Somatostatin and brain-derived neurotrophic factor mRNA expression in the primate brain: decreased levels of mRNAs during aging

Hayashi, Michihiro; Yamashita, Akiko; Shimizu, Keiko

doi:10.1016/s0006-8993(96)01317-0

Cited by 115 publications

(58 citation statements)

References 50 publications

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“…2C), perhaps reflecting its low expression level in this layer in control subjects. Consistent with previous reports of age-dependent declines in BDNF and TrkB mRNA expression levels (Hayashi et al, 1997;Romanczyk et al, 2002), we detected significant negative correlations between BDNF mRNA expression and age for both the control (r ϭ Ϫ0.62; p ϭ 0.015) and schizophrenia (r ϭ Ϫ0.52; p ϭ 0.049) groups and trends for negative correlations between TrkB mRNA and age (r ϭ Ϫ0.49, p ϭ 0.065 for the control group; r ϭ Ϫ0.48, p ϭ 0.070 for the schizophrenia group). The regression lines for subjects with schizophrenia were parallel to and shifted downward from those for control subjects (Fig.…”

Section: Expression Of Bdnf Trkb and Trkc Mrnas In The Pfc Of Subjesupporting

confidence: 92%

Relationship of Brain-Derived Neurotrophic Factor and Its Receptor TrkB to Altered Inhibitory Prefrontal Circuitry in Schizophrenia

Hashimoto¹,

Bergen²,

Nguyen³

et al. 2005

J. Neurosci.

367

292

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Dysfunction of inhibitory neurons in the prefrontal cortex (PFC), represented by decreased expression of GABA-related genes such as the 67 kDa isoform of glutamate decarboxylase (GAD 67 ) and parvalbumin (PV), appears to contribute to cognitive deficits in subjects with schizophrenia. We investigated the involvement of signaling mediated by brain-derived neurotrophic factor (BDNF) and its receptor tyrosine kinase TrkB in producing the altered GABA-related gene expression in schizophrenia. In 15 pairs of subjects with schizophrenia and matched control subjects, both BDNF and TrkB mRNA levels, as assessed by in situ hybridization, were significantly decreased in the PFC of the subjects with schizophrenia, whereas the levels of mRNA encoding the receptor tyrosine kinase for neurotrophin-3, TrkC, were unchanged. In this cohort, within-pair changes in TrkB mRNA levels were significantly correlated with those in both GAD 67 and PV mRNA levels. Decreased BDNF, TrkB, and GAD 67 mRNA levels were replicated in a second cohort of 12 subject pairs. In the combined cohorts, the correlation between within-pair changes in TrkB and GAD 67 mRNA levels was significantly stronger than the correlation between the changes in BDNF and GAD 67 mRNA levels. Neither BDNF nor TrkB mRNA levels were changed in the PFC of monkeys after a long-term exposure to haloperidol. Genetically introduced decreases in TrkB expression, but not in BDNF expression, also resulted in decreased GAD 67 and PV mRNA levels in the PFC of adult mice; in addition, the cellular pattern of altered GAD 67 mRNA expression paralleled that present in schizophrenia. Decreased TrkB signaling appears to underlie the dysfunction of inhibitory neurons in the PFC of subjects with schizophrenia.

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Section: Expression Of Bdnf Trkb and Trkc Mrnas In The Pfc Of Subjesupporting

confidence: 92%

Relationship of Brain-Derived Neurotrophic Factor and Its Receptor TrkB to Altered Inhibitory Prefrontal Circuitry in Schizophrenia

Hashimoto¹,

Bergen²,

Nguyen³

et al. 2005

J. Neurosci.

367

292

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“…However, although expression of somatostatin mRNA is reduced in frontal cortex, parietal cortex, striatum, and hippocampus, it is unchanged in the hypothalamus (255,256). The age-related decline in somatostatin gene expression in the frontal and parietal cortex of rats paralleled impaired memory performance in a modified Morris water maze test (257).…”

Section: H Somatostatin In the Cnsmentioning

confidence: 99%

Molecular Endocrinology and Physiology of the Aging Central Nervous System

2005

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Aging is associated with a progressive decline in physical and cognitive functions. The impact of age-dependent endocrine changes regulated by the central nervous system on the dynamics of neuronal behavior, neurodegeneration, cognition, biological rhythms, sexual behavior, and metabolism are reviewed. We also briefly review how functional deficits associated with increases in glucocorticoids and cytokines and declining production of sex steroids, GH, and IGF are likely exacerbated by age-dependent molecular misreading and alterations in components of signal transduction pathways and transcription factors. (Endocrine Reviews 26: 203-250, 2005)

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“…These two BDNF transcript sizes are similar to what have been reported previously in cortical regions of the primate brain. 55 BDNF RNase protection assay Visual inspection of the autoradiographic films generated in the RNase protection assay revealed protected BDNF mRNA in all samples assayed ( Figure 2a). The 0 lane of the standard curve contained no apparent signal, verifying that the RNase levels used were sufficient to digest the unprotected singlestranded riboprobe.…”

Section: Bdnf Northern Analysismentioning

confidence: 99%

Reduced brain-derived neurotrophic factor in prefrontal cortex of patients with schizophrenia

et al. 2003

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Anatomical and molecular abnormalities of excitatory neurons in the dorsolateral prefrontal cortex (DLPFC) are found in schizophrenia. We hypothesized that brain-derived neurotrophic factor (BDNF), a protein capable of increasing pyramidal neuron spine density and augmenting synaptic efficacy of glutamate, may be abnormally expressed in the DLPFC of patients with schizophrenia. Using an RNase protection assay and Western blotting, we detected a significant reduction in BDNF mRNA (mean = 23%) and protein (mean = 40%) in the DLPFC of patients with schizophrenia compared to normal individuals. At the cellular level, BDNF mRNA was expressed at varying intensities in pyramidal neurons throughout layers II, III, V, and VI of DLPFC. In patients with schizophrenia; neuronal BDNF expression was decreased in layers III, V and VI. Our study demonstrates a reduction in BDNF production and availability in the DLPFC of schizophrenics, and suggests that intrinsic cortical neurons, afferent neurons, and target neurons may receive less trophic support in this disorder.

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Somatostatin and brain-derived neurotrophic factor mRNA expression in the primate brain: decreased levels of mRNAs during aging

Cited by 115 publications

References 50 publications

Relationship of Brain-Derived Neurotrophic Factor and Its Receptor TrkB to Altered Inhibitory Prefrontal Circuitry in Schizophrenia

Relationship of Brain-Derived Neurotrophic Factor and Its Receptor TrkB to Altered Inhibitory Prefrontal Circuitry in Schizophrenia

Molecular Endocrinology and Physiology of the Aging Central Nervous System

Reduced brain-derived neurotrophic factor in prefrontal cortex of patients with schizophrenia

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