Ask about this productRelated genes to: TAAR5 Blocking Peptide
- Gene:
- TAAR5 NIH gene
- Name:
- trace amine associated receptor 5
- Previous symbol:
- -
- Synonyms:
- PNR
- Chromosome:
- 6q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-23
- Date modifiied:
- 2015-08-26
Related products to: TAAR5 Blocking Peptide
Related articles to: TAAR5 Blocking Peptide
- : Spinal cord injury (SCI) is a severe pathological condition resulting in persistent motor and sensory impairments. The trace amine-associated receptor 5 (TAAR5) is a potential modulator of central nervous system functions; however, its role in CNS repair remains poorly understood. : We comprehensively evaluated the effect of TAAR5 gene knockout on functional recovery following lateral spinal cord hemisection in TAAR5-KO and wild-type (WT) male mice. Sensorimotor recovery after SCI was assessed using the horizontal ladder, grasp, and hindlimb mobility tests. Exploratory and anxiety-like behaviors were evaluated using the open field and elevated plus maze tests before and 5 weeks after SCI. : TAAR5-KO mice exhibited accelerated recovery of sensorimotor functions, as assessed by joint mobility and grasping tests, compared to WT animals. In contrast, no significant intergroup differences were found in the Horizontal Regular Ladder test, likely due to the task complexity and an insufficient recovery period. Nevertheless, SCI induced elevated anxiety-like behavior regardless of genotype. : These findings indicate that TAAR5 deficiency exerts a positive modulatory effect on the restoration of specific components of sensorimotor function after SCI. This effect may be mediated through the modulation of dopaminergic neurotransmission and inflammatory processes. The observed beneficial effect of TAAR5 knockout identifies this receptor as a promising target for developing novel therapeutic strategies aimed at improving functional outcomes following spinal cord injury. - Source: PubMed
Publication date: 2026/03/31
Buglinina Anastasiia DRomanyuk Ekaterina AChesnokov Alexander AMilov Sviatoslav IShkorbatova Polina YuPavlova Natalia VKatolikova Nataliia VGainetdinov Raul RKalinina Daria SMusienko Pavel E - Many species use microbiome-derived metabolites as chemosensory cues, yet the chemicals involved and the sensory pathways that detect and process them remain poorly understood. Trimethylamine (TMA) is a volatile metabolite that is produced by the gut microbiome and selectively accumulated in the urine of sexually mature male mice. Here, we show that TMA regulates inter-male aggression and social dominance by activating trace amine-associated receptor 5 (TAAR5) in the main olfactory system. In wild-type mice, early aggressive behavior during male-male encounters strongly predicts eventual social status: dominant males initiate more attacks, whereas subordinate males display more defensive behaviors. Deletion of TAAR5 eliminated this asymmetry, with dominant and subordinate mice showing similar levels of aggressive and defensive behaviors. Strikingly, restoring TAAR5 expression in olfactory sensory neurons (OSNs) rescued the behavioral asymmetry, indicating that this effect is mediated by the main olfactory system and arguing against contributions from proposed TAAR5 expression in the brain. Finally, pharmacological suppression of microbial TMA production reduced inter-male aggression, and this effect was reversed by painting treated males with TMA, showing that microbiome-derived TMA is the key volatile ligand for TAAR5 in this context. Taken together, our findings identify TMA as a critical olfactory cue that signals the presence of sexually mature males and facilitates social hierarchy formation. More broadly, our results demonstrate that a microbiome-derived metabolite can shape mammalian social interactions through the main olfactory system and uncover a previously unrecognized role for the TAAR family in regulating social behavior. - Source: PubMed
Publication date: 2026/03/30
Cichy AnnikaDewan AdamHe ZhuolingFitzgerald CassandraRatkowski MadisonKrasewicz JakubOzarkar VaikhariKaye SarahTeng TiffanyZhang JingjiFeinstein PaulBozza Thomas - Elevated levels of the gut microbe-derived metabolite trimethylamine -oxide (TMAO) are associated with cardiometabolic disease risk. However, the mechanism(s) linking TMAO production to human disease are incompletely understood. Initiation of the metaorganismal TMAO pathway begins when dietary choline and related metabolites are converted to trimethylamine (TMA) by gut bacteria. Gut microbe-derived TMA can then be further oxidized by host flavin-containing monooxygenases to generate TMAO. Previously, we showed that drugs lowering both TMA and TMAO protect mice against obesity via rewiring of host circadian rhythms (Schugar et al., 2022). Although most mechanistic studies in the literature have focused on the metabolic end product TMAO, here we have instead tested whether the primary metabolite TMA alters host metabolic homeostasis and circadian rhythms via trace amine-associated receptor 5 (TAAR5). Remarkably, mice lacking the host TMA receptor () have altered circadian rhythms in gene expression, metabolic hormones, gut microbiome composition, and diverse behaviors. Also, mice genetically lacking bacterial TMA production or host TMA oxidation have altered circadian rhythms. These results provide new insights into diet-microbe-host interactions relevant to cardiometabolic disease and implicate gut bacterial production of TMA and the host receptor that senses TMA (TAAR5) in the physiologic regulation of circadian rhythms in mice. - Source: PubMed
Publication date: 2026/01/29
Mahen Kala KMassey William JOrabi DannyBrown Amanda LJaramillo Thomas CBurrows AmyHorak Anthony JDutta SumitaMrdjen MarkoMouannes NourVaradharajan VenkateshwariOsborn Lucas JYe XiayanYarbrough Dante MGrubb TregZajczenko NatalieHohe RachelBanerjee RakheeLinga PranaviLaungani DevHajjar Adeline MSangwan NaseerDwidar MohammedBuffa Jennifer ASwanson Garth RWang ZenengBrown Jonathan Mark - Recent studies indicated a connection between trace amine-associated receptor 5 (TAAR5) and emotional behaviors related to anxiety and depression; however, the neurobiological basis of this link is still unclear. Using mutant TAAR5 knockout (TAAR5-KO) mice, we explored the consequences of receptor deletion on dopamine (DA) dynamics in the ventral striatum and stress-related behaviors. Voltammetric measurements of DA in the nucleus accumbens (NAc) coupled with electrical stimulation of the ventral tegmental area (VTA) revealed that mice lacking TAAR5 display a greater DA release, while its reuptake is not affected. Behaviorally, mutants were significantly less anxious in the elevated plus maze (EPM) and consumed more sucrose in comparison with wild-type (WT) controls. The new object recognition test (NOR) did not uncover a difference between these genotypes. During predator (rat) stress exposure, mutant and WT mice showed quite distinct responses versus the behavior observed in stressless conditions. Control animals demonstrated a substantial increase in "freezing" (a sign of passive coping), while "running" and "exploring" patterns (signs of active coping) were significantly extended in mice lacking TAAR5. Short-term consequences of stress were explored 24 h following the predator exposure. The absence of TAAR5 did not prevent or reduce stress-induced anxiety in the EPM. In fact, the level of anxiety in mutants reached that observed in control mice. Furthermore, activity in NOR was significantly decreased in mice lacking TAAR5 but not in WT animals. On the other hand, predator exposure resulted in impaired NOR in the WT control, whereas mutants' performance was not altered. These findings indicate that TAAR5 deletion leads to significant DA imbalance, which might at least partly explain the better stress-coping strategy and other stress-induced behavioral consequences observed in mutant animals. - Source: PubMed
Publication date: 2025/12/25
Nemets Vsevolod VGrinevich Vladimir PPetrunina Evgeniia NBudygin Evgeny AGainetdinov Raul R - Despite their association with brain disorders, the neurophysiological roles of the trace amine-associated receptors remain poorly understood. In humans, the genomic cluster comprises nine consecutive genes, six of which code for functional proteins (TAAR1, TAAR2, TAAR5, TAAR6, TAAR8, TAAR9). While homologues of the former three are known to regulate classical monoamines and neurogenesis, the functions of the latter three remain largely unknown. In this exploratory study, we demonstrate for the first time that TAAR9 plays a significant regulatory role in the monoaminergic systems of the rat. - Source: PubMed
Publication date: 2025/11/12
Zhukov Ilya SKarpova Inessa VMurtazina Ramilya ZAlnefeesi YazenKorenkova Olga MTissen Ilia YuPalchikova Svetlana ATokareva Lydia APyurveev Sarng SShabanov Petr DKubarskaya Larisa GRozhko Mikhail AZernova Ekaterina BZolotoverkhaja Ekaterina AVolnova Anna BKalueff Allan VAlenina Natalia VGainetdinov Raul R