NADPH-diaphorase-positive neurons in the auditory cortex of young and old rats

Ouda, Ladislav; Nwabueze-Ogbo, Fidel; Druga, R; Syka, Josef

doi:10.1097/00001756-200303030-00013

Cited by 17 publications

(23 citation statements)

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“…In contrast, a substantial decrease with aging in the levels of other markers in the auditory cortex of rats was reported in the case of GABA (Ling et al 2005), NADPH-diaphorase (Ouda et al 2003) and acetylcholine (Stemmelin et al, 2000). In our study we evaluate age-related…”

Section: Introductionmentioning

confidence: 86%

Changes in parvalbumin immunoreactivity with aging in the central auditory system of the rat

Ouda¹,

Druga²,

Syka³

2008

Experimental Gerontology

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Section: Introductionmentioning

confidence: 86%

Changes in parvalbumin immunoreactivity with aging in the central auditory system of the rat

Ouda¹,

Druga²,

Syka³

2008

Experimental Gerontology

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“…Idrizbegovic et al [2006] also showed a 25% reduction in the neurons in the dorsal and ventral cochlear nucleus in 24-month-old mice. Moreover, Ouda et al [2003] found a 46% reduction in the thickness of the auditory cortex in 36-month-old rats compared to in 3-month-old rats. Our study also found fewer neurons in the auditory cortex in old C57BL/6J mice than in young mice, but the number of apoptotic neurons was much higher than in young mice.…”

Section: Discussionmentioning

confidence: 85%

The miR-34a/Bcl-2 Pathway Contributes to Auditory Cortex Neuron Apoptosis in Age-Related Hearing Loss

Huang

Ou²,

Xiong³

et al. 2017

Audiol Neurotol

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Hypothesis: The miR-34a/Bcl-2 signaling pathway may play a role in the mechanisms related to age-related hearing loss (AHL) in the auditory cortex. Background: The auditory cortex plays a key role in the recognition and processing of complex sound. It is difficult to explain why patients with AHL have poor speech recognition, so increasing numbers of studies have focused on its central change. Although micro (mi)RNAs in the central nervous system have recently been increasingly reported to be associated with age-related diseases, the molecular mechanisms of AHL in the auditory cortex are not fully understood. Methods: The auditory brainstem response was used to assess the hearing ability of C57BL/6 mice, and q-PCR, immunohistochemistry, and Western blotting were used to detect the expression levels of miR-34a and Bcl-2 in the mouse auditory cortex. TUNEL and DNA fragmentation were adopted to detect the apoptosis of neurons in the auditory cortex. To verify the relationship of miR-34a and Bcl-2, we transfected an miR-34a mimic or miR-34a inhibitor into primary auditory cortex neurons. Results: In this study, miR-34a/Bcl-2 signaling was examined in auditory cortex neurons during aging. miR-34a and apoptosis increased in the auditory cortex neurons of C57BL/6 mice with aging, whereas an age-related decrease in Bcl-2 was determined. In the primary neurons of the auditory cortex, miR-34a overexpression inhibited Bcl-2, leading to an increase in apoptosis. Moreover, miR-34a knockdown increased Bcl-2 expression and diminished apoptosis. Conclusion: Our results support a link between age-related apoptosis in auditory cortex neurons and miR-34a/Bcl-2 signaling, which may serve as a potential mechanism of the expression of AHL in the auditory cortex.

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“…Few neuronal morphometric changes were observed, and only in specific bregma levels of Te2 and Te3, which makes difficult to draw conclusions from them. Nevertheless, the increase in the number of dendrites has been said to represent compensatory mechanisms related to the reduction in cortical NADPH-d-positive neurons (Ouda et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

“…In central auditory structures, NOS activity was found in neuronal elements of the cochlea (Fessenden et al, 1994), superior olivary complex (Reuss, 1998;, inferior colliculus (IC) (Druga and Syka, 1993), and auditory cortex (AC) (Druga and Syka, 1993;Huh et al, 1998;Ouda et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

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Age‐related changes of NADPH‐diaphorase‐positive neurons in the rat inferior colliculus and auditory cortex

Sánchez‐Zuriaga

Martí-Gutiérrez

Cruz

et al. 2007

Microscopy Res & Technique

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Nitric oxide (NO) has been implied in age-related changes of the central nervous system (CNS) and the central auditory pathway. The present study was conducted to investigate whether the number of NO-producing cells and their morphometric characteristics in the inferior colliculus (IC) and the auditory cortex (AC) are changed with the increasing age of the subjects. IC and AC sections of adult and senile Wistar rats were studied using the histochemical detection of NADPH-diaphorase activity (NADPH-d), a marker for neurons containing nitric oxide synthase (NOS). Our results showed a decreased area of the somas of NADPH-d-positive neurons in the dorsal cortex (DC) of the IC and a diffuse loss of NADPH-d-positive neurons in the senile IC and primary cortical auditory area (Te1). However, an increased number of NO-producing cells have been shown by other authors in different parts of the ageing auditory pathway and CNS. It seems that age-related changes in NADPH-d-positive cells may follow a region-specific route. These changes may be related to hearing impairments with increasing age.

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NADPH-diaphorase-positive neurons in the auditory cortex of young and old rats

Cited by 17 publications

References 0 publications

Changes in parvalbumin immunoreactivity with aging in the central auditory system of the rat

Changes in parvalbumin immunoreactivity with aging in the central auditory system of the rat

The miR-34a/Bcl-2 Pathway Contributes to Auditory Cortex Neuron Apoptosis in Age-Related Hearing Loss

Age‐related changes of NADPH‐diaphorase‐positive neurons in the rat inferior colliculus and auditory cortex

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