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Afferent Neurons

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Naoki Yoshimura – 1st expert on this subject based on the ideXlab platform

  • hyperexcitability of bladder Afferent Neurons associated with reduction of kv1 4 α subunit in rats with spinal cord injury
    The Journal of Urology, 2013
    Co-Authors: William C De Groat, Ryosuke Takahashi, Tsuyoshi Yoshizawa, Takakazu Yunoki, Pradeep Tyagi, Seiji Naito, Naoki Yoshimura

    Abstract:

    Purpose: To clarify the functional and molecular mechanisms inducing hyperexcitability of C-fiber bladder Afferent pathways after spinal cord injury we examined changes in the electrophysiological properties of bladder Afferent Neurons, focusing especially on voltage-gated K channels.Materials and Methods: Freshly dissociated L6-S1 dorsal root ganglion Neurons were prepared from female spinal intact and spinal transected (T9-T10 transection) Sprague Dawley® rats. Whole cell patch clamp recordings were performed on individual bladder Afferent Neurons. Kv1.2 and Kv1.4 α-subunit expression levels were also evaluated by immunohistochemical and real-time polymerase chain reaction methods.Results: Capsaicin sensitive bladder Afferent Neurons from spinal transected rats showed increased cell excitability, as evidenced by lower spike activation thresholds and a tonic firing pattern. The peak density of transient A-type K+ currents in capsaicin sensitive bladder Afferent Neurons from spinal transected rats was sig…

  • bladder hyperactivity and increased excitability of bladder Afferent Neurons associated with reduced expression of kv1 4 α subunit in rats with cystitis
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2009
    Co-Authors: Yukio Hayashi, William C De Groat, Michael B Chancellor, Koichi Takimoto, Krisrtin A Erickson, Vickie L Erickson, Tsukasa Kirimoto, Koushi Nakano, Naoki Yoshimura

    Abstract:

    Hyperexcitability of C-fiber bladder Afferent pathways has been proposed to contribute to urinary frequency and bladder pain in chronic bladder inflammation including interstitial cystitis. However, the detailed mechanisms inducing Afferent hyperexcitability after bladder inflammation are not fully understood. Thus, we investigated changes in the properties of bladder Afferent Neurons in rats with bladder inflammation induced by intravesical application of hydrochloric acid. Eight days after the treatment, bladder function and bladder sensation were analyzed using cystometry and an electrodiagnostic device of sensory function (Neurometer), respectively. Whole cell patch-clamp recordings and immunohistochemical staining were also performed in dissociated bladder Afferent Neurons identified by a retrograde tracing dye, Fast Blue, injected into the bladder wall. Cystitis rats showed urinary frequency that was inhibited by pretreatment with capsaicin and bladder hyperalgesia mediated by C-fibers. Capsaicin-sensitive bladder Afferent Neurons from sham rats exhibited high thresholds for spike activation and a phasic firing pattern, whereas those from cystitis rats showed lower thresholds for spike activation and a tonic firing pattern. Transient A-type K+ current density in capsaicin-sensitive bladder Afferent Neurons was significantly smaller in cystitis rats than in sham rats, although sustained delayed-rectifier K+ current density was not altered after cystitis. The expression of voltage-gated K+ Kv1.4 α-subunits, which can form A-type K+ channels, was reduced in bladder Afferent Neurons from cystitis rats. These data suggest that bladder inflammation increases bladder Afferent neuron excitability by decreasing expression of Kv1.4 α-subunits. Similar changes in capsaicin-sensitive C-fiber Afferent terminals may contribute to bladder hyperactivity and hyperalgesia due to acid-induced bladder inflammation.

  • bladder overactivity and hyperexcitability of bladder Afferent Neurons after intrathecal delivery of nerve growth factor in rats
    The Journal of Neuroscience, 2006
    Co-Authors: Naoki Yoshimura, William C De Groat, Satoshi Seki, Nelson E Bennett, Yukio Hayashi, Teruyuki Ogawa, Osamu Nishizawa, Michael B Chancellor

    Abstract:

    Nerve growth factor (NGF) has been proposed as an important mediator inducing bladder overactivity under pathological conditions such as spinal cord injury, bladder outlet obstruction, or cystitis. We therefore examined the effects of chronic NGF treatment on bladder activity and the properties of bladder Afferent Neurons. In adult female rats, NGF (2.5 μg/μl) was infused continuously into the intrathecal space at the L6–S1 level of spinal cord for 1 or 2 weeks using osmotic pumps (0.5 μl/h). Bladder Afferent Neurons were labeled with axonal transport of Fast Blue injected into the bladder wall. After intrathecal injection of NGF, cystometrograms under an awake condition showed bladder overactivity revealed by time-dependent reductions in intercontraction intervals and voided volume. ELISA analyses showed significant increases in NGF levels in L6–S1 dorsal root ganglia of NGF-treated rats. In patch-clamp recordings, dissociated bladder Afferent Neurons exhibiting tetrodotoxin (TTX)-resistant action potentials from NGF-treated animals were larger in diameter and had significantly lower thresholds for spike activation compared with sham rats. In addition, the number of TTX-resistant action potentials during 600 ms depolarizing pulses was significantly increased time dependently after 1 or 2 weeks of NGF application. The density of slowly inactivating A-type K+ currents was decreased by 52% in bladder Afferent Neurons with TTX-resistant spikes after 2 week NGF treatment. These results indicate that increased NGF levels in bladder Afferent pathways and NGF-induced reduction in A-type K+ current density could contribute to the emergence of bladder overactivity as well as somal hypertrophy and hyperexcitability of bladder Afferent Neurons.

William C De Groat – 2nd expert on this subject based on the ideXlab platform

  • hyperexcitability of bladder Afferent Neurons associated with reduction of kv1 4 α subunit in rats with spinal cord injury
    The Journal of Urology, 2013
    Co-Authors: William C De Groat, Ryosuke Takahashi, Tsuyoshi Yoshizawa, Takakazu Yunoki, Pradeep Tyagi, Seiji Naito, Naoki Yoshimura

    Abstract:

    Purpose: To clarify the functional and molecular mechanisms inducing hyperexcitability of C-fiber bladder Afferent pathways after spinal cord injury we examined changes in the electrophysiological properties of bladder Afferent Neurons, focusing especially on voltage-gated K channels.Materials and Methods: Freshly dissociated L6-S1 dorsal root ganglion Neurons were prepared from female spinal intact and spinal transected (T9-T10 transection) Sprague Dawley® rats. Whole cell patch clamp recordings were performed on individual bladder Afferent Neurons. Kv1.2 and Kv1.4 α-subunit expression levels were also evaluated by immunohistochemical and real-time polymerase chain reaction methods.Results: Capsaicin sensitive bladder Afferent Neurons from spinal transected rats showed increased cell excitability, as evidenced by lower spike activation thresholds and a tonic firing pattern. The peak density of transient A-type K+ currents in capsaicin sensitive bladder Afferent Neurons from spinal transected rats was sig…

  • bladder hyperactivity and increased excitability of bladder Afferent Neurons associated with reduced expression of kv1 4 α subunit in rats with cystitis
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2009
    Co-Authors: Yukio Hayashi, William C De Groat, Michael B Chancellor, Koichi Takimoto, Krisrtin A Erickson, Vickie L Erickson, Tsukasa Kirimoto, Koushi Nakano, Naoki Yoshimura

    Abstract:

    Hyperexcitability of C-fiber bladder Afferent pathways has been proposed to contribute to urinary frequency and bladder pain in chronic bladder inflammation including interstitial cystitis. However, the detailed mechanisms inducing Afferent hyperexcitability after bladder inflammation are not fully understood. Thus, we investigated changes in the properties of bladder Afferent Neurons in rats with bladder inflammation induced by intravesical application of hydrochloric acid. Eight days after the treatment, bladder function and bladder sensation were analyzed using cystometry and an electrodiagnostic device of sensory function (Neurometer), respectively. Whole cell patch-clamp recordings and immunohistochemical staining were also performed in dissociated bladder Afferent Neurons identified by a retrograde tracing dye, Fast Blue, injected into the bladder wall. Cystitis rats showed urinary frequency that was inhibited by pretreatment with capsaicin and bladder hyperalgesia mediated by C-fibers. Capsaicin-sensitive bladder Afferent Neurons from sham rats exhibited high thresholds for spike activation and a phasic firing pattern, whereas those from cystitis rats showed lower thresholds for spike activation and a tonic firing pattern. Transient A-type K+ current density in capsaicin-sensitive bladder Afferent Neurons was significantly smaller in cystitis rats than in sham rats, although sustained delayed-rectifier K+ current density was not altered after cystitis. The expression of voltage-gated K+ Kv1.4 α-subunits, which can form A-type K+ channels, was reduced in bladder Afferent Neurons from cystitis rats. These data suggest that bladder inflammation increases bladder Afferent neuron excitability by decreasing expression of Kv1.4 α-subunits. Similar changes in capsaicin-sensitive C-fiber Afferent terminals may contribute to bladder hyperactivity and hyperalgesia due to acid-induced bladder inflammation.

  • bladder overactivity and hyperexcitability of bladder Afferent Neurons after intrathecal delivery of nerve growth factor in rats
    The Journal of Neuroscience, 2006
    Co-Authors: Naoki Yoshimura, William C De Groat, Satoshi Seki, Nelson E Bennett, Yukio Hayashi, Teruyuki Ogawa, Osamu Nishizawa, Michael B Chancellor

    Abstract:

    Nerve growth factor (NGF) has been proposed as an important mediator inducing bladder overactivity under pathological conditions such as spinal cord injury, bladder outlet obstruction, or cystitis. We therefore examined the effects of chronic NGF treatment on bladder activity and the properties of bladder Afferent Neurons. In adult female rats, NGF (2.5 μg/μl) was infused continuously into the intrathecal space at the L6–S1 level of spinal cord for 1 or 2 weeks using osmotic pumps (0.5 μl/h). Bladder Afferent Neurons were labeled with axonal transport of Fast Blue injected into the bladder wall. After intrathecal injection of NGF, cystometrograms under an awake condition showed bladder overactivity revealed by time-dependent reductions in intercontraction intervals and voided volume. ELISA analyses showed significant increases in NGF levels in L6–S1 dorsal root ganglia of NGF-treated rats. In patch-clamp recordings, dissociated bladder Afferent Neurons exhibiting tetrodotoxin (TTX)-resistant action potentials from NGF-treated animals were larger in diameter and had significantly lower thresholds for spike activation compared with sham rats. In addition, the number of TTX-resistant action potentials during 600 ms depolarizing pulses was significantly increased time dependently after 1 or 2 weeks of NGF application. The density of slowly inactivating A-type K+ currents was decreased by 52% in bladder Afferent Neurons with TTX-resistant spikes after 2 week NGF treatment. These results indicate that increased NGF levels in bladder Afferent pathways and NGF-induced reduction in A-type K+ current density could contribute to the emergence of bladder overactivity as well as somal hypertrophy and hyperexcitability of bladder Afferent Neurons.

G J Dockray – 3rd expert on this subject based on the ideXlab platform

  • cocaine and amphetamine regulated transcript mediates the actions of cholecystokinin on rat vagal Afferent Neurons
    Gastroenterology, 2010
    Co-Authors: Guillaume De Lartigue, R Dimaline, Andrea Varro, Helen E Raybould, Claire B De La Serre, G J Dockray

    Abstract:

    Background & Aims Cholecystokinin (CCK) acts on vagal Afferent Neurons to inhibit food intake and gastric emptying; it also increases expression of the neuropeptide cocaine- and amphetamine-regulated transcript (CART), but the significance of this is unknown. We investigated the role of CARTp in vagal Afferent Neurons. Methods Release of CART peptide (CARTp) from cultured vagal Afferent Neurons was determined by enzyme-linked immunosorbent assay. Expression of receptors and neuropeptides in rat vagal Afferent Neurons in response to CARTp was studied using immunohistochemistry and luciferase promoter reporter constructs. Effects of CARTp and CCK were studied on food intake. Results CCK stimulated CARTp release from cultured nodose Neurons. CARTp replicated the effect of CCK in stimulating expression of Y2R and of CART itself in these Neurons in vivo and in vitro, but not in inhibiting cannabinoid-1, melanin-concentrating hormone, and melanin-concentrating hormone-1 receptor expression. Effects of CCK on Y2R and CART expression were reduced by CART small interfering RNA or brefeldin A. Exposure of rats to CARTp increased the inhibitory action of CCK on food intake after short-, but not long-duration, fasting. Conclusions The actions of CCK in stimulating CART and Y2R expression in vagal Afferent Neurons and in inhibiting food intake are augmented by CARTp; CARTp is released by CCK from these Neurons, indicating that it acts as an autocrine excitatory mediator.

  • cholecystokinin regulates expression of y2 receptors in vagal Afferent Neurons serving the stomach
    The Journal of Neuroscience, 2008
    Co-Authors: G Burdyga, Guillaume De Lartigue, R Dimaline, Andrea Varro, Helen E Raybould, D G Thompson, R Morris, G J Dockray

    Abstract:

    The intestinal hormones CCK and PYY3–36 inhibit gastric emptying and food intake via vagal Afferent Neurons. Here we report that CCK regulates the expression of Y2R, at which PYY3–36 acts. In nodose ganglia from rats fasted up to 48 h, there was a fivefold decrease of Y2R mRNA compared with rats fed ad libitum ; Y2R mRNA in fasted rats was increased by administration of CCK, and by refeeding through a mechanism sensitive to the CCK1R antagonist lorglumide. Antibodies to Y2R revealed expression in both Neurons and satellite cells; most of the former (89 ± 4%) also expressed CCK1R. With fasting there was loss of Y2R immunoreactivity in CCK1R-expressing Neurons many of which projected to the stomach, but not in satellite cells or Neurons projecting to the ileum or proximal colon. Expression of a Y2R promoter-luciferase reporter (Y2R-luc) in cultured vagal Afferent Neurons was increased in response to CCK by 12.3 ± 0.1-fold and by phorbol ester (16.2 ± 0.4-fold); the response to both was abolished by the protein kinase C inhibitor Ro-32,0432. PYY3–36 stimulated CREB phosphorylation in rat nodose Neurons after priming with CCK; in wild-type mice PYY3–36 increased Fos labeling in brainstem Neurons but in mice null for CCK1R this response was abolished. Thus Y2R is expressed by functionally distinct subsets of nodose ganglion Neurons projecting to the stomach and ileum/colon; in the former expression is dependent on stimulation by CCK, and there is evidence that PYY3–36 effects on vagal Afferent Neurons are CCK dependent.

  • cocaine and amphetamine regulated transcript stimulation of expression in rat vagal Afferent Neurons by cholecystokinin and suppression by ghrelin
    The Journal of Neuroscience, 2007
    Co-Authors: Guillaume De Lartigue, R Dimaline, Andrea Varro, G J Dockray

    Abstract:

    The neuropeptide transmitter cocaine- and amphetamine-regulated transcript (CART) inhibits food intake and is expressed by both vagal Afferent and hypothalamic Neurons. Here we report that cholecystokinin (CCK) regulates CART expression in rat vagal Afferent Neurons. Thus, CART was virtually undetectable after energy restriction for 24 h, but administration of CCK to fasted rats increased CART immunoreactivity, and refeeding of fasted animals promptly increased CART by a mechanism sensitive to a CCK-1 receptor antagonist. In vagal Afferent Neurons incubated in serum-free medium, CART was virtually undetectable, whereas the orexigenic peptide melanin-concentrating hormone (MCH) was readily detected. The addition of CCK rapidly induced CART expression and downregulated MCH. Using a CART promoter–luciferase reporter vector transfected into cultured vagal Afferent Neurons, we showed that CCK stimulation of CART transcription was mediated by activation of protein kinase C and cAMP response element-binding protein (CREB). The action of CCK on CART expression was inhibited by the orexigenic peptide ghrelin, through a mechanism that involved exclusion of phosphorylated CREB from the nucleus. Thus, CCK reciprocally regulates expression of CART and MCH within the same vagal Afferent neuron; ghrelin inhibits the effect of CCK at least in part through control of the nuclear localization of phosphoCREB, revealing previously unsuspected modulation of gut–brain signals implicated in control of food intake.