1. 5-HTergic effects
5-HT1 receptors: agonize 5-HT1A receptors antidepressant, anxiolytic, improve delayed ejaculation and pleasure deficit (buspirone) Xuzhou psychiatric hospital psychiatry Chi Lei
Agonism of 5-HT1D receptors Treatment of migraine (sumatriptan, fluoxetine)
5-HT2 receptors: agonizes postsynaptic membrane 5-HT2A receptors, causing insomnia, anxiety and inhibiting sexual function (SSRIs)
Increases 5-HTergic, when agonizing 5-HT2A receptors can cause insomnia anxiety and inhibit sexual function. Paroxetine for premature ejaculation)
Agonizes presynaptic membrane 5-HT2A receptors, agonizing this receptor inhibits DA release.
Midbrain cortex: attenuates posterior membrane D1 receptor function, causing mental slowness and weakness
Midbrain limb: attenuates posterior membrane D2 receptor function, mildly improves nurturing symptoms
Nigrostriatal: attenuates posterior membrane D2 receptor function, causing EPS
Hypothalamic funnel: attenuates posterior membrane D2 receptor function, prolactin deinhibitory release
Agonism of 5-HT2c receptors, causing irritability and anorexia
5-HT3 receptors: agonize 5-HT3 receptors, cause headache, malignancy, vomiting (mirtazapine blocks 5-HT23 receptors, preserving the antidepressant, anxiolytic and sexual function-improving effects of agonizing 5-HT1A receptors, while avoiding the side effects of agonizing 5HT23 receptors)
5-HT4 receptors: agonism of 5-HT4 receptors increases Ach release, improves learning memory in the frontal cortex, and increases gastrointestinal motility in the digestive tract.
Other 5-HTergic effects: anti-impulsive aggression, mental stabilization (SSRIs and lithium carbonate)
Anti-compulsive, SSRIs and chlorpromazine, venlafaxine increase 5-HTergic
Sleep promotion, during sleep, pineal gland releases large amounts of 5-HT to promote sleep, increase slow-wave sleep and inhibit fast-wave sleep
Treatment of chronic pain, the effect is not as effective as the proposed NE energy
Slowing heart rate, central 5-HT energy increase can inhibit DA energy, thus slowing down the heart rate (SSRIs, lithium carbonate increase 5-HT slowing heart rate)
2. NE effect
Alpha 1 receptors: cause anxiety and insomnia, venlafaxine, Ritalin
Inhibition of attention, activation when a large number of NE release activation of α1 receptors
Improve memory, selective activation of α1 receptors (venlafaxine, fluoxetine)
Psychogenic, agonism of amygdala α1 receptors promotes activation of the midbrain-limbic DA pathway, enhances D2 receptor activity in the limbic system, causes Sch-positive symptoms hallucinatory delusions
Causes impulsive aggression, calm state, blue spot-prefrontal agonism α2 is stronger than α1, screening for behavior
Stressful state, α1 stronger than α2, prefrontal cortical vasoconstriction, inhibits cognitive function, does not effectively screen for behavior, prone to impulsive aggression
Raise blood pressure, α1 receptors can constrict systemic A-vessels, primary hypertension susceptible
Causes urinary frequency and urgency, mimetic α1 constricts bladder sphincter (venlafaxine)
Causes impotence, agonist α1 receptors contract trabecular smooth muscle in penile corpus cavernosum, penis can not be filled with blood, so can not be erect
Causes premature ejaculation, increases vas deferens, seminal vesicles, seminal duct smooth muscle peristalsis
α2 receptors: improve attention, when calm, α2 is stronger than αa1 to improve the main, when stressed α1 is stronger than α2 to inhibit the main (venlafaxine, fluoxetine moderate amount to improve attention, too much to inhibit attention)
Anxiolytic lowering of Bp, colistin activates α2 receptors in the anterior membrane and inhibits NE release
Mirtazapine blocks α2 receptors, and NE release is de-inhibited, causing anxiety and lowering blood pressure. However, mirtazapine also has a blocking alpha1 receptor effect, masking both effects and improving anxiety and sleep.
Treatment of ADHD, agonizing prefrontal cortex α2 receptors, inhibiting striatal function via frontal cortex-striatal NE pathway
For the treatment of morphine withdrawal symptoms, activation of anterior membrane alpha2 receptors inhibits blue spot NEergic release
To cause impotence, colistin activates presynaptic membrane α2 receptors to inhibit NE release and inhibits postsynaptic membrane β2 receptor function to cause erectile inability
Beta2 receptor mimetic.
Reinforces traumatic memories, increased NE release in traumatized brain, β receptor excitation upon activation of the lateral part of the base of the amygdala, reinforces traumatic memories (insulin, lithium attenuates β receptors)
Antidepressant, antidepressant only works when beta receptors are hypersensitive
Worsens non-extensive social terror, beta receptor excitation
Causes inability to sit still, large amounts of DA excite beta1 receptors
Causes tachycardia, tricyclic, venlafaxine increases NE activation of beta receptors, causes tachycardia
Weight loss, increased NE activates β3 receptors on fat cells and breaks down fat
Other NEergic effects.
Excitation of sympathetic nerves, tremor, pupil dilation, anorexia, nausea, constipation, general feeling of heat, sweating (venlafaxine)
Treatment of neuralgia, amitriptyline
3. DA-like energy
Midbrain-limbic/hyperexcitatory D2 receptors, causing positive symptoms (sertraline)
Block D2 receptors, improve positive symptoms, strong to weak order:Fluphenazine” Haloperidol” Risperidone” Chlorpromazine” Olanzapine” Methiodiazide” Clozapine” Quetiapine
Midbrain-cortex: agonizing postsynaptic membrane D1 receptors can improve negative symptoms
Atypical antipsychotics block this presynaptic membrane 5-HT2a receptor, which inhibits the release of DA, and when blocked DA de-inhibits release and improves negative symptoms and cognitive function.
Sulpiride: Blocking the presynaptic D2 receptor causes DA release, and agonizing the postsynaptic D1 receptor improves negative symptoms, which theoretically improves cognitive function, but no relevant studies have been conducted.
DA-mimetics: amantadine, bromocriptine, and levodopa strengthen the midbrain cortical pathway, improving negative symptoms and potentially improving cognitive function, but at the same time activating the pathway and worsening positive symptoms.
Substantia nigra-striatal: when agonizing striatal DA2 receptors, it inhibits myotonia and improves Parkinson’s disease
When blocking DA2 receptors, it increases muscle tone, causing Parkinson’s disease, acute dystonia, and inability to sit still
Hypothalamic-brain funnel: agonizes D2 receptors on the postsynaptic membrane when DA is released, potently inhibits prolactin release Blockade of D2 receptors by antipsychotics causes hyperprolactinemia
Treat pathway: reinforces drug-taking behavior upon agitation, DA facilitation, opioid peptide transmission
Substance of abuse: opioid, cannabis-agitates μ receptors
Amphetamines-excite DA release
Cocaine – blocking DA recycling
Alcohol, phencyclidine – antagonizes N-methyl-D-aspartate receptors and induces DA deregulatory release
Nicotine – agonizes nicotinic receptors to increase DA release, and the above substances increase the DA of this pathway to agonize the vomeronasal opioid receptors
Treatment options: SSRIs mimic 5-HTergic, agonizing DA neurons presynaptic membrane 5-HT2a receptors, inhibiting DA release, inhibiting reinforcement center, causing hyperkinetic and mental retardation. BDZ inhibits DA release by mimicking GABA, which in turn inhibits reinforcement center, causing hyperkinetic weakness.
Other DA effects: antidepressant: alcohol, nicotine, cocaine and opioids increase DA release, antidepressant
Clozapine blocks 5-HT2a receptors, increases DA release, antidepressant
Ritalin, bromocriptine, low-dose sulpiride mimic DAergic, antidepressant
TCA class inhibits presynaptic D2 receptor sensitivity and promotes DA release, and increases D2 receptor sensitivity in the postsynaptic membrane, antidepressant
Manicogenic: levodopa, bromocriptine promote mania, biphasic common
Antipsychotics, lithium, carbamazepine, sodium valproate anti-DAergic, antimanic Sulpiride selective D2 receptor blocker antimanic.