TY  - GEN
T1  - GABA Receptor mutant gbb-1 accelerates morphological aging of GABA neurons in Caenorhabditis elegans
AU  - Dhillon, I.
AU  - Momin, A.
AU  - Chin-Sang, I.
DO  - 10.17912/D7E5-WJ67
UR  - http://beta.micropublication.org/journals/biology/d7e5-wj67/
AB  - The aging of an organism is heterogeneous, that is to say, tissues and organs may age at unique rates compared to overall organism longevity. Inhibition of the insulin/insulin-like growth factor signaling (IIS), such as the daf-2 IIS receptor increases Caenorhabditis elegans longevity. The daf-2 pathway plays a key role in the regulation of metabolism and stress responses and as such, impacts the longevity of the organism (Uno and Nishida 2016). Evidence suggests that an increase in insulin signaling results in a reduction in overall lifespan and a decrease in neuronal longevity (Kenyon 2010). Recently, the gbb-1 GABA signaling pathway has also been implicated in the regulation of adult longevity (Chun et al. 2015). The GABAergic motor neurons innervate the dorsal and ventral body muscles controlling locomotion, foraging and defecation of the animal. GABA, an inhibitory neurotransmitter, has been found to decrease the lifespan of the nematodes (Chun et al. 2015), however, its role in neuronal aging has yet to be determined. The formation of ectopic neurite branches and production of axonal beads are two known phenotypes of neuronal aging in C. elegans. In this study, we examined the aging of the GABAergic motor neuron nerve cords and dorsal commissures.
PY  - 2018
JO  - microPublication Biology
ER  -