Nadph-diaphorase in the spinal trigeminal nucleus oralis and rostral solitary tract nucleus of rats

ABSTRACTExposure of the oral cavity to acidic solutions evokes not only a sensation of sour, but also of sharp or tangy. Acidic substances potentially stimulate both taste buds and acid-sensitive mucosal free nerve endings. Mice lacking taste function (P2X2/P2X3 double-KO mice) refuse acidic solutions similarly to wildtype mice and intraoral infusion of acidic solutions in these KO animals evokes substantial c-Fos activity within orosensory trigeminal nuclei as well as of the nucleus of the solitary tract (nTS) (Stratford et. al 2017). This residual acid-evoked, non-taste activity includes areas that receive inputs from trigeminal and glossopharyngeal peptidergic (CGRP-containing) nerve fibers that express TrpA1 and TrpV1 both of which are activated by low pH. We compared avoidance responses in wildtype (WT) and TrpA1/V1 double KO (TRPA1/V1Db1-/-) mice in brief-access behavioral assay (lickometer) to 1, 3, 10, 30 mM citric acid, along with 100 μM SC45647 and H2O. Both WT and TRPA1/V1Db1-/- show similar avoidance, including to higher concentrations of citric acid (10 and 30 mM; pH 2.62 and pH 2.36 respectively), indicating that neither TrpA1 nor TrpV1 is necessary for the acid avoidance behavior in animals with an intact taste system. Similarly, induction of c-Fos in the nTS and dorsomedial spinal trigeminal nucleus was similar in the WT and TRPA1/V1Db1-/-animals. Taken together these results suggest non-TrpV1 and non-TrpA1 receptors underlie the residual responses to acids in mice lacking taste function.

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Genetic Deletion of TrpV1 and TrpA1 Does Not Alter Avoidance of or Patterns of Brainstem Activation to Citric Acid in Mice

Chemical Senses ◽

10.1093/chemse/bjaa043 ◽

2020 ◽

Vol 45 (7) ◽

pp. 573-579

Author(s):

Tian Yu ◽

Courtney E Wilson ◽

Jennifer M Stratford ◽

Thomas E Finger

Keyword(s):

Citric Acid ◽

Nerve Fibers ◽

Low Ph ◽

Solitary Tract ◽

Spinal Trigeminal Nucleus ◽

Trigeminal Nucleus ◽

Taste System ◽

Acidic Solutions ◽

Trigeminal Nuclei ◽

Genetic Deletion

Abstract Exposure of the oral cavity to acidic solutions evokes not only a sensation of sour, but also of sharp or tangy. Acidic substances potentially stimulate both taste buds and acid-sensitive mucosal free nerve endings. Mice lacking taste function (P2X2/P2X3 double-KO mice) refuse acidic solutions similar to wildtype (WT) mice and intraoral infusion of acidic solutions in these KO animals evokes substantial c-Fos activity within orosensory trigeminal nuclei as well as of the nucleus of the solitary tract (nTS) (Stratford, Thompson, et al. 2017). This residual acid-evoked, non-taste activity includes areas that receive inputs from trigeminal and glossopharyngeal peptidergic (CGRP-containing) nerve fibers that express TrpA1 and TrpV1 both of which are activated by low pH. We compared avoidance responses in WT and TrpA1/V1 double-KO (TRPA1/V1Dbl−/−) mice in brief-access behavioral assay (lickometer) to 1, 3, 10, and 30 mM citric acid, along with 100 µM SC45647 and H2O. Both WT and TRPA1/V1Dbl−/− show similar avoidance, including to higher concentrations of citric acid (10 and 30 mM; pH 2.62 and pH 2.36, respectively), indicating that neither TrpA1 nor TrpV1 is necessary for the acid-avoidance behavior in animals with an intact taste system. Similarly, induction of c-Fos in the nTS and dorsomedial spinal trigeminal nucleus was similar in the WT and TRPA1/V1Dbl−/− animals. Taken together these results suggest non-TrpV1 and non-TrpA1 receptors underlie the residual responses to acids in mice lacking taste function.

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Increase in NADPH-Diaphorase-Positive and Neuronal NO Synthase Immunoreactive Neurons in the Rat Spinal Trigeminal Nucleus Following Infusion of a NO Donor—Evidence for a Feed-Forward Process in NO Production Involved in Trigeminal Nociception

Cephalalgia ◽

10.1111/j.1468-2982.2008.01791.x ◽

2009 ◽

Vol 29 (5) ◽

pp. 566-579 ◽

Cited By ~ 17

Author(s):

PM Schlechtweg ◽

J Röder ◽

MJM Fischer ◽

W Neuhuber ◽

K Messlinger

Keyword(s):

Nitric Oxide ◽

Afferent Input ◽

Central Canal ◽

Nadph Diaphorase ◽

No Production ◽

Spinal Trigeminal Nucleus ◽

Trigeminal Nucleus ◽

No Donor ◽

No Donors ◽

Nos Isoforms

Nitric oxide (NO) donors, which cause delayed headaches in migraineurs, have been shown to activate central trigeminal neurons with meningeal afferent input in animal experiments. Previous reports indicate that this response may be due to up-regulation of NO-producing cells in the trigeminal brainstem. To investigate this phenomenon further, we determined nitric oxide synthase (NOS)-containing neurons in the rat spinal trigeminal nucleus (STN), the projection site of nociceptive trigeminal afferents, following infusion of the NO donor sodium nitroprusside (SNP). Barbiturate anaesthetized rats were infused intravenously with SNP (50 μg/kg) or vehicle for 20 min or 2 h, and after periods of 3–8 h fixed by perfusion. Cryostat sections of the medulla oblongata containing the caudal STN were histochemically processed for detection of nicotineamide adenine dinucleotide phosphate (NADPH)-diaphorase or immunohistochemically stained for NOS isoforms and examined by light and fluorescence microscopy. The number of neurons positive for these markers was determined. Various forms of neurons positive for NADPH-diaphorase or immunoreactive to neuronal NOS (nNOS) were found in superficial and deep laminae of the STN caudalis and around the central canal. Neurons were not immunopositive for endothelial (eNOS) or inducible (iNOS) NOS isoforms. The number of NADPH-diaphorase-positive neurons increased time dependently after SNP infusion by a factor of more than two. Likewise, the number of nNOS-immunopositive neurons was increased after SNP compared with vehicle infusion. Around the central canal the number of NADPH-diaphorase-positive neurons was slightly increased and the number of nNOS+ neurons not changed after SNP treatment. NO donors increase the number of neurons that produce NO in the STN, possibly by induction of nNOS expression. Increased NO production may facilitate neurotransmitter release and promote nociceptive transmission in the STN. This mechanism may explain the delayed increase in neuronal activity and headache after infusion of NO donors.

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Novel Morphological Alteration and Neural Pathway of NADPH Diaphorase Positivity in the Spinal Cord with Disc Herniation of Aged Dog: A Case Report

10.20944/preprints202002.0280.v1 ◽

2020 ◽

Cited By ~ 2

Author(s):

Yinhua Li ◽

Yunge Jia ◽

Wei Hou ◽

Huibing Tan

Keyword(s):

Spinal Cord ◽

Disc Herniation ◽

Nadph Diaphorase ◽

Spinal Trigeminal Nucleus ◽

Trigeminal Nucleus ◽

Neural Pathway ◽

Lumbosacral Spinal Cord ◽

Spinal Disc ◽

Collateral Pathway ◽

Spinal Disc Herniation

Neuronal lesion or injury is a traditional approach to investigate neural circuit. Is any new neural pathway or new neurodegeneration related central nerve system injury? Spinal disc herniation can cause the spinal cord injury. However, the histological examination is still lack. It happened that a case of spinal disc herniation of a 10-year old dog was examined with NADPH diaphorase (N-d) histology. We did not find the N-d neurodegenerative aberrant in the tissue of the mid-rostral lumber segment besides the metamorphoses by the compression of the disc herniation. However, the severe neuropathological changes majorly occurred in the lumbosacral spinal cord. We found more diverse neurodegenerative alterations: the aging-related N-d body (ANB), megaloneurite and N-d homogeneous formazan globule in the lumbosacral spinal cord. We also found that a new circuit pathway (intermedial collateral pathway) showed by a megaloneurite between the lateral collateral pathway and the medial collateral pathway. The enormous notch caused by spinal disc herniation located at the mid-rostral lumber segments. The aging-related neurodegeneration occurred the specific lumbosacral segments. The homogeneous formazan globule was round or oval homogeneous N-d positivity which distributed in the gray matter and dorsal column. In the medulla oblongata, ANBs were revealed in the gracile nucleus, nucleus reticularis lateralis (ventrolateral spinal trigeminal nucleus) and middle of the spinal trigeminal nucleus.

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