Sparing and recovery of spatial alternation performance after entorhinal cortex lesions in rats

Ramirez, Julio J.; Stein, Donald G.

doi:10.1016/0166-4328(84)90029-9

Cited by 67 publications

(40 citation statements)

References 9 publications

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“…Notably, supplementation with AJC at levels utilized herein has been demonstrated to prevent the reduction in acetylcholine and decline in cognitive performance that otherwise accompanies maintenance of mice on the deficient diet (16,24). In support of this possibility, cholinergic depletion itself is sufficient to induce impairments in memory in rodents (25)(26)(27)(28)(29).…”

Section: Discussionmentioning

confidence: 70%

Supplementation with apple juice can compensate for folate deficiency in a mouse model deficient in methylene tetra hydrofoate reductase activity

Chan

Ortiz

Rogers

et al. 2011

The Journal of nutrition, health and aging

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Folate insufficiency promotes developmental as well as age-related disorders of the nervous system. The C677T variant of 5',10' methylene tetrahydrofolate reductase (MTHFR; which utilizes folate to regenerate methionine from homocysteine) displays reduced activity, and therefore promotes functional folate deficiency. Mice heterozygously lacking this gene (MTHFR+/-mice) represent a useful model for analysis of the impact of MTHFR deficiency and potential compensatory approaches. Since consumption of apple products has benefited mouse models subjected to dietary and/or genetically-induced folate deficiency, we compared the impact of supplementation with apple juice on cognitive and neuromuscular performance of mice MTHFR+/+ and +/-mice with and without dietary folate deficiency. Mice were maintained for 1 month on a standard, complete diet, or a challenge diet lacking folate, and vitamin E and containing a 50g iron/500g total diet as a pro-oxidant. Additional groups received apple juice concentrate (AJC) diluted to 0.5% (vol/vol) in their sole source of drinking water. MTHFR+/-mice demonstrated significantly impaired cognitive performance in standard reward-based T maze and the non-reward-based Y maze tests as compared to MTHFR+/+ when maintained on the complete diet; supplementation with AJC improved the performance of MTHFR+/-to the level observed for MTHFR+/+ mice. Maintenance for 1 month on the deficient diet reduced the performance of both genotypes in both tests, but supplementation with AJC prevented these reductions. MTHFR+/+ and +/-displayed virtually identical neuromuscular performance in the standard paw grip endurance test when maintained on the complete diet, and displayed similar, non-significant declines in performance when maintained on the deficient diet. Supplementation of either diet with AJC dramatically improved the performance of both genotypes. The findings presented herein indicate that supplementation with AJCs can compensate for genetic as well as dietary insufficiency in folate in a murine model of genetic folate compromise, and support the notion that dietary supplementation may be more critical under conditions of latent genetic compromise.

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Section: Discussionmentioning

confidence: 70%

Supplementation with apple juice can compensate for folate deficiency in a mouse model deficient in methylene tetra hydrofoate reductase activity

Chan

Ortiz

Rogers

et al. 2011

The Journal of nutrition, health and aging

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“…Because of the robust plasticity in the hippocampus following partial deafferentation, several studies have explored the idea that injury-induced plasticity might underlie functional recovery. Early studies assessing axonal sprouting and changes in behavior (spontaneous or reinforced alternation) were controversial (Loesche and Steward, 1977;Scheff and Cotman, 1977;Olton et al, 1982;Ramirez and Stein, 1984). Subsequent studies using a variety of behavioral tasks have failed to show a clear relationship between injury-induced plasticity and functional recovery (Ramirez, 2001).…”

Section: Discussionmentioning

confidence: 98%

Synaptogenesis in the Hippocampal CA1 Field following Traumatic Brain Injury

Scheff

Price

Hicks

et al. 2005

Journal of Neurotrauma

154

126

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Traumatic brain injury (TBI) results in both acute and chronic disruption of cognitive ability that may be mediated through a disruption of hippocampal circuitry. Experimental models of TBI have demonstrated that cortical contusion injuries can result in the loss of specific neurons in the CA3 subfield of the ipsilateral hippocampus, resulting in partial loss of afferents to the CA1 subfield. Numerous studies have documented the ability of the central nervous system to compensate for deafferentation by initiating a plasticity response capable of restoring lost synaptic contacts. The present study was designed to examine the time course of loss and replacement of synaptic contacts in stratum radiatum dendritic field of CA1. Young adult rats were subjected to a lateral cortical contusion injury and assayed for total synaptic numbers using unbiased stereology coupled with transmission electron microscopy. Injured animals demonstrated a 60% loss of synapses in CA1 at 2 days post-injury, followed by a reinnervation process that was apparent as early as 10 days post-injury. By 60 days post-injury, total synaptic numbers had approached pre-injury levels but were still significantly lower. Some animals were behaviorally tested for spatial memory in a Morris Water Maze at 15 and 30 days post-injury. While there was some improvement in spatial memory, injured animals continued to demonstrate a significant deficit in acquisition. These results show that the hippocampus ipsilateral to the cortical contusion is capable of a significant plasticity response but that synapse replacement in this area does not necessarily result in significant improvement in spatial learning.

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“…A 1.0 mA current was passed through the electrode for a period of 45 sec at each coordinate (Ramirez and Stein, 1984). Animals that received sham surgery were treated similarly, with the exception of the penetration of the electrode into the brain (note that all animals received rAAV vector injection).…”

Section: Methodsmentioning

confidence: 99%

Adeno-Associated Virus Vector Expressing Nerve Growth Factor Enhances Cholinergic Axonal Sprouting after Cortical Injury in Rats

et al. 2003

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Nerve growth factor (NGF) is known to promote both the survival of cholinergic neurons after injury and the regeneration of damaged cholinergic axons. Recent evidence has implicated NGF in the regulation of cholinergic axonal sprouting by intact neurons projecting to the hippocampus of rats, sustaining a lesion of the entorhinal cortex. We explored the possibility that NGF may regulate this lesioninduced cholinergic sprouting by injecting recombinant adeno-associated virus (rAAV) vector expressing NGF and green fluorescent protein (GFP) into the dentate gyrus of rats that were subsequently given unilateral entorhinal lesions. Sprague Dawley rats were unilaterally injected with (1) rAAV vector expressing NGF and GFP or (2) rAAV vector expressing GFP. Fourteen days after injection, the animals received lesions of the entorhinal area ipsilateral to the virus injection. Four days after lesion, GFP expression and the septodentate sprouting response in the dentate gyrus were assessed. Optical densitometric analyses revealed a significant increase in acetylcholinesterase label (a marker for cholinergic septodentate sprouting) in the ipsilateral outer molecular layer of the dentate gyrus in rats injected with rAAV vector expressing NGF. Thus, NGF-expressing rAAV vector enhanced the sprouting response of intact cholinergic neurons after unilateral entorhinal lesions in rats.

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Sparing and recovery of spatial alternation performance after entorhinal cortex lesions in rats

Cited by 67 publications

References 9 publications

Supplementation with apple juice can compensate for folate deficiency in a mouse model deficient in methylene tetra hydrofoate reductase activity

Supplementation with apple juice can compensate for folate deficiency in a mouse model deficient in methylene tetra hydrofoate reductase activity

Synaptogenesis in the Hippocampal CA1 Field following Traumatic Brain Injury

Adeno-Associated Virus Vector Expressing Nerve Growth Factor Enhances Cholinergic Axonal Sprouting after Cortical Injury in Rats

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