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what receptors do the antidepressants and antianxiety medications act on?

 what is receptors function database:

note: all the data in this page from starting the article to end and other parts of the site are DMCA protected, will report anyone who use the data for commercial usage to all parties, if you used any text from here you need to use dofollow link linking to this page, don't use all the data just part of it, for learning purpose, thanks for understanding
 
info about what reaction will happen if you agonist/antagonist the receptors,
keep in your mind, the place of the receptor can make change of the receptor function, like agonizing adrenergic β2 receptor in the heart will cause fast heart beat and hypertension, but agonizing them in the brain will cause urge to fight, by increasing reward for violence behaviors..
add to that this is just self gathering info for multiple source, as of what i understand in the over last years of testing, my info might be wrong, it's just will help you to know more about the general function of the receptor ☺

advantages:
-to cell are colored for knowing its better to agonist the receptor or antagonist it
-link for source are available (to read where i got this info, available only in excel file down, not image or html type)
-endogenous and exogenous affinity to the receptors are available
-always updated info because i never got boring from exploring ☺✌
-free

preview:

green: in (whats will happen if) cell mean = I am not sure if the information is correct in that cell
in (receptor) cell mean = transporter.
blue: in (whats will happen if) cell mean = I'm sure.
in (receptor) cell mean = better to agonist.
red:in (receptor) cell mean = better to be antagonist.
  black blue: in (receptor) cell mean = agonizing give strong benefits
   black red: in (receptor) cell mean = antagonizing give strong benefits
yellow: just additional info
auto-receptor: the receptor that product negative feedback mean it will decrease the release of it's endogenous neurotransmitter
anti-target: pharmacy companies (eg, Eli Lilly) always make sure their drugs doesn't interact with that receptor because it cause problems

 

html table:

Neurotransmitters selectivity (Ki nm) receptor what's will happened if
endogenous  exogenous  agonized/enhanced   antagonized/inhibited
serotonin /   SERT Serotonin reduction increase serotonin decrease D2 sensivity in striatal  downregulate dopamine 3 receptors
1.0 HT1A feelings of love, empathy, and connection to others by induceding oxytocin stimulation  negative feedback Antidepressants (post-synaptic receptor agonists and pre-synaptic autoreceptor antagonists serve as antidepressants depressant
1.4 HT1B induced repetitive behavior  of ocd negative feedback aggression  anxiolytic implusivity (by increasing dopamine levels and dopamine release in the nucleus accumbens the place most expressed D3 receptors)
1.6 HT1D negative feedback Vasoconstriction  inhibit/modulating release of glutamate  antidepressant affects locomotion and anxiety
2.4 HT1E might involved in the regulation of memory in humans
2.6 HT7 Autoreceptor   antidepressant & Cognition & ability to regonise old objects
2.6 HT2C increase of corticotropin releasing hormone (CRH) and vasopressin mRNA in the paraventricular nucleus and proopiomelanocortin in the anterior pituitary lobe. In rats decrease impulsivity and motivation for drug and food reduced cognitive deficits  anxiolytic or sometimes in some aspect anxiety  estradiol and progesterone decrease the receptor concentration in the ventral hippocampus  increases release serotonin,  norepinephrine and dopamine
2.8 HT2B empathy  Autoreceptor Required for behavioral effects of SSRIs pulmonary hypertension  
3.2 HT1F treatment of migraine headaches development was halted due to toxicity
3.6 HT2A hallucination anti-inflammatory  inhibit dopamine release and increases in hormonal levels of oxytocin, prolactin, ACTH, corticosterone, and renin antidepressant Serotonin syndrome antidepressant
31.0 HT6 anti-anxiety antidepressant increase GABA Antagonists enhance
cognitive performance;
blockade of signaling is
anxiogenic 
reverse a scopolamine-induced cognitive deficit but it appears that 5-HT6 receptor blockade is more consistently effective in alleviating memory deficits than increasing memory in normally functioning animals   Alzheimer's disease  block effect of ssris
39.7 HT4 Ememory & learning + antidepressant effects increase acetylcholine  respiratory depression
79.2 HT5A Autoreceptor + Memory consolidation
  implicated in the sleep-wake cycle
187.1 HT3 Serotonin syndrome   Anti-vomiting anxiolysis antidepressant
dopamine /   DAT  dopamine reduction increase dopamine
1.0  D1 in prefrontal cortex : cognition-enhancing effects  hypotension  D1 receptors in the 'direct pathway' provide a range of possible decisions derived from activity in the cortex rewarded behaviors and pleasure, One such behavior is eating + nootropic, anorectic, rewarding and profound antiparkinson effects motivation (goal directed behaviors) anxiety and depression  effective antagonist d1(mostly the cause)/d5 product inhibition of acute euphoric effects of cocaine treatment of Tourette's syndrome 
1.0 D2 D2 receptors in the 'indirect pathway' are activated to filter and select one of decisions provided by D1 receptor, add to that
increase reward for complex stuff like:  internet, big dreams , urge/enjoyment to Efficiency complete tasks (over activation if together with anxiety cause ocd) etc..
hyperactivity of adhd induce locomotion activity reduce prolactin Anti-vomiting Neuroleptic malignant syndrome antipsychotic positive symptoms extrapyramidal symptoms  especially  dystonia
  D2s negative feedback: reduce dopamine release and increase dopamine reuptake
1.0 D3 increase reward for: shopping, gambling, eating, sex, drug seeking behaviors', Risk-Taking , impulsivity Stimulation of yawning  anti-empathy effect anti-restless leg syndrome reduce prolactin Anti-vomiting block agitation induced by of D3 agonizing Blockade of the D3 receptor disrupts drug-associated cue-induced craving and stress-induced craving. fear from risk-taking stations
induce sexual fantasies poriomania (A morbid impulse to wander or journey away from home.) kleptomania (a recurrent urge to steal, typically without regard for need or profit.) Intermittent explosive disorder or IED is a clinical condition of experiencing recurrent aggressive episodes that are out of proportion of any given stressor. Pyromania: is characterized by impulsive and repetitive urges to deliberately start fires.
1.0 D4 Novelty seeking (increases the propensity for exploring to select a novel choice over familiar one (eg, human example in this is relationship cheating)) increase working memory performance and fear  reverse stress-induced working memory deficits
  associated with cheating, like in sex relationships and might other type of cheating too..
  D4.7  better cognitive performance 
x10 of D1 D5 inhibits the synthesis of melatonin    reduces burst firing  and improve motor deficits, increased motor response to administration of methamphetamine learning problems (fear memory aid by B2 and M1 receptors) that may be associated with ADHD hypertension 
noradrenalin /   NET nordraline reduction   increase nordraline
/ α1  vasoconstriction anorexia inhibit hearing system   orthostatic hypotension inhibit ejaculation but not orgasm
1.2 α1A inhibit olfactory system  
1.0 α1B no info in Wikipedia  
/ α1C  
1.6 α1D  
/ α2 vasoconstriction anti ptsd + anxiety disorders    
1.5 α2A in prefrontal cortex : cognition-enhancing effects + lowering blood pressure negative feedback: at high stimulation frequencies  
1.4 α2B emotional memory focus more on negative aspects of a situation  
1.5 α2C negative feedback : at lower levels of nerve activity  
1.3 β1 anxiolytic  in (SNS) positive feedback   lower blood pressure bronchoconstriction (less affective then β2)
1.1 β2 increase rewards for: fighting, listening rap music, social dominance nervous and excitable, increase respiration speed, fine visual Hallucinations, rather not to say empathy talk   bronchoconstriction
1.1 β3 induce fat breaking in adipose tissue / anti muscle stress effects  antidepressant and anxiolytic tremors    
histamine 102.9   H1 orthostatic hypotension Sleep-wake cycle (promotes wakefulness), body temperature, nociception, endocrine homeostasis, regulates appetite, involved in cognition   anti-sensitivity anti-insomnia anti-acne dizziness
15.8 H2     The ulcer
6.8 H3  autoreceptors   anti-vertigo increase histamine, acetylcholine, norepinephrine, serotonin, GABA release stimulant + wakefulness + cognitive enhancing at relatively low levels of receptor occupancy improve memory consolidation
17.1 H4      anti-inflammatory and antihyperalgesic effects
acetylcholine     asyt T     increase acetylcholine
1.0 M1 Secretion from salivary glands  aggression Secretion from salivary glands Gastric acid secretion from stomach and muscle spasm. olfactory behaviors (e.g. mating is the pairing of either opposite-sex or hermaphroditic organisms )    inhibit ability of recall memory Delirium hallucinations 
100.9 M2 negative feedback slow the heart rate    Responsible for decrease in sexual activity, as a study using rats confirmed
  Mediating olfactory guided behaviors (e.g. odor discrimination, aggression, mating).[10] 
235.3 M5 Stimulation of gastric acid secretion. increase dopamine release   M5 receptor knockout mice exhibit a reduction in the reinforcing effects and withdrawal symptoms of cocaine and morphine
  M4 hypersalivation inhibit D1-induced locomotion stimulation Inhibition of dopaminergic (D1 receptor) signaling negative feedback   treatment of Parkinson's disease knockout mice exhibit an increase in anxiolysis compared to wild-type mice
M3 increased secretions from stomach (emesis)   change glucose to weight gain (olanzpine)+diabetes side-effects decreases the urgency to urinate anti-asthma 
nicotine     α1 no info in the first 100 Google search result
α2 influence hippocampus-dependent learning and memory and behaviors
α3     Heterozygous α3 mice are less sensitive to nicotine-induced seizures.
α4 induced release of dopamine more sensitive to nicotine-induced hypothermia and nicotine-induced seizures and sleep disruptions altered nicotinic modulation of respiratory rhythm
α5   Knockout mice show increased nicotine intake in self-administration tests, Reduced sensitivity to nicotine-induced behavioral effects and seizures, Increased attentional performance
22.35 7,75 (nicotine) α6 increase reward and reinforcing effects  
  103,14 (nicotine)   α7 some of the cognitive effects of nicotine
    α8 no info in the first 100 Google search result
α9
α10 no info in the first 100 Google search result
β1  expressed in vertebrate skeletal muscle and placenta
β2 increase attentional performance   Knockout mice loss of nicotine-induced dopamine and GABA release, impaired development of the visual system, increased passive avoidance latency; loss of nicotine self-administration, reduced nicotine-induced antinociception, impaired learning and increased neurodegeneration in aged animals
β3 chronic exposure induced withdrawal Modulation of gene expression and increase nicotine consumption Modulate Dopamine Release  hyperalgesia, anhedonia-like effect
β4   Knockout mice display decreased anxiety-related responses; resistance to nicotine-induced seizures; decreased nicotine withdrawal Nicotine intravenous self-administration (IVSA) was lower in constitutive β4 knockout (KO) mice at all doses tested, β4KO mice have higher extracellular dopamine (DA) levels in the nucleus accumbens 
γ  expressed in adult extraocular muscle and involvement in myasthenia gravis
δ  no info in the first 100 Google search result
ε      knockout mice display impaired neuromuscular transmission, progressive muscle weakness and atrophy and associated with the human AChR deficiency syndrome 
3.04 1 (nicotine) α4β2  improvements in attentional performance release of dopamine in the nucleus accumbens   
2.24 1,38 (nicotine) α2β2  
16.47 3,48 (nicotine) α3β2
23.09 8,68 (nicotine) α4β4
32.35  23,57 (nicotine) α2β4
21.18  37,98 (nicotine) α6β4
36.18  50,78 (nicotine) α6β2
  60,47 (nicotine) α6β3β4α5
230.29  92,95 (nicotine) α3β4 anti-addiction
Sigma   σ1 hallucinogenic   nootropic and antidepressant actions in animal studies, as well as antitussive anti-amnesic  antipsychotic decreases the convulsivity 
σ2 no role in depression regulate cholesterol transporter NPC1, involved in cholesterol homeostasis  
glutamate transporter   EAAT2 induce/enhance the expression of EAAT2=reduce the development and expression of tolerance to opiates and other drugs of abuse reduced expression of EAAT2= increase addictive/drug-seeking behavior and increase in vulnerability to relapse after re-exposure to the addictive drug or its associated drug cues
NMDA   GluN1 (glycine) plasticity of synapses which is believed to underlie memory and learning
    anxiolytic (emotional blunting  no disinhibition), sedative, dissociative feeling (altered state), Reduces pain sensitivity, neuroprotective, distorts visual acuity antidepressant
GluN2A increase long term depression  short-term memory  
GluN2B (glutamate) long-term memories 
GluN2C no info
GluN2D long-term potentiation, an activity-dependent increase in the efficiency of synaptic transmission thought to underlie certain kinds of memory and learning
NMDA     antidepressant bladder issues
(MK-801)  
AMPA   AMPA motor coordination disruptions, convulsions, and neurotoxicity, enhance cognition and memory, to produce antidepressant-, antianhedonic-, and anxiolytic-like effects, and to have neurotrophic and neuroplasticity-promoting activities. increase levels of BDNF in the hippocampus and to stimulate hippocampal neurogenesis high-impact AMPAR PAMs decrease both deactivation and desensitization together to enhance and prolong synaptic currents rapidly-acting antidepressant effects of the NMDA receptor antagonist ketamine appear to be mediated through indirect/downstream activation of AMPARs antidepressant-like effects in animals are blocked by the AMPAR antagonist NBQX anticonvulsant  neuropathic pain  sedation
GluA1 centrally involved in synaptic plasticity. Expression of the GluR1 gene is significantly reduced in the human frontal cortex with increasing age
 GluA2 regulation of AMPA receptor properties and synaptic plasticity/regulates metabotropic glutamate receptor-dependent long-term depression 
 GluA3 RNA editing allow faster recovery from desensitization therefore allows continue response to stimulant
 GluA4
Metabotropic
glutamate
 receptor 
  mGluR5 nootropic and antipsychotic effects   reduce drug self-administration regardless of dose learned helplessness
mGluR3  sedative, neuroprotective, anti-addictive and anticonvulsant    anxiolytic effects without producing sedation + slightly reduce cognitive performance + inhibiting the development of tolerance to morphine + relieving the symptoms of withdrawal from chronic use of both nicotine and morphine + reducing the effects of 5HT2A agonist hallucinogens + noticable reduce of yohimbine-induced stress response   antidepressant   antidepressant
increase behavioral effects of hallucinogenic drugs
increasing analgesic effects of μ-opioid agonists
modulating dopamine receptor function
antagonizing give anxiolytic effect too but its deferent then the  anxiolytic effect produced by agonists  antidepressant and anxiolytic + boost release of dopamine and serotonin in specific brain areas
mGluR2  antipsychotic and anxiolytic  auto receptor  decreases cocaine self-administration in rats, with no effect on food self-administration
mGluR1   block adrenergic receptor activation in neurons neuroprotective agent for the treatment of stroke. analgesic Mice lacking mGluR1 had impaired motor functions, characterized by impaired balance. In the Morris watermaze test, an assay for learning abilities, those mice needed significantly more time to successfully complete the task
mGluR1a significantly inhibited sexual motivation 
mGluR4 treatment of Parkinson's disease  
mGluR6 response to light
mGluR7 inhibit cocaine and alcohol self-administration     
mGluR8 anticonvulsant + treatment for hyperalgesia
Ionotropic glutamate receptor/Kainate    GluR5   protect against seizures neuroprotective + anticonvulsant + antihyperalgesic + analgesic + anxiolytic suppresses both the withdrawal symptoms from opioids and the development of tolerance
GluR6 associated with nonsyndromic autosomal recessive mental retardation GluR6 KO mice exhibited less anxious or more risk-taking type behavior and less despair-type manifestations, and they also had more aggressive displays
GluR7 RNA editing 
KA1 regulation of antidepressant treatment-response like citalopram
KA2 no info in the first 100 Google search result just they linked to "Intracellular Trafficking"
GABA   α sedative + relaxing   antidepressant stimulant
α1 induce sleep  sedative or amnestic  
α2 anxiolytic 
α3
α4 amnesia ataxic, sedative, and analgesic effects  decreases their free consumption of and preference for alcohol
α5   do not have convulsant or anxiogenic effects but instead show cognitive- and memory-enhancing or nootropic-like effects
α6  
β sedative + relaxing antidepressant stimulant
β1    
β2  anesthetic 
β3 sedation 
α-ρ1  
α-ρ2 SSRIs like effect increase serotonin
α-ρ3
γ1   
γ2  elevated anxiety + altered emotional behavior reminiscent of melancholic depression + depression related anhedonia in the sucrose consumption test elevated serum corticosterone levels  epilepsy
γ3  Autism and autism spectrum disorders
δ      Knockout females, but not males, show improved fear conditioning Mice lacking the δ subunit show reduced sensitivity to neuroactive steroids  
ε   
θ 
π  overexpressed in pancreatic adenocarcinomas
opioid   DOR δ1 euphoria  physical dependence
DOR δ2
KOR κ1 analgesic, anxiogenic, and dissociative/hallucinogenic
KOR κ2
KOR κ3
MOR μ1 respiratory depression physical dependence Opioids down-regulate the HPA-axis to produce near-castrate testosterone levels, while also suppressing adrenocorticotropic hormone secretion from the anterior pituitary (this lead to decrease libido etc,, effect of low T)
Restless legs syndrome
increased sensitivity to physical touch and pain
MOR μ2 euphoria
MOR μ3  
 NOR depression development of tolerance to μ-opioid agonists  
 NOR ORL1  
ZOR tissue growth 
NOP   treatments for depression and Parkinson's disease
trace
 amine
receptors 
  0.71 (dopamine) TAAR1  decrease Serotonin, Noradrenaline, Dopamine, reuptake inhibition  
  TAAR2 not about depression
TAAR5
TAAR6
TAAR8
TAAR9
COMT     convert  catecholamine's to rubbish   stop convert  catecholamine's to rubbish +levodopa
fos   ΔFosB  happiness seeking behaviors (craving) anti-craving effect
c-Fos don't increase the chronic induction of ΔFosB increase the chronic induction of ΔFosB
adenosine   A1 anticonvulsant and analgesic feel more energized and awake + heart-pounding effects
A2A    wakefulness-promoting effects, Antagonism of A2A receptors in the ventrolateral preoptic area reduces inhibitory GABA neurotransmission to the tuberomammillary nucleus, a histaminergic projection nucleus that activation-dependently promotes arousal
A2B provide protection from ischemia (lack of oxygen due to blocked blood supply)  promotes progression of human oral cancer anti-inflammatory  inhibits release of interleukins that is involved in the development of spatial memories 
A3 anti-inflammatory  
cAMP     stimulant
oxidants       decrease cell death due oxidative stress smooth skin (anti-aging effect)
PDE   1   increase cAMP used in: Parkinson's disease, Alzheimer's disease, Epilepsy
2 increase cAMP used in: improving memory
3 increase cAMP used in: acute heart failure and cardiogenic shock
4 increase cAMP used in: precognitive (including long-term memory-improving), wakefulness-promoting, neuroprotective, and anti-inflammatory effects
5 increase cAMP used in: erectile dysfunction
7 increase cAMP used in: anti-inflammatory and neuroprotective induction of dopaminergic neurogenesis
10 motor and cognitive deficits and increased anxiety increase cAMP used in: erectile dysfunction, treatment for schizophrenia
9   increase cAMP used in: improve learning and memory 
11 poorly understood, in part due to the lack of selective inhibitors
Oxytocin   Oxytocin love (mostly because androgen Neurotransmitter "Oxytocin" have wake biding affinity to Vasopressin 1A)    
Vasopressin   1A social recognition (mostly this is empathy of SSRIs + testosterone directly suppresses oxytocin in mice) Romantic attachment (physical and physiological) emotional talk + increase ability to trust others + increase generosity  Oxytocin evokes feelings of contentment, reductions in anxiety, and feelings of calmness and security when you are with your friend reduced anxiety-like behavior  greatly impaired social recognition abilities social isolation deficits in circadian rhythms and olfaction
1B aggression ability to recognize recently investigated mice reduced social motivation or awareness
2 antidiuretic   
Orexin   OX1 happiness  happiness seeking behaviors wakefulness + regulates energy expenditure + increase appetite + body temperature and locomotion
OX2  
 P-glycoprotein     prevent drugs from across BBB (involved in tolerance) cause some peripherally acting drugs to have central nervous system action too
 estrogen receptor   ERα  induced increase in SHBG which lower free testosterone + upregulation of gonadal testosterone production due to reduced negative feedback by androgens on the hypothalamic–pituitary–gonadal axis undersized testes, stimulate cell proliferation in breast tissue maintenance of bone integrity antidepressant-like effects  
Erβ anti-proliferative in reproductive tissue anxiolytic  antidepressant, anxiolytic, cognitive-enhancing, and stress-relieving up-regulates oxytocin receptors increase sexual motivation cognitive impairment , and development of AD pathology Abnormalities in gene expression associated with ER-β have also been linked to autism spectrum disorder
GPER GPER and ERβ play a modulator role in breast development, ERα is the main receptor responsible for estrogen-mediated breast tissue growth  anxiogenic Lordosis to front  
Estrogen-related receptor   ERRα   ERRalpha KO mice:-reduced body weight, resistant to high-fat diet induced obesity
ERRβ ERRβ Null Mice: show severely impaired placental formation.
ERRγ protect pre-menopausal women from age-related hearing loss  
Membrane estrogen receptor   Gq-mER no info
Erx
ER-X
Androgen receptor    AR have important role in prostate cancer    
GPRC6A mediate rapid, non-genomic prostate cancer cell responses to testosterone increase skeletal muscle strength, indicating potential anabolic effects, implicated in the antigonadotropic effects of androgens
14nM(Kd)   ZIP9  increase skeletal muscle strength, indicating potential anabolic effects, implicated in the antigonadotropic effects of androgens
progesterone receptor    PR-A serve to antagonize the effects of PR-B   delayed but otherwise normal mammary ductal development at puberty impaired lobuloalveolar development of the mammary glands
PR-B positive regulator of the effects of progesterone
PR-C  
mPRγ no info
mPRδ
mPRα
mPRβ
mPRϵ
AdipoR1
AdipoR2
Glucocorticoid receptor     LINKED TO PTSD
Mineralocorticoid
Cannabinoid     CB1 anxiolytic increase appetite, novelty, appreciation for food, music, art, analgesic, decrease short-term memory    
 CB2 anti-inflammation  preventing cognitive impairment and loss of neuronal markers anti-cancer properties
NAGly
(GPR18)
anti-inflammatory without producing any psychoactive effects
GPR55 altered blood pressure regulation 
GPR119 body weight loss by reduction in food intake     
Neuropeptide Y receptor   Y1   regulation of appetite, anxiety, BIBP-3226 has anxiogenic and anorectic effects
Y2 reducing alcohol consumption in addicted rats[6][7] and anxiolytic effects
Y4  
Y5 anorectic, antidepressant and anxiolytic effects
 peroxisome proliferator-activated receptor gamma    PPAR-γ uprgulate SERT + increase production of serotonin (the result is antidepressant effect)  
Melanocortin    MC1R  hyperpigmentation primarily of the hair and skin decrease sensitivity to pain
MC2R  upregulates levels of cAMP by activating adenylyl cyclase  
MC3R    increased fat mass despite decreased food intake 
MC4R  powerful  treatments for  female and male sexual dysfunction via activation of the central oxytocin system, have been found to promote pair bond   produce pronounced antidepressant- and anxiolytic-like effects  Obesity
MC5R    male mice decreases aggressive behavior, promotes defensive behavior and encourages other male mice to attack MC5R-deficient males through pheremonal signals decreased production of sebum
Thyroid hormones   T3     weight loss, tremor, headache, upset stomach, vomiting, diarrhea, stomach cramps
    nervousness, irritability, insomnia, excessive sweating, increased appetite, fever, changes in menstrual cycle, sensitivity to heat
 
ZINC RECEPTOR   GPR39 SSRIs upregulate this (involved in the antidepressant response)
Histone deacetylase    HDAC2   treatment for Parkinson's Disease prevented cognitive and behavioral impairments in mice with Alzheimer's Disease
HDAC1 no info in Wikipedia
HDAC3  
HDAC4 regulates bone and muscle development
HDAC5  involved in memory consolidation 
HDAC6 Mutations in this gene have been associated to Alzheimer's disease
HDAC8      
HDAC9
HDAC10 HDAC10 has been shown to interact with Histone deacetylase 2, and Nuclear receptor co-repressor 2
HDAC11 upregulation of HDAC11 expression has also been seen in various cancer cells
Sirtuin implicated in influencing cellular processes like aging, transcription, apoptosis, inflammation implicated in influencing cellular processes like aging, transcription, apoptosis, inflammation ( nicotinamide inhibit this)
COX   COX-1       
COX-2  suppressing inflammatory neurodegenerative pathways in mental illness
Neurotensin   NTS1   blocked the effects of stimulant drugs including MDMA
NTS2
GHB receptor   GPR172A do not produce a sedative effect, instead causing a stimulant effect followed by convulsions at higher doses, thought to be mediated through increased Na+/K+ current and increased release of dopamine and glutamate  
Angiotensin II   AT1  increase vasoconstriction, aldosterone synthesis and secretion, increased vasopressin secretion reduce fear memory recall 
AT2 inhibition of cell growth Over expression of the AT2 receptor down-regulated the AT1 receptor Decrease of dopamine synthesis  
AT3  no info in the first 100 Google search result
AT4 induce release of oxytocin (anxiolytic effect) enhances learning and memory and cognition     
vitamin D receptor    VDR increase calcium absorption loss of bone density
regulates the expression of more than 900 genes  (cell growth and development, immune function, and metabolic control)
Melatonin    MT1      MT1 receptor knockout mice exhibit depression-like behaviour and reduced mobility in the forced swim test compared to wild-type mice.
MT2   MT2 receptor knockout mice do not exhibit luzindole-mediated antidepressant-like actions, as seen in wild-type mice.
GPR50  Physiological function of GPR50 remains unclear, although studies implicate the receptor in energy homeostasis [12].
calcium   α2δ-1     anticonvulsant, analgesic, and anxiolytic effects (opiates and benzo-like effect)
Sodium   Nav1.2   mutations in this gene have been linked to several seizure disorders and autism, infantile spasms bitemporal glucose hypometabolism , and bipolar disorder
Nav1.3 anti-Neuropathic pain 
Nav1.4  Mutations in the gene are associated with hypokalemic periodic paralysis, hyperkalemic periodic paralysis, paramyotonia congenita, and potassium-aggravated myotonia 
Nav1.5 cardiac diseases is associated with mutations (Long QT syndrome type 3)
Nav1.8 treatment of chronic pain
Nav1.9  pain relief inti-inflammatory 
Potassium channels   K2P2.1 anxiolytic and antidepressive effect   
Kv7.1   Mutations in the gene can lead to a defective protein and several forms of inherited arrhythmias as Long QT syndrome, Short QT syndrome, and Familial Atrial Fibrillation
Kv7.2 anticonvulsants
G protein-coupled receptor kinase   GRK6   upregulate D2/D3 receptor upregulate mu-opiates receptors
GRK2 The agonist-dependent phosphorylation of the rat D1A receptor was substantially increased  upregulate β2 adrenergic receptors  upregulate mu-opiates receptors
GRK3 upregulate mu-opiates receptors upregulate KOR-opiates receptors
GRK5  
Retinoid receptor    RAR-alpha 1   Knock-out mice studies showed that a deletion in one of the copies of the RARA gene did not create any observable defect, while deletion of both copies shoes symptoms similar to that of Vitamin A deficiency. This proved that all 3 subtypes of RARs work redundantly.  Ro41-5253 (1 mg/kg) treatment downregulated RARα protein expression in hypothalamic PVN and hypothalamus, and increased the protein levels of BDNF, PSD95, SYP and MAP2 in the hippocampus. We concluded that Ro41-5253 had antidepressant-like effects on CUMS rats by downregulating HPA axis hyperactivity and improving the hippocampal neuronal deficits as the absence of retinoid receptors results in a reduced expression of the DA D2 receptor/mutations for the acid retinoic receptors demonstrated in mice could reduce expression of D1 and D2 receptors and do impair dopamine signaling
 RAR-alpha 2
 RAR-alpha 3
RAR-beta limits growth of many cell types by regulating gene expression associated with cancer onset/progression
RAR-gamma shown to interact with NCOR1 Depression, Mood changes, Suicidal ideation anti-cancer  
RXR downregulation of thyroid stimulating hormone significant increase in cholesterol levels and a decrease in total thyroxine levels 
 RXR-alpha regulating their transcription (unknown what it is) RXR heterodimer in the absence of ligand is bound to hormone response elements complexed with corepressor protein. Binding of agonist ligands to RXR results in dissociation of corepressor and recruitment of coactivator protein, which, in turn, promotes transcription of the downstream target gene into mRNA and eventually protein.  
RXR-beta involved in mediating the effects of retinoic acid (RA). This  increasing both DNA binding and transcriptional function on their respective response elements Induction of apoptosis (associated to RARa activation)
RXR-gamma the antiproliferative effects of retinoic acid (RA).  Adapalene (CD-271) is a dual RAR and RXR agonist, used in the treatment of acne (which make sure that rxr is upregulate ht1a presynpatic receptors and dopamine 2) very strong acne treatment suppression of thyroid function ablation of Rxrgamma in mice leads to depressive-like behaviors including increased despair and anhedonia, which were accompanied by reduced expression of dopamine D2 receptor in the shell of nucleus accumbens (NAc) and altered serotonin signaling (proberly increase singling of serotonin)
Nuclear receptor  NCOR1  assists nuclear receptors in the down regulation of target gene expression (unknown what it is) Loss of function of this protein significantly increases the strength and power of mouse muscles
NCOR2  
Neurokinin    TACR1 has been associated with the transmission of stress signals and pain 99% human receptor occupancy might be required for consistent psycho-pharmacological or other therapeutic effects prevent chemotherapy-induced nausea and vomiting  anti-pain
TACR2    antidepressant and anxiolytic treatment of asthma
TACR3 dose-dependently suppress luteinizing hormone (LH) secretion, though not that of follicle-stimulating hormone (FSH), and consequently to dose-dependently decrease estradiol and progesterone levels in women and testosterone levels in men

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