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Annely Haase

Publications and source records attributed to Annely Haase.

2 recordsLinked to original sources

Cellular expression patterns of acetylcholinesterase activity during grasshopper development.

We examined the expression of acetylcholinesterase (AChE) in the nervous system and epidermal body structures during embryonic and larval development of two grasshopper species: Locusta migratoria and Schistocerca americana. Histochemical labelling was blocked by the enzyme inhibitors eserine and BW284c51, but not by iso-OMPA, showing that the staining reflected true AChE activity. The majority of staining was localized on the cell surface but granular intracellular staining was also visible in many cell bodies. In both species, the cellular expression of AChE followed a similar but complex spatiotemporal staining pattern. Initially, mainly epidermal tissue structures were stained in the various body appendages (stages 25%-30%). Labelling subsequently appeared in outgrowing neurons of the central nervous system (CNS) and in the nerves innervating the limbs and dorsal body wall (stages 30%-40%). The latter staining originated in motoneurons of the ventral nerve cord. In a third phase (after 45%), the somata of certain identified mechanosensory neurons started to express AChE activity, presumably reflecting cholinergic differentiation. Staining was also found in repo-positive glial cells of the CNS, longitudinal glia of connectives, glia of the stomatogastric nervous system and glial cells ensheathing peripheral nerves. Glial cells remained AChE-positive during larval to adult development, whereas motoneurons lost their AChE expression. The expression pattern in non-neuronal cells and glutamatergic motoneurons and the developmental appearance of AChE prior to synaptogenesis in the CNS suggest non-cholinergic functions of AChE during grasshopper embryogenesis.

Acetylcholinesterase↗

Nitric oxide and cyclic nucleotides are regulators of neuronal migration in an insect embryo.

The dynamic regulation of nitric oxide synthase (NOS) activity and cGMP levels suggests a functional role in the development of nervous systems. We report evidence for a key role of the NO/cGMP signalling cascade on migration of postmitotic neurons in the enteric nervous system of the embryonic grasshopper. During embryonic development, a population of enteric neurons migrates several hundred micrometers on the surface of the midgut. These midgut neurons (MG neurons) exhibit nitric oxide-induced cGMP-immunoreactivity coinciding with the migratory phase. Using a histochemical marker for NOS, we identified potential sources of NO in subsets of the midgut cells below the migrating MG neurons. Pharmacological inhibition of endogenous NOS, soluble guanylyl cyclase (sGC) and protein kinase G (PKG) activity in whole embryo culture significantly blocks MG neuron migration. This pharmacological inhibition can be rescued by supplementing with protoporphyrin IX free acid, an activator of sGC, and membrane-permeant cGMP, indicating that NO/cGMP signalling is essential for MG neuron migration. Conversely, the stimulation of the cAMP/protein kinase A signalling cascade results in an inhibition of cell migration. Activation of either the cGMP or the cAMP cascade influences the cellular distribution of F-actin in neuronal somata in a complementary fashion. The cytochemical stainings and experimental manipulations of cyclic nucleotide levels provide clear evidence that NO/cGMP/PKG signalling is permissive for MG neuron migration, whereas the cAMP/PKA cascade may be a negative regulator. These findings reveal an accessible invertebrate model in which the role of the NO and cyclic nucleotide signalling in neuronal migration can be analyzed in a natural setting.

Actins↗