2015Neurochemical JournalRequires access

The expression of the TrkA and TrkB high-affinity neurotrophin receptors in the rat hippocampus after intracerebroventricular administration of Aβ(25–35)

M. Yu. Stepanichev, А. О. Тишкина, Н. А. Лазарева, E. K. Mart’yanova, Г. Р. Тухбатова, А. О. Кулагина, С. В. Саложин, N. V. Gulyaeva

Open publisher page 0 citations

Abstract

We studied the changes in the expression of high-affinity TrkA and TrkB receptors of the nerve-growth factor and brain-derived neurotrophic factor in the rat hippocampus at different time points after the administration of Aβ(25–35) into the lateral cerebral ventricles. Studies on TrkA and TrkB expression were performed using immunohistochemistry and the method of the real-time polymerase chain reaction. We found that intracerebroventricular administration of Aβ(25–35) to rats resulted in long-term alterations in the system of neurotrophic signaling in the hippocampus. Expression of the TrkA receptor increased 28 days after treatment, whereas expression of the TrkB receptor increased 12 days and then decreased by 28 days after the treatment. Thus, alterations in neurotrophin signaling may be involved in the mechanisms that are responsible for Aβ(25–35)-induced impairment of hippocampal functions in rats.

About this research paper

What this paper is about

We studied the changes in the expression of high-affinity TrkA and TrkB receptors of the nerve-growth factor and brain-derived neurotrophic factor in the rat hippocampus at different time points after the administration of Aβ(25–35) into the lateral cerebral ventricles. Studies on TrkA and TrkB expression were performed using immunohistochemistry and the method of the real-time polymerase chain reaction. We found that intracerebroventricular administration of Aβ(25–35) to rats resulted in long-term alterations in the system of neurotrophic signaling in the hippocampus. Expression of the TrkA receptor increased 28 days after treatment, whereas expression of the TrkB receptor increased 12 days and then decreased by 28 days after the treatment. Thus, alterations in neurotrophin signaling may be involved in the mechanisms that are responsible for Aβ(25–35)-induced impairment of hippocampal functions in rats.

Why it matters

A significance statement is not available in the OpenAlex record.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

We studied the changes in the expression of high-affinity TrkA and TrkB receptors of the nerve-growth factor and brain-derived neurotrophic factor in the rat hippocampus at different time points after the administration of Aβ(25–35) into the lateral cerebral ventricles. Studies on TrkA and TrkB expression were performed using immunohistochemistry and the method of the real-time polymerase chain reaction. We found that intracerebroventricular administration of Aβ(25–35) to rats resulted in long-term alterations in the system of neurotrophic signaling in the hippocampus. Expression of the TrkA receptor increased 28 days after treatment, whereas expression of the TrkB receptor increased 12 days and then decreased by 28 days after the treatment. Thus, alterations in neurotrophin signaling may be involved in the mechanisms that are responsible for Aβ(25–35)-induced impairment of hippocampal functions in rats.

Key concepts: Tropomyosin receptor kinase B, Tropomyosin receptor kinase A, Low-affinity nerve growth factor receptor, Neurotrophin, Hippocampus, Nerve growth factor, Internal medicine, Neurotrophic factors

Related papers

Back to paper searchBrowse research topicsOriginal source
The expression of the TrkA and TrkB high-affinity neurotrophin receptors in the rat hippocampus after intracerebroventricular administration of Aβ(25–35) — Research Paper | ScholarLens