Crypt cells of the zebrafish Danio rerio mainly project to the dorsomedial glomerular field of the olfactory bulb.
ABSTRACT The olfactory mucosa of the zebrafish consists of 3 morphological types of olfactory receptor neurons (ORNs): ciliated, microvillous, and crypt cells. Previous studies in the zebrafish have revealed differential projections of ciliated and microvillous ORNs, which project to different glomerular fields. However, the bulbar targets of zebrafish crypt cells were not identified. Here, we analyze the relationship between crypt cells of the olfactory epithelium and dorsal glomerular fields of the zebrafish olfactory bulbs, as wells as the connections between these bulbar regions and forebrain regions. For this purpose, a lipophilic carbocyanine tracer (DiI) was used in fixed tissue. Application of DiI to the dorsomedial glomerular field mainly labeled crypt cells in the zebrafish olfactory epithelium. By contrast, application of DiI to the dorsolateral glomerular fields mainly labeled bipolar ORNs and only occasionally crypt cells. Bulbar efferent cells (mitral cells) contacting these dorsal glomerular fields project to different telencephalic areas, with the posterior zone of the dorsal telencephalic area (Dp) as the common target. However, dorsomedial and dorsolateral glomerular fields projected differentially to the ventral telencephalon, the former projecting to the ventrolateral supracommissural region. Retrograde labeling from the ventrolateral supracommissural region revealed mitral cells associated with 2 large glomeruli in the bulbar dorsomedial region, which putatively receives inputs from the crypt cells, indicating the existence of a crypt cell olfactory subsystem with separate projections, in the zebrafish. The comparative significance of the secondary olfactory pathways of zebrafish that convey information from crypt cells is discussed.
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- "In this latter species, acute treatment with fluoxetine (10 mg/kg) reverts the locomotoryinhibiting effect of exposure to CAS (Barbosa et al., 2012). In the crucian carp, Schrecksreaktion is in part mediated by structures which receive primary and secondary olfactory projections which are conducted by the medial bundle of the medial olfactory tract (Hamdani et al., 2000; Døving and Lastein, 2009); in zebrafish, these projections integrate into a circuit of amygdala-like structures in the telencephalon, as well as hypothalamic structures (Gayoso et al., 2011, 2012). Serotonergic innervation of such structures has been described in zebrafish (Kaslin and Panula, 2001; Lillesaar et al., 2009), as well as monoamine oxidase activity and immunoreactivity (Anichtchik et al., 2006), the presence of 5-HT 1A -like, 5-HT 1B and 5-HT 2C receptors (Norton et al., 2008; Schneider et al., 2012), and serotonin transporters (Norton et al., 2008). "
ABSTRACT: Alarm reactions to a substance secreted by the damaged skin of conspecifics and closely-related species are increasingly being recognized as fear-like responses in fish. The neurochemical underpinnings of these effects are so far unknown; however, given the role of the serotonergic system on defensive behavior, it is possible that the alarm reaction is mediated by this monoamine. Exposure to conspecific alarm substance (CAS) increased anxiety-like behavior in the light/dark test in zebrafish and decreased nocifensive behavior. These effects were accompanied by increases in blood glucose, hemoglobin, epinephrine and norepinephrine levels, as well as extracellular levels of serotonin in the brain. Pretreatment with fluoxetine blocked the anxiogenic effects of CAS on the light/dark test as well as all physiological parameters and the increase in extracellular brain 5-HT, but not the reduction in nocifensive behavior. Conversely, pretreatment with the 5-HT1AR antagonist WAY 100635 blocked the effects on nocifensive behavior, but not the effects on anxiety-like behavior nor on physiological parameters. These results point to an important and complex role of the serotonergic system in the mediation of fear-potentiated behavior in the light/dark test and in fear-induced analgesia in zebrafish.Pharmacology Biochemistry and Behavior 09/2014; DOI:10.1016/j.pbb.2014.07.003 · 2.82 Impact Factor
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ABSTRACT: The ability to detect and avoid predators is essential to survival. Various animals, from sea urchins to damselfly larvae, use injury of conspecifics to infer the presence of predators. In many fish, skin damage causes the release of chemicals that elicit escape and fear in members of the shoal. The chemical nature of the alarm substance ("Schreckstoff" in German), the neural circuits mediating the complex response, and the evolutionary origins of a signal with little obvious benefit to the sender, are unresolved. To address these questions, we use biochemical fractionation to molecularly characterize Schreckstoff. Although hypoxanthine-3 N-oxide has been proposed to be the alarm substance, it has not been reliably detected in the skin and there may be other active components. We show that the alarm substance is a mixture that includes the glycosaminoglycan (GAG) chondroitin. Purified chondroitins trigger fear responses. Like skin extract, chondroitins activate the mediodorsal posterior olfactory bulb, a region innervated by crypt neurons that has a unique projection to the habenula. These findings establish GAGs as a new class of odorants in fish, which trigger alarm behavior possibly via a specialized circuit.Current biology: CB 02/2012; 22(6):538-44. DOI:10.1016/j.cub.2012.01.061 · 9.92 Impact Factor
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ABSTRACT: Imprinting on kin occurs during the sixth day of larval development in zebrafish and depends on olfactory signals. In rodents, the immediate early gene egr1 is involved in maintaining the dopaminergic phenotype of periglomerular olfactory bulb cells in an activity dependent way. Furthermore, egr1 is upregulated in medial amygdalar dopamine cells in some rodents (prairie voles) dependent on social pheromone interactions. Thus, we aimed to investigate whether egr1 is involved in imprinting processes and later kin recognition in zebrafish in olfactory centers, such as the olfactory bulb and suspected medial amygdala. In the present paper, we focus on a basic investigation of basal egr1 expression throughout zebrafish brain development and its co-localization with tyrosine hydroxylase as a marker for dopaminergic neurons. Indeed, there is unambiguous co-localization of egr1 and tyrosine hydroxylase in the zebrafish olfactory bulb and hypothetical medial amygdala. Furthermore, as in rodents, ipsilateral transient olfactory deprivation through Triton X-100 treatment of the olfactory epithelium leads to downregulation of egr1 and tyrosine hydroxylase expression in the olfactory bulb, but apparently not in secondary olfactory targets of the zebrafish brain. This indicates that similar processes might be at work in zebrafish and rodent olfactory systems, but their more specific involvement in imprinting in zebrafish has to be further tested.Journal of chemical neuroanatomy 09/2012; 46(1-2). DOI:10.1016/j.jchemneu.2012.09.002 · 2.52 Impact Factor