Physiological and immunohistochemical characterization of cisplatin-induced neuropathy in mice

Verdú, Enrique; Vilches, J; Rodríguez, Francisco; Ceballos, Dolores; Valero, Antoni; Navarro, Xavier

doi:10.1002/(sici)1097-4598(199903)22:3<329::aid-mus5>3.0.co;2-8

Cited by 83 publications

(55 citation statements)

References 44 publications

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“…This observation implies that a loss of functional marker was earlier than a loss of structural marker. Such a difference may be in concordance with a previous study on a mouse model of cisplatin neuropathy that found decrease in VIP + nerves at an early stage followed by PGP 9.5 + nerve degeneration at a later stage 35. Multiple mechanisms underlie such a time window in the denervation of PGP 9.5 + and VIP + sudomotor nerves, including decreased synthesis or impaired axonal transport of neuropeptide at the early stage of FAP and progressive axonal degeneration as the disease burden increases 36.…”

Section: Discussionsupporting

confidence: 93%

Sudomotor innervation in transthyretin amyloid neuropathy: Pathology and functional correlates

Chao

Huang

Chiang

et al. 2015

Annals of Neurology

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ObjectiveAutonomic neuropathy is a major component of familial amyloid polyneuropathy (FAP) due to mutated transthyretin, with sudomotor failure as a common manifestation. This study aimed to investigate the pathology and clinical significance of sudomotor denervation.MethodsSkin biopsies were performed on the distal leg of FAP patients with a follow‐up duration of 3.8 ± 1.6 years. Sudomotor innervation was stained with 2 markers: protein gene product 9.5 (PGP 9.5), a general neuronal marker, and vasoactive intestinal peptide (VIP), a sudomotor nerve functional marker, followed by quantitation according to sweat gland innervation index (SGII) for PGP 9.5 (SGIIPGP 9.5) and VIP (SGIIVIP).ResultsThere were 28 patients (25 men) with Ala97Ser transthyretin and late onset (59.9 ± 6.0 years) disabling neuropathy. Autonomic symptoms were present in 22 patients (78.6%) at the time of skin biopsy. The SGIIPGP 9.5 and SGIIVIP of FAP patients were significantly lower than those of age‐ and gender‐matched controls. The reduction of SGIIVIP was more severe than that of SGIIPGP 9.5 (p = 0.002). Patients with orthostatic hypotension or absent sympathetic skin response at palms were associated with lower SGIIPGP 9.5 (p = 0.019 and 0.002, respectively). SGIIPGP 9.5 was negatively correlated with the disability grade at the time of skin biopsy (p = 0.004), and was positively correlated with the interval from the time of skin biopsy to the time of wheelchair usage (p = 0.029).InterpretationThis study documented the pathological evidence of sudomotor denervation in FAP. SGIIPGP 9.5 was functionally correlated with autonomic symptoms, autonomic tests, ambulation status, and progression of disability. Ann Neurol 2015;78:272℃283

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Section: Discussionsupporting

confidence: 93%

Sudomotor innervation in transthyretin amyloid neuropathy: Pathology and functional correlates

Chao

Huang

Chiang

et al. 2015

Annals of Neurology

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“…Immunocytochemistry Mice were perfused transcardially with 9 g/l NaCl followed by Zamboni's fixative [27]. The spinal cord, DRG, plantar footpads and toes were removed, post-fixed with Zamboni's fixative for 2 h, and then cryoprotected with 300 g/l sucrose in PBS overnight.…”

Section: Methodsmentioning

confidence: 54%

Prolonged preservation of nerve function in diabetic neuropathy in mice by herpes simplex virus-mediated gene transfer

Chattopadhyay¹,

Mata²,

Goss³

et al. 2007

Diabetologia

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Aims/hypothesis The aim of this study was to determine whether prolonged expression of neurotrophin-3 (NT-3) in mice, achieved by herpes simplex virus (HSV)-mediated gene transfer with gene expression under the control of an HSV latency promoter, can provide protection against the progression of diabetic neuropathy over a 6 month period. Materials and methods Mice with diabetes induced by streptozotocin were inoculated s.c. into both hind feet with a non-replicating HSV vector containing the coding sequence for NT-3 under the control of the HSV latencyassociated promoter 2 (LAP2) elements or with a control vector. Nerve function was evaluated by electrophysiological and behavioural measures over the course of 6 months after the onset of diabetes. Results Animals inoculated with the NT-3-expressing vector, but not animals inoculated with control vector, showed preservation of sensory and motor nerve amplitude and conduction velocity measured electrophysiologically, small fibre sensory function assessed by withdrawal from heat, autonomic function measured by pilocarpine-induced sweating, skin innervation assessed by protein gene product 9.5 staining of axons, and density of calcitonin gene-related peptide terminals in the spinal cord measured by immunohistochemistry 5.5 months after vector inoculation. Conclusions/interpretation These results indicate that the continuous production of NT-3 by LAP2-driven expression of the transgene from an HSV vector over a 6 month period protects against progression of diabetic neuropathy in mice, and provide a proof-of-principle demonstration for the development of a novel therapy for preventing the progression of diabetic neuropathy.

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“…Another model demonstrated that cisplatin causes a decrease in SNCV progressing in parallel with a decrease of neuropeptide expression in the terminal nerve fibers (calcitonin gene-related peptide, vasoactive intestinal peptide), associated to a lesser degree with a mechanical hypoalgesia. 51 After this, Aloe et al 52 also reported a heat hypoalgesia with a decrease in catecholaminergic nerve fibers density and an increase in substance P levels. More recently, Ta et al 45 have developed a model with a reported mechanical allodynia and a heat hyperalgesia (Table 2).…”

Section: Platinum Compoundsmentioning

confidence: 99%

Animal Models of Chemotherapy-Evoked Painful Peripheral Neuropathies

et al. 2009

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Summary:This review examines recent preclinical research on toxic peripheral neuropathy and potential therapeutic developments. Chemotherapy-induced peripheral neurotoxicity is a major clinical problem because it represents the dose-limiting side effects of a significant number of antineoplastic drugs. Patients are unable to complete full or optimal treatment schedules. The incidence of chemotherapy-induced peripheral neuropathy varies depending on the drugs and schedules used, and this can be quite high, particularly when neurophysiological methods are used to make a diagnosis. However, even when chemotherapy-induced peripheral neuropathy is not a doselimiting side effect, its onset may severely affect the quality of life of cancer patients and cause chronic discomfort. As such, improved understanding of the pathophysiology of chemotherapy-induced neurotoxicity need for animal models is clinically relevant and will assist in the development of future neuroprotective strategies and also in the design of novel chemotherapies with improved toxicity profiles. In this review, the features of animal models of chemotherapy-induced painful neuropathy developed for 20 years, due to the administration of the most widely used drugs, such as platinum drugs, taxanes, and vinca alkaloids, will be discussed. In a second part, data available on neuroprotectants and treatment strategies, evaluated using these previous animal models in the attempt to prevent neuropathic pain, will be summarized.

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Physiological and immunohistochemical characterization of cisplatin-induced neuropathy in mice

Cited by 83 publications

References 44 publications

Sudomotor innervation in transthyretin amyloid neuropathy: Pathology and functional correlates

Sudomotor innervation in transthyretin amyloid neuropathy: Pathology and functional correlates

Prolonged preservation of nerve function in diabetic neuropathy in mice by herpes simplex virus-mediated gene transfer

Animal Models of Chemotherapy-Evoked Painful Peripheral Neuropathies

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