GDNF family receptor α-1 in catfish: Possible implication to brain dopaminergic activity

Advances in Reproductive Endocrinology and Neuroendocrine Research Using Catfish Models

“…Neurotoxicity studies are important to identify promising neuroprotective agents for example, ascorbic acid for Al-induced neurotoxicity which was demonstrated using C. gariepinus [ 102 ]. In line with this, Mamta and Senthilkumaran [ 67 ] used 1-methyl-1,2,3,6-tetrahydropyridine (MPTP), to demonstrate the interaction of GDNF and DA-ergic system in catfish brain. In addition, controlled release of sex steroids using osmotic pump altered brain GnRH1 and CA-ergic system dimorphically in the African catfish providing insights into the reproductive toxicity of sex steroid analogues during gonadal recrudescence [ 103 ].…”

“…In the Indian stinging catfish, high temperature decreases DA activity and increases NA activity, which is a stimulatory signal for GTH-II [ 57 ]. Mamta and Senthilkumaran [ 67 ] demonstrated gfrα-1 plausibly entrains GnRH-GTH either directly or indirectly, by partially targeting CA-ergic activity. In addition, another study in catfish demonstrated catecholestrogens (CE) related enzymatic changes in during GnRH analogue-induced ovulation and suggesting E 2 modulation of catechol- O -methyltransferase (COMT) activity [ 68 ].…”

“…In many animal models including catfish, RNA knockdown can be achieved more feasibly using siRNA, shRNA or esiRNA. In this line, in vivo and in vitro transient gene silencing using PEI mediated siRNA/shRNA/esiRNA has been standardized and well established at tissue and cellular levels in gonads and brain as well as at animal level in our laboratory using various fish models including catfish [ 67 , 85 , 136 , 165 , 188 , 220 , 221 ] to functionally characterize many important factors related to teleostean reproduction. In addition, Senthilkumaran [ 168 ] compared mammalian and piscine oocyte maturation with a note on sperm maturation citing the involvement of hsd20b vis-à-vis 17α,20β-DP in addition to T and 11-KT [ 140 , 222 ].…”

Implicating transforming growth factor-β and sex steroids in the regulation of brain-gonadal functions

“…[29] Based on this premise, it is worthwhile to investigate the impact of Tgf-β and the modulatory action of a brain-pituitary-gonadal axis. The earlier report investigated Tgf-β as a vital molecule that regulates the survival of neurons synergistically with neurotrophic factors GDNF, BDNF, neurotrophin, and neuropeptides [6,30] in turn, these factors regulate the release of active TGF also modulation of Leydig cell steroidogenesis with androgenic steroids. Our recent finding revealed that the prominent Tgf-β mRNA and protein expression appear to propose a significant impact on growth factor signaling at the level of the brain.…”

“…[4] A previous study reported the neuroprotective effects of Tgf-β, receptors (1-3), activin A, and GDNF for DA-ergic neurons in vitro, protein expression increases the survival of Th-immunoreactive DA-ergic in mice and catfish. [5,6] Tgf-β is an essential growth factor involved in various functions, that is, apoptosis, sex differentiation, cellular proliferation, and growth also act as a paracrine factor which plays key roles in gonadal functions [7] such as stimulation of follicular development and steroid hormone 17β-estradiol (E2) and androgen (T) production in mammals. [8] In rainbow trout, Tgf-β stimulates the proliferation of spermatogonial and primordial germ cells [9] and prevents the maturation of oocytes in zebrafish.…”