No coin nor oath required. For personal study only.
Insect flight is one of the most energy-demanding processes in the animal kingdom. Migratory locusts, such as Locusta migratoria are able to perform long lasting flights. At the onset of flight, a cascade of metabolic events takes place, resulting in the mobilization of lipids. This mobilization is under the control of adipokinetic hormones (AKHs). These are synthesized and released by the adipokinetic cells in the corpus cardiacum, a small organ connected to the cerebral ganglion by two paired nerves, the nervi corporis cardiaci I and II (NCC I and II). Neurons in the lateral part of the protocerebrum, axons of which run through the NCC II, make direct synaptic contact with the adipokinetic cells. Electrical stimulation of the NCC II in vitro results in an elevation of the cAMP content in the adipokinetic cells and in the release of adipokinetic hormones. The question arises with regard to the identity of the neurotransmitter functioning at the synaptic contact between the NCC I1 axons and the adipokinetic cells. Immunocytochemical studies suggest a role for Locusta-tachykinin I (LomTK I). To find out whether LomTK I effects the release of AKH I, in vitro incubations were carried out. Corpora cardiaca (CC) were excised and incubated in pools of five CC in a physiological buffer. Following incubation, the CC were incubated for another 30 min in buffer to which LomTK I was added. It appeared that LomTK I had a dosedependent effect on the release of AKH. The maximal response was reached at 75 gM LomTK i. The immunocytochemical and physiological results strongly support the hypothesis that LomTK I is involved as a neurotransmitter in the regulation of adipokinetic hormone release.
π SIMILAR VOLUMES