Spatial performance correlates with in vitro potentiation in young and aged Fischer 344 rats

Deupree, David L.; Turner, Dennis A.; Watters, Carter L.

doi:10.1016/0006-8993(91)90164-q

Cited by 113 publications

(56 citation statements)

References 32 publications

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“…This link has been strengthened by studies in which hippocampal LTP in aged rats was found to be related to individual differences in spatial learning ability (Barnes and McNaughton, 1985;Deupree et al, 1991;Davis et al, 1993;Bach et al, 1999). Such correlative studies reinforce the idea that the hippocampus plays a key role in spatial memory formation, but whether a selective deficit in LTP per se explains the spatial learning deficit in aged animals is unclear (Shors and Matzel, 1997;McEachern and Shaw, 1999).…”

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confidence: 85%

“…Spatial learning is particularly impaired in aged rats, but some aged subjects show severe deficits in spatial learning, whereas others are indistinguishable from young controls (Gage et al, 1984;Barnes and McNaughton, 1985;Deupree et al, 1991;Quirion et al, 1995;Backman et al, 1996). The basis for this variability is unknown, but it is well documented that spatial learning in rodents is strongly hippocampus dependent (Morris et al, 1982(Morris et al, , 1990Hollup et al, 2001).…”

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confidence: 99%

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Theta-Frequency Synaptic Potentiation in CA1In VitroDistinguishes Cognitively Impaired from Unimpaired Aged Fischer 344 Rats

et al. 2002

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Hippocampal-dependent learning and memory deficits have been well documented in aging rodents. The results of several recent studies have suggested that these deficits arise from weakened synaptic plasticity within the hippocampus. In the present study, we examined the relationship between hippocampal long-term potentiation (LTP) in vitro and spatial learning in aged (24-26 months) Fischer 344 rats. We found that LTP induced in the CA1 region using theta-frequency stimulation (5 Hz) is selectively impaired in slices from a subpopulation of aged rats that had shown poor spatial learning in the Morris water maze. LTP at 5 Hz in aged rats that did not show learning deficits was similar to that seen in young (4-6 months) controls. We also found that 5 Hz LTP amplitude strongly correlated with individual learning performance among aged rats. The difference in 5 Hz LTP magnitude among aged rats was not attributable to an altered response to 5 Hz stimulation or to differences in the NMDA receptormediated field EPSP. In addition, no performance-related differences in LTP were seen when LTP was induced with 30 or 70 Hz stimulation protocols. Finally, both 5 Hz LTP and spatial learning in learning-impaired rats were enhanced with the selective muscarinic M 2 antagonist ]benzodiazepin-6-one). These findings reinforce the idea that distinct types of hippocampal LTP offer mechanistic insight into age-associated cognitive decline.

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confidence: 85%

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Theta-Frequency Synaptic Potentiation in CA1In VitroDistinguishes Cognitively Impaired from Unimpaired Aged Fischer 344 Rats

et al. 2002

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“…Several studies have demonstrated that the magnitude of NMDA receptor-dependent LTP at hippocampal CA1 synapses attenuates with age [45][46][47]. The ability of leptin to induce LTP in adult hippocampus is also markedly reduced in aged animals [29].…”

Section: Leptin-driven Changes In Synaptic Efficacy Display Parallelsmentioning

confidence: 99%

Leptin regulation of hippocampal synaptic function in health and disease

Irving

Harvey

2014

Phil. Trans. R. Soc. B

104

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The endocrine hormone leptin plays a key role in regulating food intake and body weight via its actions in the hypothalamus. However, leptin receptors are highly expressed in many extra-hypothalamic brain regions and evidence is growing that leptin influences many central processes including cognition. Indeed, recent studies indicate that leptin is a potential cognitive enhancer as it markedly facilitates the cellular events underlying hippocampal-dependent learning and memory, including effects on glutamate receptor trafficking, neuronal morphology and activity-dependent synaptic plasticity. However, the ability of leptin to regulate hippocampal synaptic function markedly declines with age and aberrant leptin function has been linked to neurodegenerative disorders such as Alzheimer's disease (AD). Here, we review the evidence supporting a cognitive enhancing role for the hormone leptin and discuss the therapeutic potential of using leptin-based agents to treat AD.

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“…The LTP deficit explanation is made more plausible by recent in vitro findings on age-related deficits of LTP induction (Deupree et al, 1991(Deupree et al, , 1993Moore et al, 1993) and new evidence suggesting that such an LTP induction failure in old rats may result from a reduction in the net synaptic input in old pyramidal cells . The latter effect may partly be a consequence of a reduced number of f unctional synaptic contacts made by a given CA3 pyramidal cell axon (Barnes et al, 1992;Barnes, 1994) or reduced temporal summation in old hippocampal cells (Rosenzweig et al, 1997).…”

Section: Effect Of Age On Experience-dependent Place Field Plasticitymentioning

confidence: 99%

The Effect of Aging on Experience-Dependent Plasticity of Hippocampal Place Cells

et al. 1997

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The firing characteristics of 1437 CA1 pyramidal neurons were studied in relation to both spatial location and the phase of the theta rhythm in healthy young and old rats performing a simple spatial task on a rectangular track. The old rats had previously been found to be deficient on the Morris spatial learning task. Age effects on the theta rhythm per se were minimal. Theta amplitude and frequency during rapid eye movement sleep were virtually identical. During behavior, theta frequency was slightly reduced with age. In both groups, cell firing occurred at progressively earlier phases of the theta rhythm as the rat traversed the place field of the cell (i.e., there was "phase precession," as reported by others). The net phase shift did not differ between age groups. The main finding of the study was a loss of experience-dependent plasticity in the place fields of old rats. During the first lap around the track on each day, the initial sizes of the place fields were the same between ages; however, place fields of young rats, but not old, expanded significantly during the first few laps around the track in a given recording session. As the place fields expanded, the rate of change of firing with phase slowed accordingly, so that the net phase change remained constant. Thus changes in field size and phase precession are coupled. A deficit in plasticity of place fields in old rats may lead to a less accurate population code for spatial location.

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Spatial performance correlates with in vitro potentiation in young and aged Fischer 344 rats

Cited by 113 publications

References 32 publications

Theta-Frequency Synaptic Potentiation in CA1In VitroDistinguishes Cognitively Impaired from Unimpaired Aged Fischer 344 Rats

Theta-Frequency Synaptic Potentiation in CA1In VitroDistinguishes Cognitively Impaired from Unimpaired Aged Fischer 344 Rats

Leptin regulation of hippocampal synaptic function in health and disease

The Effect of Aging on Experience-Dependent Plasticity of Hippocampal Place Cells

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