MindMap Gallery noradrenergic effect
This is a mind map about noradrenergic effects, including serotonergic effects (agonism), stimulating 5-HT 1A receptors, blocking 5-HT 2A receptors, etc.
Edited at 2024-03-12 22:22:34This is a mind map about bacteria, and its main contents include: overview, morphology, types, structure, reproduction, distribution, application, and expansion. The summary is comprehensive and meticulous, suitable as review materials.
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This is a mind map about the reproductive development of animals, and its main contents include: insects, frogs, birds, sexual reproduction, and asexual reproduction. The summary is comprehensive and meticulous, suitable as review materials.
This is a mind map about bacteria, and its main contents include: overview, morphology, types, structure, reproduction, distribution, application, and expansion. The summary is comprehensive and meticulous, suitable as review materials.
This is a mind map about plant asexual reproduction, and its main contents include: concept, spore reproduction, vegetative reproduction, tissue culture, and buds. The summary is comprehensive and meticulous, suitable as review materials.
This is a mind map about the reproductive development of animals, and its main contents include: insects, frogs, birds, sexual reproduction, and asexual reproduction. The summary is comprehensive and meticulous, suitable as review materials.
Psychotropic Drug Neurotransmitter Effects
Serotonergic effects of SSRIs
Serotonergic effects (agonism)
Selective serotonin reuptake/recycling inhibitors (SSRIs) block the 5-HT recycling transporter → increase the concentration of 5-HT in the synaptic cleft → enhance 5-HT energy → "two antibodies", "two essences" and "three gods" "Four Systems"
Two resistance
anti-anxiety
Short-term (2-3 days): 5-HT → postsynaptic membrane 5-HT 2A receptor → arousal → anxiety
In patients with anxiety disorders, the initial dose of SSRIs should be low
Long-term (2 weeks): 5-HT → postsynaptic membrane 5-HT 1A receptor → promote DA release → anti-anxiety
antidepressant
5-HT→post-synaptic membrane 5-HT 1A receptor→promotes DA release→antidepressant
Two sperm
mental retardation
5-HT → Presynaptic membrane 5-HT 2A receptor → Inhibit DA release → Mental retardation → Unable to feel the appropriate emotional response
Insomnia
5-HT→GABA presynaptic membrane 5-HT 1 receptor→Inhibit GABA release→Insomnia
5-HT→Post-synaptic membrane 5-HT 1A receptor/2A receptor→Promote NE release/arousal→Insomnia
SSRIs should be taken in the morning (except fluvoxamine) and should not be taken in the evening
three gods
Dizziness and headache
5-HT→5-HT3 receptor→constrict cerebral blood vessels→cerebral ischemia and hypoxia→dizziness and headache
Mirtazapine → 5-HT 1A receptor → anti-anxiety/anti-depressant, while blocking 5-HT3 receptor → improve dizziness and headache
extrapyramidal reaction
5-HT→Nigral-striatal pathway Presynaptic membrane 5-HT 2A receptor→Inhibition of DA release→Extrapyramidal response
Promote itching
SSRIs increase 5-HT energy and cause local or systemic itching
Four systems
gastrointestinal system
5-HT→post-synaptic membrane 5-HT 1A receptor→promotes DA release in the medulla oblongata vomiting center
feel sick and vomit
5-HT→Gastrointestinal 5-HT 3 receptor→Promote DA release
Nausea, vomiting, diarrhea
5-HT→Gastrointestinal tract 5-HT 4 receptor→Promote intestinal acetylcholine release→Increase intestinal motility
diarrhea
circulatory system
5-HT→Presynaptic membrane 5-HT 2A receptor→Inhibits DA release in the medulla oblongata cardiovascular center
Reduce heart rate, average 4-8 beats/min
reproductive system
5-HT→Presynaptic membrane 5-HT 2A receptor→Inhibits DA release in the nucleus accumbens
Inhibit sexual desire, sexual excitement, and orgasm
5-HT→Presynaptic membrane 5-HT 2A receptor→Inhibits DA release in the hypothalamic infundibular pathway→
Mild to moderate hyperprolactinemia → Suppression of androgens → Suppression of sexual function
5-HT inhibits NO synthase → inhibits NO synthesis
Inhibit penile congestion and erection
skeletal system
5-HT inhibits bone formation
Patients over 50 years old taking SSRIs have increased risk of fractures
The effect of SSRIs on increasing 5-HT energy is from strong to weak: paroxetine>escitalopram>sertraline>fluoxetine>citalopram>fluvoxamine
Agonizes 5-HT 1A receptors
Buspirone stimulates 5-HT 1A receptor → increases DA and NE energy → "two antibodies" and "two highs"
Two resistance
Buspirone→post-synaptic membrane 5-HT 1A receptor→promotes DA release in the ventromedial part of the prefrontal cortex
Anti-anxiety, anti-depression
Two highs
Improve sexual function
Buspirone → Post-synaptic membrane 5-HT 1A receptor → Promote central DA release → Promote the release of oxytocin from the posterior pituitary gland
Promote sexual arousal and ejaculation
Increase alertness
Buspirone → postsynaptic membrane 5-HT 1A receptor → NE release → stimulates α1 receptor
Increase alertness → insomnia
Blocks 5-HT 2A receptors
Atypical antipsychotics block 5-HT 2A receptors → disinhibited release of DA → "one long" and "three antibodies"
a long
QT interval prolongation
Three antibodies
Anti-negative symptoms and cognitive impairment
Atypical antipsychotics → block dorsolateral prefrontal cortex 5-HT 2A receptors → DA disinhibitory release → postsynaptic membrane D1 receptors
Anti-negative symptoms and cognitive impairment
Anti-mood disorder
Atypical antipsychotics → block ventromedial 5-HT 2A receptors in the prefrontal cortex → disinhibitory release of DA → postsynaptic membrane D1 receptors
Antidepressant, antianxiety
Anti-extrapyramidal reaction
Atypical antipsychotics → block 5-HT 2A receptors in the nigra-striatal pathway → disinhibitory release of DA → attenuate the blocking effect of antipsychotics on postsynaptic membrane D2 receptors
Anti-extrapyramidal reaction
Both blocking 5-HT 2A receptors and stimulating 5-HT 1A receptors can increase DA energy, and their three-antibody effects are similar.
Blocks 5-HT 3 receptors
Vortioxetine blocks 5-HT 3 receptors→strongly inhibits GABA interneurons→disinhibitory excitability of NE neurons→"two antibodies" and "two lows"
Two resistance
antidepressant
Vortioxetine → blocks 5-HT 3 receptors → NE neuron deinhibition → NE release
antidepressant
Anti-cognitive impairment
Vortioxetine → blocks 5-HT 3 receptors → disinhibitory release of NE, acetylcholine, and glutamate
Anti-cognitive impairment
Two lows
Decreased intestinal motility
Vortioxetine → blocks 5-HT 3 receptors → reduces intestinal motility
constipate
reduced sexual inhibition
Vortioxetine → blocks 5-HT 3 receptors
Reduce inhibition of sexual arousal and ejaculation
Noradrenergic effects of SNRIs
Curative effect
"Depression" "Pain" "Children" "Women"
antidepressant
anti-anxiety depression
Blocks 5-HT recycling (dulled emotion) > Blocks NE recycling, SSRIs > SNRIs
SSRIs block 5-HT recycling from strong to weak: paroxetine > escitalopram > sertraline > fluoxetine > citalopram > fluvoxamine
anti-blocking depression
Block NE recycling (increase power) > Block 5-HT recycling
SNRIs block NE recycling from strong to weak: reboxetine > milnacipran > duloxetine > venlafaxine > fluoxetine > sertraline > fluvoxamine > citalopram
Anti-pain
SNRIs (milnacipran, duloxetine, venlafaxine) increase -HT and NE energy and treat chronic pain
Fighting Attention Deficit Hyperactivity Disorder (ADHD)
SNRIs (methylphenidate, atomoxetine) increase NE and DA energy and resist ADHD
Anti-urinary incontinence
Duloxetine increases NE energy → stimulates α1 receptors in the internal bladder sphincter → contracts the internal bladder sphincter → resists stress urinary incontinence; excessive contraction will cause difficulty in urination
narcolepsy
SNRIs (venlafaxine) increase NE energy
Adverse reactions
mental system
"Four causes": causing anxiety and insomnia, causing irritability, causing mania, and causing mental illness
hypervigilance
Duloxetine increases NE energy → stimulates α1 receptors → hypervigilance →
anxiety, insomnia
Chlorpromazine blocks α1 receptors and can fight anxiety and insomnia
irritable, irritable
Chlorpromazine blocks α1 receptors and can resist irritability and irritation
suicidal tendencies
Hyperarousal increases impulsivity
Neurogenic frequent urination
depersonalization
delirium
induce mania
Venlafaxine increases NE energy → (excessive) stimulation of brain beta receptors → (induced mania) antidepressant
Increase clarity of perceived signals and increase clarity of thinking
Promote attention switching (situation-dependent shifting)
Increase memories of positive emotions (think good things)
exacerbating psychosis
The locus coeruleus-ventral tegmental part of the midbrain excites the NE energy pathway → stimulates α1 receptors → activates D2 receptors in the limbic system → induces psychosis
Use venlafaxine with caution/not in patients with schizophrenia
nervous system
"Two heads" - headache, dizziness; "Two muscles" - myofiber tremors, muscle twitching (epilepsy)
Headache, drowsiness
Milnacipran increases NE energy → stimulates α1 receptors on cerebral blood vessels → constricts cerebral blood vessels → cerebral ischemia and hypoxia → dizziness, headache, and drowsiness
Dizziness, tinnitus
Methylphenidate increases NE energy → stimulates vascular α1 receptors → constricts vestibular blood vessels → dizziness; drivers or those operating dangerous machines should use it with caution
Constrict cochlear blood vessels → tinnitus, hearing loss
extrapyramidal reaction
Milnacipran increases NE energy → stimulates striatal beta receptors → inhibits striatal DA energy → tremors, akathisia, bruxism, etc.
Propranolol blocks beta receptors and treats tremor, akathisia, bruxism, etc.
epileptic seizure
Bupropion increases NE energy → stimulates α1 receptors in temporal lobe cortex → hypervigilance → induces epilepsy
circulatory system
"Fast heart rate, high blood pressure, orthostatic hypotension"
heart
increase heart rate
Venlafaxine increases NE energy → stimulates β1 receptors → increases heart rate → induces angina pectoris and myocardial infarction
Metoprolol blocks β1 receptors → reduces heart rate
Reduce heart rhythm variability
Bupropion increases NE energy → stimulates β1 receptors → increases heart rate → reduces heart rhythm variability and is susceptible to premature ventricular contractions
Myocardial ischemia
Methylphenidate increases NE energy → stimulates vascular α1 receptors → contracts coronary arteries → myocardial ischemia → supraventricular tachycardia, acute myocardial infarction, and sudden death
hypertension
Venlafaxine increases NE energy→stimulates α1 receptors→constricts blood vessels→increases blood pressure
Use with caution: patients with coronary heart disease or cerebral hemorrhage. Contraindications: Patients with uncontrolled hypertension
orthostatic hypotension
Venlafaxine increases NE energy → stimulates α2 receptors in the medullary cardiovascular center → reduces NE release → orthostatic hypotension → syncope
Antipsychotics block α1 receptors → relax peripheral venous vascular smooth muscle → cause orthostatic hypotension
Relax local venous smooth muscle→
nasal congestion
Painless parotid gland enlargement
Angioedema (dorsal foot or ankle)
Atypical antipsychotics block α1 receptors from strong to weak
Clozapine (high) = quetiapine = risperidone = paliperidone = haloperidol > peropilone (moderate) = olanzapine = ziprasidone = lurasidone = blonan Serin > Aripiprazole (low) > Sulpiride (none) = Amisulpride
reproductive system
"Increases sexual desire, causes impotence and testicular pain"
increase libido
Duloxetine increases NE energy → enhances mesolimbic DA pathway activity → promotes DA release in the phrenic nucleus accumbens → stimulates D1 receptors → enhances sexual desire (increases the frequency of masturbation)
Inhibit sexual excitement
Impotence
Duloxetine increases NE energy → stimulates α1 receptors in the corpus cavernosum → contracts trabecular smooth muscle → the penis cannot become engorged and erect → impotence
Chlorpromazine blocks α1 receptors → dilates trabecular smooth muscle → congestion of corpus cavernosum → priapism → compression of urethra →
Difficulty urinating, urinary retention;
Continuous congestion → hypoxia, pain;
Hypoxia for 24-72 hours → cavernous fibrosis → permanent impotence
vaginal dryness
Bupropion increases NE energy → stimulates vaginal α1 receptors → contracts vaginal wall blood vessels → inhibits vaginal congestion → decreases vaginal secretions → vaginal dryness
Premature ejaculation
Milnacipran increases NE energy→stimulates α1 receptors→increases the smooth muscle peristalsis ability of the vas deferens, seminal vesicles, and seminal ducts→increases the contraction of prostate smooth muscle→promotes sperm leakage into the urethral bulb→causing premature ejaculation and semen discharge during urination.
Chlorpromazine blocks α1 receptors → inhibits peristalsis and contraction → inhibits the leakage of semen into the bulb of the urethra → delays ejaculation
testicle pain
Milnacipran increases NE energy → stimulates testicular α1 receptors → contracts testicular blood vessels → testicular ischemia and pain
abortion
Atomoxetine increases NE energy→stimulates α1 receptors→constricts blood vessels→insufficient blood supply to the uterus and fetus→abortion and reduced Apgar scores in neonatal health assessment
digestive system
"Dry mouth, constipation"
Dry mouth, anorexia
Atomoxetine increases NE energy → inhibits salivary gland secretion/inhibits gastrointestinal motility → dry mouth/anorexia and weight loss
obstructive jaundice
Milnacipran increases NE energy → stimulates Oddis sphincter α1 receptors → contracts Oddis sphincter → poor bile flow → indigestion/obstructive jaundice, right upper quadrant tenderness/liver damage/dark urine
pancreatitis
Methylphenidate increases NE energy → contracts the sphincter of Oddis → bile flows into the pancreas → pancreatic enzyme is activated into pancreatic enzyme → pancreatitis → fever, shock/blood amylase higher than 500U/pancreatic juice stimulates the peritoneum
constipate
Milnacipran increases NE energy → stimulates α1 receptors → inhibits intestinal motility → constipation
metabolic system
"Sweating, hot flashes"
Sweating, hot flashes
Venlafaxine increases NE energy → stimulates adipocyte β3 receptors → promotes lipolysis → sweating and hot flashes
urinary system
"Difficulty urinating"
Difficulty urinating
Duloxetine increases NE energy → stimulates α1 receptors in the internal bladder sphincter → contracts the bladder sphincter →
Frequent urination and urgency
Continued contraction → difficulty urinating
Contraction fatigue → urinary incontinence
Clozapine inhibits α1 receptors → relaxes the internal bladder sphincter → nocturnal enuresis and daytime urinary incontinence
Syndrome of inappropriate antidiuretic hormone secretion
Duloxetine increases NE energy → stimulates the locus coeruleus-supraoptic nucleus NE pathway → promotes ADH release → increases the permeability of the distal convoluted tubule and collecting duct to water → increases water reabsorption but no change in sodium reabsorption → hyponatremia Symptoms, hypernatremia→Cell edema→
Headache, fatigue, confusion
Anorexia, vomiting, belching
Other effects
increased intraocular pressure
Milnacipran increases NE energy → stimulates the α1 receptor of the pupillary muscle → contracts the pupillary muscle → dilates the pupil and narrows the anterior chamber angle → increases intraocular pressure
Use with caution: People with glaucoma or increased intraocular pressure. Contraindications: Untreated angle-closure glaucoma.
piloerection
Milnacipran increases NE energy→stimulates α1 receptors→contracts arrector pili muscles→piloerection
skin numbness
Bupropion increases NE energy → inhibits incoming pain signals from the dorsal horn of the spinal cord → numbness
distal limb ischemia
hair loss
Methylphenidate increases NE energy → continues to shrink hair follicle blood vessels → hair follicle dystrophy → hair loss
itching
Atomoxetine increases NE energy→stimulates α1 receptors→constricts blood vessels→
Ischemia of nerves in terminal limbs → itching of hands and feet
Prolonged contraction of skin blood vessels (pallor) → Damaging re-expansion of blood vessels (cyanosis) → Hypoxia (pain) → Raynaud’s phenomenon
Contraction of arterioles → cellular hypoxia → acidosis → early melanocyte apoptosis → local skin loss of pigment → vitiligo
Raynaud's phenomenon
Vitiligo
influenza
Bupropion increases NE energy → activates lymphocytes → produces stress immunosuppressive proteins → increases infection and influenza rates
Anti-α2 adrenergic autoreceptor
Psychotropic drugs increase NEergic pathways
Block NE recycling→increase NE energy
Block NE neuron presynaptic membrane α2 receptor → NE disinhibitory release → increase NE energy conduction
Antidepressants that block α2 receptors: mirtazapine, trazodone
Atypical antipsychotics block α2A receptors from strong to weak: risperidone (moderate) = aripiprazole = lurasidone > clozapine (weak) > olanzapine > quetiapine
dopaminergic effect
Schizophrenia
mesolimbic pathway
Arouses dopamine D2 receptors (DA hyperactivity) → positive symptoms
Memory reorganization, abnormal excitement → hallucination
Abnormal excitement of primitive thinking (intuition) → primary delusion
Explaining abnormal experiences → secondary delusions
Recall ability decreases but familiarity remains → false memory → delusion
Tricyclic antidepressants, sertraline, bupropion, and methylphenidate block DA recycling and can worsen delusions and hallucinations when used alone in schizophrenia.
Blocks dopamine D2 receptors
Improve delusions and hallucinations
For positive symptoms, except for clozapine and olanzapine, the other atypical antipsychotics are equivalent to typical antipsychotics
D2 receptor upregulation
During prolonged treatment with antipsychotics, D2 receptors are upregulated by an average of 34%. Sudden discontinuation or reduction of the drug → rebound enhancement of D2 receptor function → rapid onset of DA hypersensitivity psychosis.
Symptoms are the same every time
The knowledge structure and motivation orientation have not changed.
mesencephalocortical pathway
Negative and depressive symptoms in schizophrenia
D1 receptor agonist
Functional insufficiency → negative symptoms, depressive symptoms
Function enhancement→Improve negative symptoms and depressive symptoms
Low-dose sulpiride and amisulpride can improve negative symptoms and depressive symptoms
Dopamine mimetic drugs (amantadine, bromocriptine, levodopa) can not only improve negative symptoms and depressive symptoms, but also worsen positive symptoms.
Improve cognitive impairment in schizophrenia
dopamine↑
Atypical antipsychotics block presynaptic membrane 5-HT2A receptors in the mesencephalocortical pathway → disinhibitory release of DA → improve cognitive impairment
working memory
executive cognitive functions
verbal fluency
DA and cognitive function form an inverted U shape
NMDA receptor activity↑
Clozapine, olanzapine, and amisulpride mimic glutamatergic → agonize NMDA receptors
Brain-derived neurotrophic factor↑
Ziprasidone = risperidone > clozapine, increases the concentration of brain-derived neurotrophic factor
Activity of GABA interneurons containing somatostatin action site↑
Clozapine, olanzapine, sodium valproate, clonazepam mimic GABAergic
nigrostriatal pathway
Agonizes D2 receptors
Levodopa → activates striatal D2 receptors → inhibits muscle tone → improves Parkinson’s syndrome
Block D2 receptors
Antipsychotics → block striatal D2 receptors →
Block 65%-80% → antipsychotic
Block >80%→increase muscle tone→drug-induced parkinsonism, akathisia, acute dystonia (extrapyramidal reaction)
D2 receptor hypersensitivity
Long-term use of antipsychotics → increased D2 receptor sensitivity (adaptive hypersensitivity) → hypotonia → tardive dyskinesia
hypothalamic-infundibular pathway
norprolactin
Dopamine D2 receptor partial agonists (bromocriptine, aripiprazole) → stimulate prolactin cell D2 receptors → inhibit prolactin secretion
rising prolactin
Antipsychotics → block D2 receptors on prolactin cells → disinhibitory release of prolactin
Hyperprolactinemia: women>25ug/L, men>20ug/L
Mild: <50ug/L, loss of sexual desire, infertility
Moderate: 51-75ug/L, oligomenorrhea
Height: >100ug/L, hypogonadism, amenorrhea, galactorrhea
Hyperprolactinemia → negative feedback inhibition → luteinizing hormone ↓ → progesterone ↓, follicle-stimulating hormone ↓ → estrogen ↓, testosterone ↓
Spirit
Progesterone-mimetic GABAergic effects: progesterone ↓→anxiety, irritability
Estrogen 5-HT mimetic effects: Estrogen ↓ → Anxiety, depression
breast
Men → breast feminization, women → breast congestion (tenderness), galactorrhea
reproduction
Testosterone↓→Male sperm count, decreased libido, impotence, delayed ejaculation, inability to ejaculate (anorgasmia)
Estrogen ↓→ Female sexual desire decreases, vaginal lubrication decreases, and sexual intercourse pain
Estrogen ↓, progesterone ↓ → Oligomenorrhea, delayed menstruation, amenorrhea, infertility; delayed sexual maturity in children and adolescents
Progesterone ↓→ Prostaglandins ↑→ Severe uterine contraction→ Dysmenorrhea
cardiovascular
coronary heart disease
Estrogen↓→promotes vascular hardening
water and sodium retention
Ankle edema, weight gain
pulmonary embolism
Hyperprolactinemia→Adenosine diphosphate↑→Platelet activation→Venous thrombosis of lower extremities
endocrine
Osteoporosis
Estrogen↓, Testosterone↓→Bone Density↓
hirsutism in women
tumor
Pituitary adenoma, breast cancer, endometrial cancer, prostate cancer
Other antidopaminergic effects
intermittent limb movement disorder
DA antagonists (olanzapine, risperidone, quetiapine) → intermittent limb movements during sleep → discontinuous sleep at night and sleepiness during the day
Pigmentation
Levodopa metabolic pathway ① is converted into DA, ② is converted into melanin → pigmentation
Intestinal motility
Levodopa → stimulates D2 receptors → inhibits intestinal motility → constipation
Sulpiride and metoclopramide → block D2 receptors → promote intestinal motility
mood disorder
dysthymia
Insufficient DA energy in the nucleus accumbens → mild depression lasting more than 2 years
major depressive disorder
Reward pathway DA energy is very low → anhedonia
Bupropion inhibits the recycling of NE and DA → effective in treating refractory depression
anxiety disorder
social phobia
Low DA → social phobia
Loneliness, Parkinson's disease, DA blockers
Increase DA ability → improve social phobia
Monoamine oxidase inhibitors →Hindered degradation of monoamines (5-HT, NE, DA) → Increased concentrations of 5-HT, NE and DA → Increased DA energy
obsessive-compulsive disorder
DA can increase → cause compulsion
Atypical antipsychotics → block 5-HT2A receptors → disinhibitory release of DA → worsen obsessive-compulsive disorder
Atypical antipsychotics (amisulpride 325 mg/d) → block D2 receptors → strengthen the anti-obsessive effect
other
increase libido
Prefrontal cortex → DA conduction → Nucleus accumbens → Enhanced response to pleasant stimuli → Susceptible to addiction and sexual arousal
Levodopa, DA agonists, DA recycling blockers (bupropion, methylphenidate) → increase sexual desire
irritable
Prefrontal cortex → DA conduction → amygdala → enhanced response to aversive stimuli → susceptible to irritability (bupropion)
Antipsychotics, benzodiazepines, mood stabilizers → inhibit DA energy → anti-irritability
impulse control disorder
Dopaminergic drugs → can replace the pleasure derived from the release of DA from the midbrain tegmentum → relieve impulse control disorders
Methylphenidate - kleptomania; Bupropion - pathological gambling, trichotillomania
catatonia
Bromocriptine → stimulates the nigrostriatal DA pathway → improves akinetic mutism, the maximum dose is 40 mg/d
substance abuse
reward access
Midbrain tegmental area → DA conduction → prefrontal cortex → glutamate conduction → nucleus accumbens → drug-seeking behavior
reward delivery
dopamine
An exciting sense of desire for a reward that is about to be received, for example: the pleasure of flirting between men and women
Opium
Produce a calming sense of happiness in response to a reward that has been received, for example: acute drinking → stimulate the release of β-endorphin → pleasure
reward material
opium, marijuana
Stimulate μ receptor → increase DA energy
Amphetamine
Promote DA release→increase DA energy
cocaine
Block DA recycling→increase DA energy
Alcohol, ketamine, phencyclidine
Antagonize NMDA receptors → disinhibitory release of DA → increase DA energy
nicotine
Stimulate nicotine receptors → promote DA release → increase DA energy
Benzodiazepines → Mimic GABA-A receptors → Inhibit DA release → Loss of motivation and weakness → Treat alcohol abuse