The reproductive biology of Calanus finmarchjcus was investigated at a permanent station in the Norwegian Sea (Weathership Stn M, 66" N, 2" E) during a time series between March and June 1997 The temporal development of female abundance, egg production rate and gonad development stage in relation to the phytoplankton production cycle is described Abundance of females, copepodite stage 5 and males as well as female gonad morphology were examlned from MrP2 net samples taken daily from the upper 100 m. Daily egg production rate and number of spawn.ing females we]-e determined from 50 individual females placed in multiwells or beakers. Once a week a multinet haul from 1000-500-250-100-50-0 m was performed to study the depth d~stribution of females and gonad development stages. Results show that the reproductive period of C. finmarchicusin the Atlantic rcqion of the Norwegian Sea can be subdivided in 3 periods in relation to phytoplankton devrlopmt,nt.(1) During the prebloom over a period of 49 d mean egg production rate was 8 eggs female-' d ' and an average of 47 of the females were mature. (2) Coincident with the bloom in mid May the e g g production rate increased up to a maximum of 44 eggs female-' d-' while more than 80% of the females were mature. (3) After the bloom at the beginning of June, egg production decreased, and mature females were only rarely found. Feedlng expenments indicate that food quantity limited egg production prior to the bloom, while presumably food quality was not sufficient dunng postbloom. However, due to high female abundance the total population egg production prior to the bloom was the same as during the bloom. This implies that the reproduction of C. finmarchicus in the Norwegian Sea is to some extent decoupled from the phytoplankton bloom.

The feeding ecology of Calanus finmarchicus was investigated during spring 1997 at a permanent station in the Norwegian Sea (Stn M, 66"N, 2"E) as part of the TASC (Trans Atlantic Study of Calanus finmarchicus) project time-series investigations. The phytoplankton bloom began in mid May, coinciding m t h the onset of the stratification, and was mainly composed of d~atoms and prymnesiophytes. Daily Ingestion of phytoplankton by C. finmarchicus was about 2% of body carbon for the long period before the bloom, 30% during the bloom and 14 % after the bloom. Due to their low abundance, ingestion of ciliates represented only 2 to 6 O/o of the phytoplankton ingestion. Body carbon and carbon/nitrogen ratio decreased significantly before the bloom indicating a deficit in carbon ingestion and the use of storage lipid during this period.

No abstract

Neuropeptide Y (NPY), a member of the pancreatic polypeptide family, is an orexigenic hormone. GnRH-1 neurons express NPY receptors. This suggests a direct link between metabolic function and reproduction. However, the effect of NPY on GnRH-1 cells has been variable, dependent on metabolic and reproductive status of the animal. This study circumvents these issues by examining the role of NPY on GnRH-1 neuronal activity in an explant model that is based on the extra-central nervous system origin of GnRH-1 neurons. These prenatal GnRH-1 neurons express many receptors found in GnRH-1 neurons in the brain and use similar transduction pathways. In addition, these GnRH-1 cells exhibit spontaneous and ligand-induced oscillations in intracellular calcium as well as pulsatile calcium-controlled GnRH-1 release. Single-cell PCR determined that prenatal GnRH-1 neurons express the G protein-coupled Y1 receptor (Y1R). To address the influence of NPY on GnRH-1 neuronal activity, calcium imaging was used to monitor individual and population dynamics. NPY treatment, mimicked with Y1R agonist, significantly decreased the number of calcium peaks per minute in GnRH-1 neurons and was prevented by a Y1R antagonist. Pertussis toxin blocked the effect of NPY on GnRH-1 neuronal activity, indicating the coupling of Y1R to inhibitory G protein. The NPY-induced inhibition was independent of the adenylate cyclase pathway but mediated by the activation of G protein-coupled inwardly rectifying potassium channels. These results indicate that at an early developmental stage, GnRH-1 neuronal activity can be directly inhibited by NPY via its Y1R.