Background Scallops are among the best-studied bivalve mollusks. However, adult nervous system and neurogenesis studies of scallops are limited. Here, we studied the localization of neurotransmitters (serotonin/5-HT, FMRFamide, catecholamines) in adult ganglia and larvae of Azumapecten farreri using histochemical and immunohistochemical methods. Results We found peptide FMRFamide in all adult scallop ganglia, whereas 5-HT-like immunoreactive (lir) somata were exclusively detected in the cerebropleural, pedal, and accessory ganglia. Scallop larval neurogenesis starts with the emergence of the 5-HT-lir neurons, which are part of the apical organ (AO) at the early veliger stage. Near the AO, paired anlagen of cerebral ganglion (CG) developed. 5-HT-lir neurites of the CG innervate the velum, ventral, and dorsal parts of the larva at the late veliger stage. Scallop pediveligers possess 5-HT-lir CG, pleural ganglia, and immunopositive signals in the developing enteric nervous system. FMRFamide-lir is first detected in dorsal, ventral, and AO cells of early veligers. Later, FMRFamide-lir extends to the visceral nervous cord, all ganglia, as well as in the enteric nervous system in pediveligers. Catecholaminergic neurons are detected near the larval mouth, in the vellum, and in the stomach in veligers. Conclusions We described the distribution of neurotransmitters of the ganglia in adult scallops and the larval neurodevelopment in A. farreri. Immunostaining of neurotransmitters showed that the gross anatomy of adult scallop ganglia, in general, is similar to that in other bivalves, but complicated by the complexity of the structure of the ganglia and the appearance of additional ganglia not described in other molluscs. A comparison of larval neuromorphology suggests that 5-HT-lir structures are more conservative than FMRF-lir structures in Bivalvia. Notably, the latter are much more distributed in scallop A. farreri larvae than in other studied bivalves.
Sleep–wake cycle disorders are an important symptom of many neurological diseases, including Parkinson’s disease, Alzheimer’s disease, and multiple sclerosis. Circadian rhythms and sleep–wake cycles play a key role in maintaining the health of organisms. To date, these processes are still poorly understood and, therefore, need more detailed elucidation. The sleep process has been extensively studied in vertebrates, such as mammals and, to a lesser extent, in invertebrates. A complex, multi-step interaction of homeostatic processes and neurotransmitters provides the sleep–wake cycle. Many other regulatory molecules are also involved in the cycle regulation, but their functions remain largely unclear. One of these signaling systems is epidermal growth factor receptor (EGFR), which regulates the activity of neurons in the modulation of the sleep–wake cycle in vertebrates. We have evaluated the possible role of the EGFR signaling pathway in the molecular regulation of sleep. Understanding the molecular mechanisms that underlie sleep–wake regulation will provide critical insight into the fundamental regulatory functions of the brain. New findings of sleep-regulatory pathways may provide new drug targets and approaches for the treatment of sleep-related diseases.
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