Neuroendocrine system of Crustaceans and Reproduction

Endocrine system of decapoda The crustacean endocrine system, like that of other higher invertebrates, has neurosecretory cells and some classical endocrine glands. The following are the principal endocrine areas. The eye stalk contains a number of, so called, Xorgans including medulla externa (me), sensory pore, medulla interna (mi), and medulla terminalis (mt)

 and the neurohemal organ, the sinus gland (sg). Axons from neurosecretory cells in the brain and other parts of the nervous system pass to the sinus gland via a neurosecretory tract. The postcommisural organs receive axons from 4 neurosecretory cells in each side of the circumesophageal connectives: only one is shown on the left side.

 The pericardeal organs are located over openings of branchiocardiac veins into the aorta: Numerous nerves run from the nervous system to the organs. The dorsal nerve of the heart (n. dors) and nerves to muscles (n. mot) are also shown. The androgenic gland often is a vermiform mass of secretory cells attached to the distal portion of vas deferens. The ovaries secrete female sex steroids in many species.

 The generalized neurosecretory system (except the eyestalk) consist of cerebral neurosecretory cells (ns 1-5) and thoracic ganglia neurosecretory cells. Axons of neurosecretory cells in all parts of the brain pass to the sinus gland, but only axons from ganglionic neurosecretory cells pass out through the pedal nerves. The Y-organ is an endocrine gland without innervation; it is an ovoid disk of hypertrophied epidermis, which secretes molting hormone.

Molting cycle
Molting, that is the periodic shedding of the exoskeleton, is under endocrine regulation in crustaceans as well as in other arthropods. The event of exoskeleton shedding is termed, ecdysis, and names of the other phases in the molt cycle relate to ecdysis. Thus, the molt period starts with the proecdysis, which leads into the ecdysis. The period immediately following ecdysis is called metecdysis, and periods between molts are called anecdysis.

 During proecdysis, the epidermis starts to separate from the old cuticule (exoskeleton) and the epidermal cells enlarge and begin to secrete the new exoskeleton. Minerals and macromolecules are reabsorbed from the old exoskeleton and temporarily stored elsewhere for later incorporation into the new exoskeleton. Amino acids are stored in the hemolymph, while Ca is deposited at various locations depending on species.

 The muscles of the major limb segments atrophy during proecdysis so that the limbs can be pulled out through the narrow basal segment at ecdysis. Regeneration of lost limbs also begins during proecdysis. At ecdysis, the old exoskeleton cracks open, typically in the rear end, and the animal backs out of the old shell. When newly emerged, the new exoskeleton is pale and soft.

 In many species the molted animal eats the old exoskeleton to regain some of the minerals and other nutrients. During metecdysis, Ca and other components are laid down in the new exoskeleton and the limb muscles grow.

Ecdysone in lobster
Molting in crustaceans is induced by the steroid, 20-hydroxyecdysone, which is produced and released as a precursor from the Y-gland,the concentration of 20-hydroxyecdysone in hemolymph of a lobster during the molt cycle. The molting event, or ecdysis, is indicated by an M. The peak in 20-hydroxyecdysone occurs just prior to the molt.

 There is however more to the story, because 20-OH ecdysone is not the only hormone controlling molting. Already in 1905 there was a paper reporting that bilateral ablation of the eyestalks of crabs accelerated the molting cycle. an eyestalk ablation experiment with lobster. Again, 20-hydroxyecdysone concentrations in hemolymph were measured during the molting cycle.

 One of the groups, ablation substantially reduced the lag before the 20hydroxyecdysone peak and thereby also the time to molt. The net effect of eyestalk ablation is pretty dramatic. This picture shows two lobster siblings. The larger animal was bilaterally eyestalk ablated at the 2nd larval stage and then kept under identical conditions during 5 months.

 The explanation for this dramatic effects is that ecdysone release from the Y-gland is under negative control of a peptide hormone, moltinhibiting hormone (MIH), which is released from the sinus gland of the eyestalk. MIH is a protein with a molecular weight of 7000-9000, depending on species. MIH release, in turn, is stimulated by a neurotransmitter, 5-HT. Exactly how the periodicity of molting is regulated seems to be a matter of current research.

Reproduction
Already in 1943 it was demonstrated that the sinus gland is involved in reproductive regulation as well. In a classic experiment, Panouse showed that eyestalk ablation from prawn females leads to rapid increase in ovarian size and to precocious egg deposition.

 It was further demonstrated that an ovarianinhibiting factor was released by the sinus gland. The factor is now known to be a peptide hormone with a MW of 7,000 8,000, and it is generally called, gonad-inhibiting hormone (GIH). The sinus gland is the GIH-releasing organ, but the source of this neurohormone is the medulla terminalis (mt) X-organ.

 In females, the GIH level in the plasma varies during the course of the annual reproduction cycle and ovary development is stimulated when the GIH concentration of the hemolymph is low. In many species, sexual maturation and molt cycle is synchronous. In such species, follicle growth and oocyte development appear to be related not only to the absence of GIH but also to the low levels of 20-OH ecdysone present at the beginning of each molt cycle.

Vitellogenesis
In all oviparous species that have been investigated, the yolk of the egg is not produced in the follicle itself but elsewhere in the body and is transported to the oocyte. The yolk protein is called vitellogenin (VTG) in arthropods and well as in chordates. The process of vitellogenin production and its subsequent transport to and uptake by oocytes is collectively called vitellogenesis.

 In crustaceans, VTG synthesis occurs in an organ, called the fat body, and possibly at other sites as well. VTG is transported in the hemolymph to the ovaries where the protein is incorporated into the oocytes. The follicle cells that surround the oocyte have an extensive tubular network through which the VTG molecules can pass. Uptake of VTG in the oocyte occurs by means of receptor mediated endocytosis.

 There seems to be two targets for GIH: (1) Inhibition of VTG synthesis, and (2) binding of VTG to the membrane receptors on the oocyte. When the level of GIH in the hemolymph goes down the vitellogenesis can proceed, which leads to maturation of the follicle.

Endocrine control of Reproduction

In insects sexual differentiation is by genetic mechanism. But in Crustacea both sexual differentiation and gonadal activity are influenced byhormones situation resembling as in vertebrates. Most of Malacostraca are unisexual only few groups show protandric hermaphroditism. In these Crustacea sex is determined genetically but morphological and functional expression of sex is very much influenced by hormones.

 At the time of hatching/ at the end of larval periodindistinguishable with reference to sexes. During successive molt sexual differentiation commences but only completes after gonadal maturity. Sexual dimorphismPenis in male and oostegites in female. In undifferentiated young crustacean primordial of vasdeference are present in both the sexes. Attached near each vasdeference is androgenic gland. In genetic female androgenic gland fail to develop but in the male the glands enlarge to form a solid strand of cells.

 Androgenic gland secrets male hormone. Young male ----------Remove Androgenic gland----- instead of spermatocytes-----oocyte development commences