The visualisation of cardiovascular innervation in the guinea pig using antiserum to protein gene product 9.5 (pgp 9.5)

Gulbenkian, S.; Wharton, John; Polak, Julia M.

doi:10.1016/0165-1838(87)90122-6

Cited by 257 publications

(98 citation statements)

References 44 publications

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“…For negative controls only the diluent was used for first-layer incubation. Antibody against the general neuronal marker protein gene product 9.5 (PGP 9.5, human, 1:4000) (Gulbenkian et al, 1987) was used to confirm neuronal staining with NOS antibody.…”

Section: Immunocytochemical Studiesmentioning

confidence: 99%

Nitric oxide, and not vasoactive intestinal peptide, as the main neurotransmitter of vagally induced relaxation of the guinea pig stomach

Desai

Warner

Bishop

et al. 1994

British J Pharmacology

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Hammersmith Hospital, Du Cane Road, London W12 ONN 1 Nitric oxide synthase (NOS) The cross-sections of the stomach wall showed NOS-positive neurones mainly in the myenteric plexus ganglia and NOS-positive nerve fibre varicosities in the circular muscle layer. 4 Relaxations induced by vagal stimulation were almost completely prevented by L-NAME with an IC50 value of 5.5 x 10-6M. This inhibition was reversed by L-arginine (2 mM).5 VIP (100nM) induced reproducible relaxations of the stomach. These were unaffected by tetrodotoxin (2f1M) or Nw-nitro-L-arginine methyl ester (L-NAME, 100 AM).6 Desensitization to the relaxant effect of VIP partially reduced relaxations induced by vagal stimulation, glyceryl trinitrate or sodium nitroprusside but not noradrenaline. 7 These results show that NO has a neuronal origin in the guinea pig stomach, and support NO, and not VIP, as the major neurotranmitter of vagally induced gastric relaxation in the guinea pig.

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Section: Immunocytochemical Studiesmentioning

confidence: 99%

Nitric oxide, and not vasoactive intestinal peptide, as the main neurotransmitter of vagally induced relaxation of the guinea pig stomach

Desai

Warner

Bishop

et al. 1994

British J Pharmacology

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“…Neuropeptide Y is a sympathetic neurotransmitter that is coreleased with NE (37) but is under different controls of biosynthesis and metabolism (23). In addition, to determine whether there was structural loss of the sympathetic nerve fibers, we measured tissue protein gene product (PGP) 9.5, a panneuronal marker (24,28) unrelated to sympathetic neurotransmitters.…”

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confidence: 99%

Desipramine attenuates loss of cardiac sympathetic neurotransmitters produced by congestive heart failure and NE infusion

Liang

Yatani

Himura

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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. Desipramine attenuates loss of cardiac sympathetic neurotransmitters produced by congestive heart failure and NE infusion. Am J Physiol Heart Circ Physiol 284: H1729-H1736, 2003. First published January 23, 2003 10.1152/ajpheart. 00853.2002We reported recently that inhibition of neuronal reuptake of norepinephrine (NE) by desipramine prevented the reduction of sympathetic neurotransmitters in the failing right ventricle of right heart failure animals. In this study, we studied whether desipramine also reduced the sympathetic neurotransmitter loss in animals with left heart failure induced by rapid ventricular pacing (225 beats/min) or after chronic NE infusion (0.5 g ⅐ kg Ϫ1 ⅐ min Ϫ1 ). Desipramine was given to the animals for 8 wk beginning with rapid ventricular pacing or NE infusion. Animals receiving no desipramine were studied as controls. We measured myocardial NE content, NE uptake activity, and sympathetic NE, tyrosine hydroxylase, and neuropeptide Y profiles by histofluorescence and immunocytochemical techniques. Effects of desipramine on NE uptake inhibition were evidenced by potentiation of the pressor response to exogenous NE and reduction of myocardial NE uptake activity. Desipramine treatment had no effect in sham or saline control animals but attenuated the reduction of sympathetic neurotransmitter profiles in the left ventricles of animals with rapid cardiac pacing and NE infusion. In contrast, the panneuronal marker protein gene product 9.5 profile was not affected by either rapid pacing or NE infusion, nor was it changed by desipramine treatment in the heart failure animals. The study confirms that excess NE contributes to the reduction of cardiac sympathetic neurotransmitters in heart failure. In addition, it shows that the anatomic integrity of the sympathetic nerves is relatively intact and that the neuronal damaging effect of NE involves the uptake of NE or its metabolites into the sympathetic nerves. neuronal uptake activity; histofluorescence; tyrosine hydroxylase; neuropeptide Y; protein gene product 9.5 EARLIER STUDIES FROM OUR LABORATORY have shown that right heart failure produced by progressive pulmonary constriction and tricuspid valve avulsion is associated with a selective reduction of norepinephrine (NE) reuptake and downregulation of myocardial ␤-adrenoceptor density in the failing right ventricle (33). The sympathetic nerve terminal profiles, as measured by catecholaminergic histofluorescence, and tyrosine hydroxylase and neuropeptide Y immunocytochemistry are also reduced only in the failing right ventricle (27). These findings suggest that the reductions of myocardial ␤-adrenoceptors and sympathetic nerve neurotransmitters in congestive heart failure (CHF) are caused by local mechanisms occurring only in the failing myocardium; the correspondent left ventricle is relatively unaffected despite exposure to the same systemic elevation of plasma catecholamines (33). A similar chamber specific reduction of myocardial ␤-adrenoceptors was reported in humans with right heart fail...

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“…Morphometric analysis revealed that the population of the spiral ganglion cells was significantly decreased in the prediabetic and diabetic WBN/Kob rats at 7 months of age in comparison with that of the agematched control Wistar rats. PGP 9.5 is a novel neuron-specific protein found in all types of mammalian nerves [4,[7][8][9][10]. This protein is uniformly distributed in the cytosol and nucleoplasm as a soluble protein in the spiral ganglion cells of the cochlea [11,12]; therefore, changes in the immunoreactivity for anti-PGP 9.5 serum may reflect structural and functional alterations of these cells.…”

Section: Discussionmentioning

confidence: 99%

“…Although the functional significance of PGP 9.5 is still unclear, this protein may play an essential role in the ubiquitin-related metabolism in nervous tissues. Recently, PGP 9.5 has been increasingly used as a convenient neural marker in neurophysiological studies [7][8][9][10][11][12]. In the present study, therefore, we examined the immunoreactivity for PGP 9.5 in the spiral ganglion cells of the cochlea in prediabetic and diabetic WBN/Kob rats by an immunohistochemical method with computer-assisted image analysis and compared the results with those obtained from normal age-matched Wistar rats in order to reveal the functional changes in the spiral ganglion cells from a quantitative point of view.…”

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Changes in the immunoreactivity of protein gene product (PGP) 9.5 in the cochlea of spontaneously diabetic WBN/Kob rats

1997

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In our previous study, hearing impairment of spontaneously diabetic WBN/Kob rats was first detected as an elevation of the hearing threshold in the auditory brainstem response in animals expressing glucose intolerance, then as a decrease in the number of spiral ganglion cells in the cochlea, and finally as oedematous changes in the stria vascularis [1]. Atrophy of the spiral ganglion was also reported as the most common pathological change in the cochlea of diabetic patients [2]. On the other hand, functional changes in the spiral ganglion cells caused by diabetes mellitus remain to be examined.Protein gene product (PGP) 9.5 is a ubiquitin carboxyl-terminal hydrolase [3] prevalent in cells of neural origin [4][5][6]. Although the functional significance of PGP 9.5 is still unclear, this protein may play an essential role in the ubiquitin-related metabolism in nervous tissues. Recently, PGP 9.5 has been increasingly used as a convenient neural marker in neurophysiological studies [7][8][9][10][11][12]. In the present study, therefore, we examined the immunoreactivity for PGP 9.5 in the spiral ganglion cells of the cochlea in prediabetic and diabetic WBN/Kob rats by an immunohistochemical method with computer-assisted image analysis and compared the results with those obtained from normal age-matched Wistar rats in order to reveal the functional changes in the spiral ganglion cells from a quantitative point of view. Diabetologia (1997) 40: 173-178 Changes in the immunoreactivity of protein gene product (PGP) 9.5 in the cochlea of spontaneously diabetic WBN/Kob rats Summary The mechanism of hearing impairment due to diabetes mellitus was examined in relation to changes in the level of the immunoreaction for the protein gene product 9.5 in the cochlea of spontaneously diabetic WBN/Kob rats. At 7 months (33 weeks) of age, when half of the males of this strain manifest diabetes, male WBN/Kob rats were divided into two groups as follows: one group consisted of prediabetic animals showing slightly decreased tolerance to glucose with a normal plasma concentration of glucose, normal urinary excretion of glucose, and functional hearing impairment (assessed in terms of elevation of hearing threshold). The second group consisted of diabetic animals with glucose intolerance, high plasma glucose level, polyuria, urinary glucose excretion, and more apparent elevation of hearing threshold. According to morphometric analysis of the spiral ganglion, the number of ganglion cells was significantly smaller in both the prediabetic and the diabetic animals than in the age-matched control Wistar rats. The staining intensity for protein gene product 9.5 was increased in some spiral ganglion cells of diabetic animals, but decreased in others according to quantitative immunohistochemical analysis. On the other hand, the immunoreactivity for protein gene product 9.5 was similar in the prediabetic animals to that in the control Wistar rats. These results suggest that numerical and immunohistochemical changes in the spiral ganglion cells r...

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The visualisation of cardiovascular innervation in the guinea pig using antiserum to protein gene product 9.5 (pgp 9.5)

Cited by 257 publications

References 44 publications

Nitric oxide, and not vasoactive intestinal peptide, as the main neurotransmitter of vagally induced relaxation of the guinea pig stomach

Nitric oxide, and not vasoactive intestinal peptide, as the main neurotransmitter of vagally induced relaxation of the guinea pig stomach

Desipramine attenuates loss of cardiac sympathetic neurotransmitters produced by congestive heart failure and NE infusion

Changes in the immunoreactivity of protein gene product (PGP) 9.5 in the cochlea of spontaneously diabetic WBN/Kob rats

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