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The cochlea forms a key element of the human auditory system in the temporal bone. Damage to the cochlea continues to produce significant impairment for sensory reception of environmental stimuli. To improve this impairment, the optical cochlear implant forms a new research approach. A prerequisite for this method is to understand how light propagation, as well as scattering, reflection, and absorption, takes place within the cochlea. We offer a method to study the light distribution in the human cochlea through phantom materials which have the objective to mimic the optical behavior of bone and Monte-Carlo simulations. The calculation of an angular distribution after scattering requires a phase function. Often approximate functions like Henyey-Greenstein, two-term Henyey-Greenstein or Legendre polynomial decompositions are used as phase function. An alternative is to exactly calculate a Mie distribution for each scattering event. This method provides a better fit to the data measured in this work., (© 2023 The Authors. Journal of Biophotonics published by Wiley‐VCH GmbH.)

CRH is known as the main stimulator of ACTH release. In representatives of all nonmammalian vertebrates, CRH has also been shown to induce TSH secretion, acting directly at the level of the pituitary. We have investigated which cell types and receptors are involved in CRH-induced TSH release in the chicken (Gallus gallus). Because a lack of CRH type 1 receptors (CRH-R1) on the chicken thyrotropes has been previously reported, two hypotheses were tested using in situ hybridization and perifusion studies: 1) TSH secretion might be induced in a paracrine way involving melanocortins from the corticotropes; and 2) thyrotropes might express another type of CRH-R. For the latter, we have cloned a partial cDNA encoding the chicken CRH-R2. Neither alpha-melanotropin (alpha-MSH) nor its powerful analog Nle4,d-Phe7-MSH could mimic the in vitro TSH-releasing effect of ovine CRH. The nonselective melanocortin receptor blocker SHU91199 did not influence CRH- or TRH-induced TSH secretion. On the other hand, we have found that thyrotropes express CRH-R2 mRNA. The involvement of this CRH receptor in the response of thyrotropes to CRH was further confirmed by the fact that TSH release was stimulated by human urocortin III, a CRH-R2-specific agonist, whereas the TSH response to CRH was completely blocked by the CRH-R blocker astressin and the CRH-R2-specific antagonist antisauvagine-30. We conclude that CRH-induced TSH secretion is mediated by CRH-R2 expressed on thyrotropes.