Elsevier

Neuroscience

Volume 101, Issue 4, 30 November 2000, Pages 807-810
Neuroscience

Letter to Neuroscience
Increase in AMPA receptors in aged memory-impaired rats is not associated with increase in monoamine oxidase B levels

https://doi.org/10.1016/S0306-4522(00)00459-0Get rights and content

Abstract

Aged rats may be behaviorally classified as either cognitively impaired or unimpaired based upon their performance in the Morris water maze task. In aged Long–Evans rats, emergence of functional deficits has been related to the increase in the α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor subtype in most hippocampal subfields, not observed in other brain structures. As AMPA receptors expressed in astrocytes may participate in the delayed and long-term glial response to injury, we investigated whether astrocytes participate in the increase of AMPA receptor observed in these aged rats. To this end, distribution of monoamine oxidase B, used as an astroglial marker, was characterized by quantitative autoradiography in the hippocampus and septum of young adults (six months) and aged (24–25 months) rats using [3H]lazabemide. Specific binding to brain sections of young, aged unimpaired, and aged impaired animals were calculated densitometrically. Compared to young animals, all hippocampal subfields in the aged unimpaired group showed a significant age-related increased labeling, which was not present in the aged impaired group. This contrasts with the increased glial transcription described in this last group.

We propose that increase in AMPA receptors in the aged memory-impaired animals may be related to an atypic astrocytic reactivity.

Section snippets

Conclusion

The present study indicates that atypical hippocampal astrocytic reactivity may participate in age-memory impairment. If true, although it may be part of the gliopathic changes easily evidenced by MAO-B analysis, the AMPA receptor increase characterized in AI rats may also be viewed as a neuronal compensatory mechanism to help counteract the loss of cognitive function. Nevertheless, further experiments are required in order to validate this hypothesis and to clarify the origin and reasons for

Experimental procedures

Experiments were performed using male Long–Evans rats obtained from Charles River Breeding Farms (St Constant, Quebec, Canada). Animal care and experimental procedures comformed to the McGill Animal Care Committee and the Canadian Council for Animal Care guidelines; all efforts were made to minimize animal suffering and to use only the number of animals necessary to produce reliable scientific data. Aged (24–25 months old) and young adult (six months old) Long–Evans rats were screened using the

Acknowledgements

We gratefully acknowledge Dr J. G. Richards, Hoffmann La Roche (Basel) for the generous gift of [3H]lazabemide. Supported by MRCC, SGR 97-00128 and FIS 00/0232.

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