Altered modulatory actions of serotonin on dentate granule cells of aged rats

Baskys, Andrius; Niesen, Charles E.; Carlen, Peter L.

doi:10.1016/0006-8993(87)90574-9

Cited by 41 publications

(2 citation statements)

References 30 publications

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“…S5). Furthermore, no age‐related changes in the Ca 2 + ‐dependent postburst afterhyperpolarization have been observed in DG granule cells (Baskys et al ., ; Niesen et al ., ; Reynolds & Carlen, ). Therefore, S1928 phosphorylation cannot account for increased calcium influx and reduced neuronal excitability with normal aging observed in CA1 hippocampal pyramidal neurons (Landfield & Pitler, ; Moyer et al ., ; Moyer & Disterhoft, ; Thibault & Landfield, ).…”

Section: Discussionmentioning

confidence: 98%

Surface L‐type Ca²⁺ channel expression levels are increased in aged hippocampus

Nunez-Santana

Antion³

et al. 2013

Aging Cell

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Summary Age-related increase in L-type Ca2+ channel (LTCC) expression in hippocampal pyramidal neurons has been hypothesized to underlie the increased Ca2+ influx and subsequent reduced intrinsic neuronal excitability of these neurons that lead to age-related cognitive deficits. Here, using specific antibodies against Cav1.2 and Cav1.3 subunits of LTCCs, we systematically re-examined the expression of these proteins in the hippocampus from young (3–4 month old) and aged (30–32 month old) F344xBN rats. Western blot analysis of the total expression levels revealed significant reductions in both Cav1.2 and Cav1.3 subunits from all three major hippocampal regions of aged rats. Despite the decreases in total expression levels, surface biotinylation experiments revealed significantly higher proportion of expression on the plasma membrane of Cav1.2 in the CA1 and CA3 regions and of Cav1.3 in the CA3 region from aged rats. Furthermore, the surface biotinylation results were supported by immunohistochemical analysis that revealed significant increases of Cav1.2 immunoreactivity in the CA1 and CA3 regions of aged hippocampal pyramidal neurons. In addition, we found a significant increase in the level of phosphorylated Cav1.2 on the plasma membrane in the dentate gyrus of aged rats. Taken together, our present findings provide clear evidence that age-related cognitive deficits cannot be attributed to a global change in L-type channel expression nor to the level of phosphorylation of Cav1.2 on the plasma membrane of hippocampal neurons. Rather increased expression and density of functional LTCCs on the plasma membrane may underlie the age-related increase in L-type Ca2+ channel activity in CA1 pyramidal neurons.

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Section: Discussionmentioning

confidence: 98%

Surface L‐type Ca²⁺ channel expression levels are increased in aged hippocampus

Nunez-Santana

Antion³

et al. 2013

Aging Cell

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“…For example, spine and synapse number in hippocampal slices are increased relative to perfusion-fixed hippocampus in vivo (Kirov et al, 1999); it was possible that age could have affected this process, leading to a spurious conclusion regarding the effects of age on synaptic transmission in the intact brain. In general, replication in vivo of such prominent effect as age on hippocampal neurophysiology provides a foundation for the interpretation of other studies on the effects of the aging process, which are currently technically possible only in the in vitro preparation (for example, Barnes & McNaughton, 1980;Baskys et al, 1987;Billard et al, 1997;Campbell et al, 1996;Jouvenceau et al, 1998;Magnusson, 1998;Norris et al 197;Ouanounou et al 1999;Potier et al, 1992;Reynolds & Carlen, 1989;Rosenzweig et al, 1997;Shankar et al, 1998, Shen & Barnes, 1996.…”

Section: Discussionmentioning

confidence: 99%

Age‐Related Decrease in the Schaffer Collateral‐Evoked EPSP in Awake, Freely, Behaving Rats

2000

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Synaptic response size in the CA1 region of the hippocampus in aged rats is reduced for a given stimulus intensity, compared with that elicited in young rats. Consistent with the in vitro findings of reduced Schaffer collateral-evoked CA1 EPSPs in old rats, the population currents evoked to iontophoretically applied AMPA are also smaller relative to the presynaptic fiber potential amplitude. On the other hand, the size of the presynaptic fiber potential and amplitude of unitary intra-cellularly recorded EPSP responses do not change across age in the CA1 region. These electrophysiological findings are consistent with the hypothesis that old rats have fewer functional synaptic contacts per Schaffer collateral axon than do young rats. The possibility that this age change arises as a result of a differential tissue recovery response to in vitro preparation was examined in the present study. CA1 presynaptic fiber potential and EPSP amplitudes evoked by the stimulation of Schaffer collateral afferents were studied in intact, freely behaving young and old rats. We confirmed in vivo the pattern of electrophysiophysiological results previously reported in vitro and found significant correlations between the synaptic response amplitudes and the accuracy of spatial behavior in the Morris swim task. The data suggest that changes in functional connectivity of old rats may be a significant contributor to cognitive changes during aging.

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