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unknown, and further studies will be necessary to elucidate its mode of
action.
Thus, declining levels of ecdysteroid and an increase in dopamine
released from nerve endings in the CA act together to shut down JH
biosynthesis by the CA after the last larval ecdysis (
Fig. 3.3
A). These factors
apparently target different steps on the JH biosynthetic pathway to ensure
the cessation of JH synthesis, allowing the initiation of metamorphosis.
2.3.2 Glutamate
The neurotransmitter glutamate has been shown to affect JH biosynthesis in
the cockroach,
Diploptera punctata
(
Pszczolkowski, Lee, Liu, & Chiang,
1999
). Glutamate causes an increase in cytosolic calcium concentration in
CA cells, which stimulates JH synthesis. Glutamate has also been shown
to stimulate JH synthesis in
Drosophila
larvae (
Huang et al., 2011
), and the
molecular mechanisms of this effect on JH synthesis have been studied well.
Glutamate is the natural stimulatory ligand of the
N
-methyl-
D
-aspartate
(NMDA) subtype of glutamate receptor, and in
Drosophila
a mutation of this
receptor influences JH biosynthesis; the expression of the regulatory gene
Decapentaplegic
(
Dpp
) and the JH biosynthetic enzyme gene
JHAMT
declines. In addition, a mutant of the gene
Mothers against decapentaplegic
(
mad
), which is located downstream of Dpp in the pathway that regulates
the transforming growth factor beta (TGF-
b
) receptor signaling pathway,
decreased
JHAMT
expression so that JH biosynthesis declined. Based on
these results, it is suggested that glutamate produced by the brain binds to
NMDA receptors in CA cells to induce
Dpp
expression, in turn activating
the TGF-
b
pathway, which enhances
JHAMT
expression. As a result, JH
biosynthesis is activated. It is not known whether this signaling pathway
is involved in the control of JH synthesis in other insect species, including
Bombyx
.
(C) Dose-dependent inhibition of JH synthesis. CC
-
CA complexes of day 0 fifth in-
star larvae were cultured with various concentrations of dopamine for 6 h followed
by the determination of JH synthetic activity (N¼3
-
4, SE). Ratio was calculated as
in (B). (D) Prevention of the inhibitory action of dopamine by a dopamine D1 re-
ceptor antagonist. CC
-
CA complexes from day 0 fifth instar larvae were cultured
with or without 0.1
m
M antagonist, R(þ)-SCH23390, and 100
m
M dopamine for 6 h
and then determined the JH synthetic activity (N¼3, SE). Ratio was calculated
as in (B). (E) Fluctuation of the mRNAs of two isoforms of dopamine D1 receptors,
BmDopR1 and BmDopR2,
in the CA during development (N¼3, SD).
