaxine for,
  • anxiolytics
  • benzodiazepines as,
  • GABA,
  • probability of dependence,
  • anxious misery,
  • anxious mood,
  • anxious self-punishment,
  • apathetic recovery, ,
  • apathetic temperament,
  • apathy,
  • circuits,
  • in depression,
  • aphasia,
  • apical dendrites, ,
  • in pyramidal cell,
  • apnea, obstructive sleep,
  • symptoms shared with other disorders,
  • Apo-E protein, and Alzheimer’s disease, ,
  • apoptosis, ,
  • from gene expression,
  • and necrosis,
  • programmed into genome,
  • APP. See amyloid precursor protein (APP)
  • appetite
  • changes in,
  • circuits,
  • histamine-1 with 5HT2C antagonism,
  • reduced,
  • appetite suppressants, interaction with MAOIs,
  • apprehensive expectations,
  • apraxia,
  • arborization, of neurons,
  • arcuate nucleus,
  • aripiprazole, , ,
  • actions as mood stabilizer,
  • and cardiometabolic risk,
  • in combos for bipolar disorder, , ,
  • as CYP 2D6 substrate, ,
  • and diabetes,
  • dosage with carbamazepine,
  • pharmacological actions,
  • pharmacological icon,
  • raising levels of,
  • and sedation, ,
  • switching from sedating agent to,
  • testing for cocaine abuse treatment,
  • and weight gain risk,
  • armodafinil (Nuvigil), for wakefulness,
  • aromatic amino acid decarboxylase (AAADC), ,
  • arousal
  • deficient daytime,
  • desensitization in prefrontal cortext,
  • and dopamine,
  • excessive, and ADHD, ,
  • mechanisms,
  • norepinephrine projections regulation of,
  • simultaneous deficient and excessive, in ADHD,
  • spectrum of cognitive dysfunction in ADHD
  • ADHD treatment,
  • deficit arousal,
  • excessive arousal,
  • arousal combos,
  • arousal spectrum, ,
  • ascending reticular activating system,
  • asenapine,
  • Asendin (amoxapine), ,
  • asociality, ,
  • Asperger’s syndrome,
  • assaultiveness,
  • astrocytes, and Alzheimer’s disease,
  • atherosclerosis, from repetitive autonomic responses,
  • atomoxetine, , , ,
  • for ADHD, ,
  • mechanism of action,
  • with stress and comorbidity,
  • CYP450 2D6 impact on plasma levels,
  • for fibromyalgia,
  • for weight loss,
  • atorvastatin
  • and CYP 450 3A4,
  • risk of muscle damage,
  • ATPase,
  • attention
  • in ADHD patients,
  • CSTC loop to regulate,
  • impaired, in schizophrenia,
  • provoking circuits for,
  • attention deficit hyperactivity disorder (ADHD), , , ,
  • adults with,
  • vs. children, ,
  • prevalence of,
  • treatment, ,
  • arousal spectrum of cognitive dysfunction
  • ADHD treatment,
  • deficit arousal,
  • excessive arousal,
  • atomoxetine for, ,
  • mechanism of action,
  • brain restructuring and,
  • causes,
  • and comorbidity, priority for treatment,
  • deficit arousal and,
  • desensitizing arousal in prefrontal cortext,
  • dopamine signals in prefrontal cortext,
  • how not to treat,
  • impact of development,
  • from improper neuronal migration,
  • information processing,
  • mania vs, ,
  • noradrenergic treatment, ,
  • atomoxetine,
  • norepinephrine signals in prefrontal cortext,
  • pharmacy,
  • selective attention circuit,
  • simultaneous deficient and excessive arousal,
  • stimulants for, , ,
  • mechanism of action,
  • stress
  • comorbidities and arousal levels,
  • and comorbidity,
  • sustained attention circuit,
  • symptoms and circuits, ,
  • DSM-IV,
  • matching,
  • symptoms shared with schizophrenia,
  • timing of onset,
  • tuning cortical pyramidal neurons,
  • attention deficit, vs. attention deficit disorder,
  • attitudes, hostile,
  • atypical antipsychotic agents,
  • for ADHD, with stimulants,
  • administration frequency,
  • in bipolar depression,
  • pharmacological actions,
  • cardiometabolic risk and,
  • cardiometabolic risk management,
  • clozapine as,
  • vs. conventional,
  • hit-and-run receptor binding properties,
  • hypothetical action over time,
  • for mania, actions,
  • for mania and bipolar depression, mechanism of action,
  • as mood stabilizers,
  • for nonpsychotic mania symptoms,
  • properties, ,
  • and weight gain risk,
  • auditory association cortex,
  • auditory hallucinations,
  • Aurorix. See moclobemide (Aurorix, Manerix)
  • autism, ,
  • cognitive symptoms,
  • irritability in children with,
  • risperidone for irritability,
  • autonomic nervous system,
  • autoreceptors,
  • autosomal dominant pattern, classic,
  • AV965,
  • Aventyl. See nortriptyline (Pamelor, Endep, Aventyl)
  • avoidance,
  • avolution, ,
  • “awakening”, ,
  • axoaxonic synapses, , , ,
  • axodendritic synapses, ,
  • Axokine,
  • axon hillock, ,
  • of pyramidal neuron,
  • axon terminals. See also presynaptic axon terminals
  • alpha 2 receptors on,
  • axonal growth cone, ,
  • docking,
  • axons, , ,
  • in basket neurons,
  • in double bouquet cells,
  • growth of,
  • in mature brain,
  • myelination of fibers,
  • neurotrophins control of growth,
  • in pyramidal cell,
  • for transport function,
  • axosomatic synapses, ,
  • Azilect. See rasaligine (Agilect/Azilect)
  • Azilect/Agilect (rasaligine),
  • for Parkinson’s disease,

 
 

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