Brainstem auditory evoked potentials in rats with streptozotocin-induced diabetes

Rubini, R.; Biasiolo, Fabrizio; Fogarolo, Fabiano; Magnavita, Vincenzo; Martini, Alessandro; Fiori, M.

doi:10.1016/0168-8227(92)90131-a

Cited by 17 publications

(10 citation statements)

References 32 publications

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“…The finding that MNCV and SNCV in diabetic rats only increased marginally throughout the experiment does not just reflect a disturbed maturation: if diabetes is induced in full-grown rats, deficits in MNCV and SNCV develop as in young adult rats, although the rate of development appears to be slightly slower [27,28]. The increased interpeak latency III-V in the BAEP and VEP p1 latency found in diabetic rats is in agreement with earlier studies [12,29,30]. In line with previous observations, the latencies of the flash-evoked VEP were not affected by cataract formation in diabetic rats [12].…”

Section: Discussionsupporting

confidence: 86%

Nerve conduction velocity and evoked potential latencies in streptozotocin‐diabetic rats: effects of treatment with an angiotensin converting enzyme inhibitor

Manschot

Gispen

Kappelle

et al. 2003

Diabetes Metabolism Res

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Section: Discussionsupporting

confidence: 86%

Nerve conduction velocity and evoked potential latencies in streptozotocin‐diabetic rats: effects of treatment with an angiotensin converting enzyme inhibitor

Manschot

Gispen

Kappelle

et al. 2003

Diabetes Metabolism Res

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“…For central auditory function, STZ-induced diabetes in rats (less then 5 months) showed no effect on ABR interpeak latencies, but increased peripheral (I and II) and central (IV) peak latencies (Notvest and Inserra 1987; Rubini et al 1992). For longer duration of STZ induced diabetes (over 6 months), prolongation of central transmission times (increased late interpeak latencies) were observed in rats (Biessels et al 1999, 2001; Manschot et al 2003).…”

Section: Discussionmentioning

confidence: 88%

Interactions of hearing loss and diabetes mellitus in the middle age CBA/CaJ mouse model of presbycusis

et al. 2009

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Recently, we characterized the more severe nature of hearing loss in aged Type 2 diabetic human subjects. The current study prospectively assessed hearing abilities in middle age CBA/CaJ mice with Type 1 diabetes mellitus (T1DM) (STZ injection) or Type 2 diabetes mellitus (T2DM) (high fat diet), for a period of 6 months. Blood glucose, body weight and auditory tests (Auditory Brainstem Response-ABR, Distortion Product Otoacoustic Emissions-DPOAE) were evaluated at baseline and every 2 months. Tone and broadband noise-burst responses in the inferior colliculus were obtained at 6 months. Body weights of controls did not change over 6 months (~32g), but there was a significant (~5g) decline in the T1DM, while T2DM exhibited ~10g weight gain. Blood glucose levels significantly increased: 3 fold for T1DM, 1.3 fold for T2DM; with no significant changes in controls. ABR threshold elevations were found for both types of diabetes, but were most pronounced in the T2DM, starting as early as 2 months after induction of diabetes. A decline of mean DPOAE amplitudes was observed in both diabetic groups at high frequencies, and for the T2DM at low frequencies. In contrast to ABR thresholds, tone and noise thresholds in the inferior colliculus were lower for both diabetic groups. Induction of diabetes in middle-aged CBA/CaJ mice promotes amplification of age-related peripheral hearing loss which makes it a suitable model for studying the interaction of age-related hearing loss and diabetes. On the other hand, initial results of effects from very high blood glucose level (T1DM) on the auditory midbrain showed disruption of central inhibition, increased response synchrony or enhanced excitation in the inferior colliculus.

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“…The latencies of auditory and visual potentials were found to be prolonged in STZ-diabetic rats Rubini et al, 1992) and BB/W diabetic rats (Chakrabarti et al, 1991;Sima et al, 1992), indicating impaired CNS conduction velocities in diabetes. In hippocampal slices from STZ-diabetic rats, long-term potentiation (LTP) induced by 100-Hz stimulation was impaired, whereas long-term depression (LTD) was enhanced compared with control rats (Biessels et al, 1998;Gispen and Biessels, 2000;Kamal et al, 2000), indicating that altered hippocampal synaptic plasticity occurs in type 1 STZdiabetic rats.…”

Section: Electrophysiological Changesmentioning

confidence: 94%

C‐peptide and Central Nervous System Complications in Diabetes

Sima

2003

Journal of Diabetes Research

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Substantial evidence collected from clinical data and experimental studies has indicated that CNS is not spared from diabetes complications. Impairments in CNS function are well documented in both type 1 and type 2 diabetic patients as well as in various animal models of diabetes, in terms of alterations in cognition, neuropsychology, neurobehavior, electrophysiology, structure, neurochemistry and apoptotic activities. These data suggest that primary diabetic encephalopathy exists as a definable diabetic complication. The mechanisms underlying this CNS complication are not clear. Experimental studies have suggested that neuronal apoptosis may play an important role in neuronal loss and impaired cognitive function. In diabetes multiple factors are responsible for neuronal apoptosis, such as a perturbed IGF system, hyperglycemia and the aging process itself. Recent data suggest that insulin/C-peptide deficiency may exert an eminent role. Administration of C-peptide partially corrects the perturbed IGF system in the brain and prevents neuronal apoptosis in hippocampus of type 1 diabetes. In neuroblastoma SH-SY5Y cells C-peptide provides a dose-dependent stimulation on cell proliferation and an anti-apoptotic effect as well. These studies provide a basis for administration of C-peptide as a potentially effective therapy for type 1 diabetes.

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Brainstem auditory evoked potentials in rats with streptozotocin-induced diabetes

Cited by 17 publications

References 32 publications

Nerve conduction velocity and evoked potential latencies in streptozotocin‐diabetic rats: effects of treatment with an angiotensin converting enzyme inhibitor

Nerve conduction velocity and evoked potential latencies in streptozotocin‐diabetic rats: effects of treatment with an angiotensin converting enzyme inhibitor

Interactions of hearing loss and diabetes mellitus in the middle age CBA/CaJ mouse model of presbycusis

C‐peptide and Central Nervous System Complications in Diabetes

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