- DCAR-1; seven transmembrane receptor for dihydrocaffeic acid (a water-soluble repellent)
- DOP-4; (D1-like) dopamine receptor
- NPR-1; receptor for flp-18- and flp-21-encoded peptides
- OCTR-1; octopamine receptor
- OCR-2; TRPV (transient receptor potential channel, vanilloid subfamily; mammalian capsaicin receptor-like channel)
- OSM-9; TRPV (transient receptor potential channel, vanilloid subfamily; mammalian capsaicin receptor-like channel)-cation selective. Among "thermoTRPs" (TRPA, TRPM, TRPV)
- SER-3; octopamine receptor
- SER-5; serotonin receptor (5-HT6R-like)
- SRA-6; G protein-coupled seven transmembrane receptor
- SRB-6; G protein-coupled seven transmembrane receptor
- TMC-1; Na+-sensitive ion channel required for salt taste chemosensation and high salt avoidance behavior
- TRPA-1; transient receptor potential ion channel
- TYRA-2; tyramine receptor
- UNC-8; mechanically gated ion channel subunit; amiloride-sensitive Na+ channel (ASC) protein (DEG/ENaC subunit)
(Wormbase; Chatzigeorgiou et al., 2013; Altun, 2011; Ezcurra et al, 2011; Aoki et al., 2011; Tobin et al., 2002; Coates and de Bono , 2002; de Bono M. et al., 2002; Tavernarakis et al., 1997; Troemel et al., 1995)
- ASH is the main nociceptor and leads to avoidance responses from noxious stimuli, which include hyperosmolarity, nose touch, volatile repellent chemicals (1-octanol), heavy metals (Cd++ and Cu++), detergents/SDS, protons, high salt and alkaloids, such as quinine. There is stimulus-specific downstream signaling in ASH; a mutation in the glutamate receptor subunit, glr-1 which acts in synaptic targets of the ASH neurons, eliminates the response to nose touch but not to osmotic repellents. Similarly, ITR-1 (inositol 1,4,5-trisphosphate receptor) functions in nose touch- and benzaldehyde-avoidance but not in other known ASH-mediated avoidance behaviors. ASH-mediated aversive responses are modulated by monoamines and peptides. Receptors for 5-HT (SER-5), DA (DOP-3, DOP-4), and OA (OCTR-1, SER-3) appear to function directly in the ASH neurons for these effects. Food or 5-HT enhances a subset of ASH-mediated aversive responses (to nose touch, but not to soluble repellants, e.g.) Similarly, DA enhances aversive responses via DOP-4 on ASH, while TA and OA delay or inhibit these reponses through distinct subsets of TA and OA receptors. Inhibition by TA and OA requires the release of multiple neuropeptides from a number of additional neurons. These neuropeptides activate peptide receptors within the ASH-mediated circuit itself and on sensory neurons outside the circuit, suggesting these monoamine-initiated peptidergic signaling cascades can have global effects.
(Chatzigeorgiou et al., 2013; Ezcurra et al., 2011; Komuniecki et al., 2011; Walker et al, 2009; Bargmann, 2006; de Bono & Villu Maricq, 2005; Hilliard et al, 2004; Hiliard et al., 2002; Hart et al., 1999; Sambongi et al., 2000; Sambongi et al., 1999; Troemel et al., 1995; Bargmann et al, 1990; Culotti & Russell 1978).
- Lightsensation (350-470 nm range); when a flash of light is focused on the head of a worm moving forward, the animal halts and initiates reversals. Ablation of ASJ, AWB, ASK and ASH neurons together leads to a severe deficit in this head avoidance response while ablation of them individually or in different combinations does not yiled a significant defect suggesting functional redundancy
(Ward et al., 2008).
- Electrosensory navigation; C. elegans moves toward the negative pole of an electric field. Killing the ASJ or ASH neurons leads to significant disruption in electrotaxis while killing ASK, AWB or AWC has a weaker effect (Gabel et al., 2007).
- ASH and ADL are proposed to mediate social feeding behavior in response to repulsive cues (e.g. high O2 levels); ablation of ASH and ADL abolishes social feeding behavior transforming social animals to solitary feeders; avoidance of high O2 levels that facilitate aggregation is promoted by OCR-2 and OSM-9, and the transmembrane protein ODR-4, acting in the nociceptive neurons ASH and ADL. ASH and ADL, in turn, transmit information about aversive stimuli in the environment to a circuit that is responsible for aggregation, rapid locomotion, and food bordering behavior (Rogers et al., 2006; de Bono et al., 2002).
- Modulates innate immune response to pathogenic bacteria. ASH, ASI, AQR, PQR, and URX neurons control the unfolded protein response (UPR) and a p38 mitogen-activated protein kinase signaling pathway required for innate immunity (Singh & Aballay, 2012.) Loss of OCTR-1 signaling in ASH and ASI increases the general immune function of the nematodes; OCTR-1 functions in these neurons to actively suppress innate immune responses by down-regulating the expression of noncanonical UPR genes in nonneuronal tissues (Sun et al., 2011s)
- Plays role in establishment of asymmetric fates of AWCL/R neurons during development via NSY-5/INX-19 gap junctions (Schumacher et al., 2012.)