Paraneuronal pseudobranchial neurosecretory system in tank goby Glossogobius giuris with special reference to novel neurohaemal contact complex.

Various putative oxygen chemosensory cells are reported to be present throughout the vertebrate body performing pivotal roles in respiration by initiating responses during acute hypoxia. Since air-breathing fishes often are exposed to the oxygen-deficient milieu, in such conditions various chemosensory cells operate in an orchestrated fashion. The Pseudobranchial neurosecretory system (PSNS) a newly discovered system, is one of these. It has been placed in the category of "Diffuse NE systems (DNES)". It is found in all the catfish species and in some other non-catfish group of teleosts. In catfishes, it is present in close association with the carotid labyrinth- a chemosensory structure, known in fish and amphibians. The presence of this system in Glossogobius giuris, in association with the pseudobranch, a structure considered to be precursor of carotid labyrinth, is a significant finding. In an attempt to study the structure and organization of the pseudobranchial neurosecretory system in a non-catfish species of teleost, the present investigation was undertaken on a goby G. giuris. The histological observations, using a neurosecretion-specific stain, revealed the presence of this system in G. giuris. The findings are discussed in the light of the association of PSNS with pseudobranch and the type of "neurohaemal contact complex" formed between this neurosecretory system and the elements of the circulatory system.

Streptozotocin-induced diabetes causes upregulation of serotonin (5-HT)2A/C receptors in lumbosacral cord motoneurons and down regulation of serotonergic paraneurons in the urethra.

Lower urinary tract (LUT) dysfunction is the most common complication of diabetes mellitus (DM). An involvement of the 5-HT2A receptor in spinal micturition control has been demonstrated in urethane anaesthetized DM rats in which i.v. administration of the 5-HT2A/2C receptor agonist 2,5-methoxy-4-iodoamphetamine (DOI), stimulated high frequency oscillations (HFOs) and improved micturition. However, the mechanisms involved in these effects are not completely understood. The present work showed that 5-HT2A and -2C receptors were upregulated in lumbosacral cord motoneurons, and the number of serotonergic paraneurons were downregulated in the urethra in DM group. The importance of the downregulation of urethral paraneurons in DM remains to be elucidated but may be related to the reduced urethral sensation caused by the disease. We suggest that targets of 5-HT receptor agonists for improvement of voiding function may be found both in the LUT and lumbosacral spinal cord.

Corrigendum: Inflammation and Tissue Remodeling in the Bladder and Urethra in Feline Interstitial Cystitis.

[This corrects the article DOI: 10.3389/fnsys.2018.00013.].

Inflammation and Tissue Remodeling in the Bladder and Urethra in Feline Interstitial Cystitis.

Interstitial cystitis/bladder pain syndrome (IC/BPS) is a debilitating chronic disease of unknown etiology. A naturally occurring disease termed feline interstitial cystitis (FIC) reproduces many features of IC/BPS patients. To gain insights into mechanisms underlying IC/BPS, we investigated pathological changes in the lamina propria (LP) of the bladder and proximal urethra in cats with FIC, using histological and molecular methods. Compared to control cat tissue, we found an increased number of de-granulated mast cells, accumulation of leukocytes, increased cyclooxygenase (COX)-1 expression in the bladder LP, and increased COX-2 expression in the urethra LP from cats with FIC. We also found increased suburothelial proliferation, evidenced by mucosal von Brunn's nests, neovascularization and alterations in elastin content. Scanning electron microscopy revealed normal appearance of the superficial urethral epithelium, including the neuroendocrine cells (termed paraneurons), in FIC urethrae. Together, these histological findings suggest the presence of chronic inflammation of unknown origin leading to tissue remodeling. Since the mucosa functions as part of a "sensory network" and urothelial cells, nerves and other cells in the LP are influenced by the composition of the underlying tissues including the vasculature, the changes observed in the present study may alter the communication of sensory information between different cellular components. This type of mucosal signaling can also extend to the urethra, where recent evidence has revealed that the urethral epithelium is likely to be part of a signaling system involving paraneurons and sensory nerves. Taken together, our data suggest a more prominent role for chronic inflammation and tissue remodeling than previously thought, which may result in alterations in mucosal signaling within the urinary bladder and proximal urethra that may contribute to altered sensations and pain in cats and humans with this syndrome.

Evidence for an urethro-vesical crosstalk mediated by serotonin.

AIM: To study the contribution of urethral serotonin for the urethro-vesical crosstalk METHODS: Urethane-anesthetized female rats and TPH1-/- mice underwent isovolumetric or urethral-opened cystometries during intravesical or intraurethral infusion of saline or serotonin solutions. Human and rat bladders and urethrae were immunoreacted against serotonin and neuronal markers. Serotonin concentration and TPH1 mRNA were determined in rat tissue by HPLC and qPCR. RESULTS: In rats, under isovolumetric conditions, intraurethral serotonin infusion, but not saline, evoked bladder contractions. This was abolished by urethral anesthesia and by treatment with serotonin receptor antagonists. Serotonin infusion into the bladder had no effect. Under urethral-opened conditions, serotonin infusion reduced the frequency and increased the amplitude of reflex voiding contractions, compared to saline infusion. TPH1-/- mice, under urethral-opened conditions, exhibited increased frequency and reduced amplitude of voiding contractions compared to WT. Serotonin concentration and TPH1 mRNA expression were higher in the urethra than in the bladder. Cells 5-HT+ were found in the human and rat urethral epithelium, close to a sub-epithelial network of cholinergic and sensory fibers, but not in the bladder. CONCLUSIONS: Serotonin, produced and released by urethral cells activates an urethro-vesical pathway that enhances bladder reflex contractions.