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Related Experiment Video

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Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

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Alterations in calcium signaling and a decrease in Bcl-2 expression: possible correlation with apoptosis in aged

R P Ureshino¹, C R Bertoncini, M J S Fernandes

¹Department of Pharmacology, Federal University of São Paulo, São Paulo, Brazil.

Journal of Neuroscience Research

|September 24, 2009

Summary

Aging brains exhibit altered calcium (Ca2+) signaling and increased oxidative stress, leading to heightened apoptosis and cell death in the striatum. These changes in calcium handling and reduced Bcl-2 expression contribute to age-related neurodegeneration.

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Area of Science:

Neuroscience
Cell Biology
Aging Research

Background:

Aging is linked to functional deficits and increased susceptibility to neurodegenerative diseases.
Altered calcium (Ca2+) homeostasis is a known factor in neurodegeneration.
The aged striatum's susceptibility to cell death warrants investigation.

Purpose of the Study:

To investigate Ca2+ signaling and apoptosis in the aged rat striatum.
To identify age-related changes in glutamate receptor expression and function.
To explore the role of mitochondrial Ca2+ and reactive oxygen species (ROS) in aged striatal apoptosis.

Main Methods:

Electrophysiological recordings of Ca2+ responses to glutamate and NMDA.
Immunostaining for glutamate receptor subunits (NR1).
Measurement of mitochondrial Ca2+ content and ROS levels.
Assessment of Bcl-2 protein expression and apoptosis markers.

Main Results:

Aged striatum showed enhanced Ca2+ responses to glutamate and NMDA, dependent on external Ca2+.
Increased expression of NMDA receptor subunit NR1 was observed in aged rats.
Elevated mitochondrial Ca2+ and ROS levels were found in aged animals.
Aged striatum exhibited decreased Bcl-2 protein and increased apoptosis.

Conclusions:

Altered Ca2+ handling, particularly via NMDA receptors, contributes to aged striatal vulnerability.
Increased ROS accumulation and reduced Bcl-2 expression promote apoptosis in the aged striatum.
These age-related molecular changes may underlie neurodegeneration in the rat striatum.