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Rearrangement of centromeric satellite DNA in hippocampal neurons exhibiting long-term potentiation

1992; Elsevier BV; Volume: 14; Issue: 1-2 Linguagem: Inglês

10.1016/0169-328x(92)90016-5

1872-6941

Filio Billia, Andrius Baskys, Peter L. Carlen, Umberto De Boni,

Genetics and Neurodevelopmental Disorders

In situ hybridization in conjunction with three-dimensional reconstruction was used to examine the topology of satellite DNA (sDNA) sequences in hippocampal CA1 neurons. In slices fixed immediately after preparation, 4–5 signals/nucleus were detected in CA1, CA3 and dentate neurons, 70–80% of 154 neurons examined in these 3 areas displayed all signals at the nuclear periphery. In the remaining fraction of neurons, sDNA signals were divided between the nucleolus and the nuclear periphery. sDNA signals were consistently localized to the nuclear midplane. Slices left to equilibrate in artificial cerebral spinal fluid for 1 h, in the absence of potentiation, exhibited a significant increase in the total number of signals/nucleus in CA1 and dentate neurons. This increase in the number of signals occurred in both nucleolar and peripheral compartments, with the number of the nucleolar compartment nearly doubling. The total number of signals/nucleus was found to be consistently reduced in tetanized CA1 neurons (4.89 ± 0.09 signals/nucleus, n = 195, P < 0.05) as compared to neurons from unpotentiated slices (5.27 ± 0.10 signals/nucleus, n = 81). A similar decrease in the total number of signals/nucleus was also observed in CA1 neurons exposed to N-methyl-d-aspartate (NMDA), from 5.27 ± 0.10 signals/nucleus (n = 81) to 5.00 ± 0.08 signals/nucleus (n = 215, P < 0.05). In contrast, dentate neurons, employed as internal controls, did not exhibit any change in number and compartmentalization of sDNA signals. These results suggest that tetanic stimulation, resulting in long-term potentiation in CA1 neurons, is associated with changes in the number of detectable sDNA signals, possibly through increased clustering, and that these changes may be mediated by NMDA receptor activation.