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  • The neural circuitry involved in the production of

    2023-05-24

    The neural circuitry involved in the production of the EOD, its modulations, and in the sensory processing of communication signals has been well characterized (Bell and Maler, 2005; Chacron et al., 2011; Krahe and Maler, 2014; reviewed in Metzner, 1999). Pacemaker cells located in the pacemaker nucleus (PM) in the hindbrain synapse onto relay cells that project their MK-8245 receptor down the spinal cord to eventually synapse onto the electromotor neurons in the spinal cord. Axons of these electromotor neurons make up the electric organ in the fish’s tail and the rate of the action potentials of these cells, entrained by the PM, determines the frequency of a fish’s EOD. Modulations of the EODf, such as the JAR and chirps, are produced by changes in the firing rate of neurons in the sublemniscal (SPPn) and chirp (PPn-C) prepacemaker nuclei located in the mesencephalon and diencephalon, respectively. Neurons from the SPPn and PPn-C project to the PM to ultimately induce changes in the EODf (Heiligenberg et al., 1996). Electrosensory input reaches the electrosensory lateral line lobe (ELL) via primary afferents from the electroreceptors in the skin. The ELL output neurons target the rhombencephalic nucleus praeeminentialis and the midbrain torus semicircularis, from where electrosensory information is relayed to the tectum opticum and the diencephalic nucleus electrosensorius. The latter projects to SPPn and thus closes the sensory-motor loop. Though the neural circuits involved in electric signaling behavior and electrosensory processing have been well studied, little is known about local steroid production in the brain and its effects within these circuits on signal production. To date, three studies have indicated an effect of aromatase activity on behavior in weakly electric fish. Firstly, Dulka and Maler (1994) demonstrated that testosterone implants feminize the baseline EODf in A. leptorhynchus, while also increasing female chirping behavior. The authors suggested that aromatization was likely responsible for these observed effects, because they were similar to those seen following estradiol administration in a sister species, Apteronotus rostratus (Meyer et al., 1987). Zucker (1997) showed that when fadrozole, an aromatase inhibitor, was administered alongside testosterone implants there was no effect on baseline EODf, effectively confirming the previous hypothesis that testosterone was being aromatized. This study did not, however, assess if this were also true for chirping behavior. Finally, Jalabert et al. (2015) showed that fadrozole injections in another species of weakly electric fish, Gymnotus omarorum, decreased the physical aggression of dominant fish; however, there was no comment of an effect on electric signaling behavior. Together these studies provide evidence to suggest an effect of aromatase activity in weakly electric fish, though it is currently unclear where aromatase is expressed in the neural circuit to affect these behaviors. The goal of this study was to identify the expression pattern of cyp19a1b mRNA in the brain of A. leptorhynchus to: 1) determine whether aromatase mRNA is expressed in brain nuclei underlying electrocommunication behavior, and 2) compare the mRNA expression pattern in a species of weakly electric fish with that of non-electrogenic teleosts.
    Material and methods
    Results
    Discussion Aromatase mRNA expression was detected in non-breeding A. leptorhynchus in forebrain regions that have been previously associated with social behavior in other teleosts, most notably the telencephalon, preoptic area, hypothalamus, and pituitary gland (reviewed in Diotel et al., 2010). Aromatase mRNA was not detected in any midbrain or hindbrain regions in A. leptorhynchus. This latter MK-8245 receptor finding suggests that if aromatase activity in the brain is involved in electric signaling behavior, its effects most likely occur at the level of regulation upstream of the pre- and pacemaker nuclei. Since cyp19a1a (ovarian aromatase) expression was not assessed in this study, we cannot exclude the possibility that there may be low levels of its expression in the brain, though there is currently little evidence for this finding in teleosts.