Memory impairment and morphological changes in rats induced by active fragment of anti-nerve growth factor-antibody

Nabeshima, Toshitaka; Ogawa, Shin-ichi; Ishimaru, Hirohisa; Kameyama, Tsutomu; Fukuta, Takanori; Takeuchi, Rie; Hayashi, Kyozo

doi:10.1016/s0006-291x(05)81222-7

Cited by 28 publications

(10 citation statements)

References 11 publications

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“…Our results confirm and extend previous findings using immunodeprivation (Nabeshima et al, 1991;Van der Zee et al, 1995) by indicating that even a partial reduction in NGF availability leads to measurable effects on spatial learning and memory. Lack of a more robust behavioral deficit may be the result of compensatory changes induced by decreased levels of NGF, and presumably reduced numbers and sizes of basal forebrain cholinergic cells, throughout development.…”

Section: Discussionsupporting

confidence: 92%

“…Although numerous studies have indicated that NGF is capable of exerting potent influences on basal forebrain cholinergic neurons, the actions of endogenous NGF on these neurons has not been rigorously examined. Studies using immunoneutralization have been hampered by the limited diffusion of antibodies in the CNS, the limited developmental time window and doses examined, and the potential cross-reactivity of NGF antibodies with other members of the neurotrophin family (Vantini et al, 1989;Nabeshima et al, 1991;Li et al, 1995;Van der Zee et al, 1995). Although the gene deletion approach circumvents these problems, the poor viability of animals homozygous for NGF gene disruption precludes analysis of the role of NGF in the survival or function of cholinergic neurons past the neonatal period (Crowley et al, 1994).…”

Section: Abstract: Ngf; Neurotrophin; Cholinergic; Learning; Memory;mentioning

confidence: 99%

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Disruption of a Single Allele of the Nerve Growth Factor Gene Results in Atrophy of Basal Forebrain Cholinergic Neurons and Memory Deficits

Chen¹,

Nishimura²,

Armanini³

et al. 1997

J. Neurosci.

201

121

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Administration of nerve growth factor (NGF) to aged or lesioned animals has been shown to reverse the atrophy of basal forebrain cholinergic neurons and ameliorate behavioral deficits. To examine the importance of endogenous NGF in the survival of basal forebrain cholinergic cells and in spatial memory, mice bearing a disruption mutation in one allele of the NGF gene were studied. Heterozygous mutant mice (ngfϩ/Ϫ) have reduced levels of NGF mRNA and protein within the hippocampus and were found to display significant deficits in memory acquisition and retention in the Morris water maze. The behavioral deficits observed in NGF-deficient mice were accompanied by both shrinkage and loss of septal cells expressing cholinergic markers and by a decrease in cholinergic innervation of the hippocampus. Infusions of NGF into the lateral ventricle of adult ngfϩ/Ϫ mice abolished the deficits on the water maze task. Prolonged exposure to NGF may be required to induce cognitive effects, because reversal of the acquisition deficit was seen after long (5 weeks) but not short (3 d) infusion. Although NGF administration did not result in any improvement in the number of septal cells labeled for choline acetyltransferase, this treatment did effectively correct the deficits in both size of cholinergic neurons and density of cholinergic innervation of the hippocampus. These findings demonstrate the importance of endogenous NGF for survival and function of basal forebrain cholinergic neurons and reveal that partial depletion of this trophic factor is associated with measurable deficits in learning and memory.

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Section: Discussionsupporting

confidence: 92%

Section: Abstract: Ngf; Neurotrophin; Cholinergic; Learning; Memory;mentioning

confidence: 99%

Disruption of a Single Allele of the Nerve Growth Factor Gene Results in Atrophy of Basal Forebrain Cholinergic Neurons and Memory Deficits

Chen¹,

Nishimura²,

Armanini³

et al. 1997

J. Neurosci.

201

121

View full text Add to dashboard Cite

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“…4, 30 animals were divided into three groups (n ϭ 10): (1) OB ϩ palm oil, (2) OB ϩ EPA, and (3) OB ϩ EPA ϩ anti-NGF (Sigma). The feeding time for EPA was 7 weeks, and anti-NGF (12 l) was intracerebroventricularly administrated for 10 d (Nabeshima et al, 1991;Nitta et al, 1996). Animal learning and memory were tested in the Morris water maze for 6 d. After decapitation, brains were quickly removed on ice and OB surgery checked for each experiment.…”

Section: Methodsmentioning

confidence: 99%

Increased Phospholipase A2 Activity and Inflammatory Response But Decreased Nerve Growth Factor Expression in the Olfactory Bulbectomized Rat Model of Depression: Effects of Chronic Ethyl-Eicosapentaenoate Treatment

Song¹,

Zhang²,

Manku³

2009

J. Neurosci.

167

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An increased inflammatory response and deficient synthesis of neurotrophic factors (NTFs) may contribute to the etiology of depression. However, the interrelationship between inflammation and NTFs is unknown. Recently, ethyl-eicosapentaenoate (EPA) has been used to treat depression. The mechanism by which EPA benefits depression is also unclear. Using the olfactory bulbectomized (OB) rat model of depression, this study evaluated two pathways from bulbectomy to the induction of depression-like changes (the inflammation-hypothalamic-pituitary-adrenal axis-stress response pathway and inflammation-nerve growth factor-memory pathway) and the effect of EPA on these pathways. When compared with sham-operated rats fed a control diet, significantly increased locomotor and rearing activities in an "open field," impaired memory in the Morris water maze, increased expression of corticotrophin-releasing factor (CRF), and increased secretion of corticosterone were found in OB rats. mRNA expression of nerve growth factor (NGF) was significantly lower in the hippocampus, and phospholipase A2 (PLA2) was higher in the hypothalamus; this change was associated with increased interleukin-1␤ (IL-1␤) and prostaglandin E2 (PGE2) in the serum and brain. EPA treatments normalized these behavioral impairments and reduced CRF expression and corticosterone secretion. EPA also reduced serum concentrations of IL-1␤ and PGE2, but reversed NGF reduction. Similar to the effects of EPA, the anti-inflammatory drug celecoxib significantly reduced blood PGE2, IL-1␤, and corticosterone concentrations and increased NGF expression in OB rats. Furthermore, anti-NGF treatment blocked EPA effects on behavior. These results suggest that an interaction exists between inflammation and NGF in the depression model. EPA may improve depression via its anti-inflammation properties and the upregulation of NGF.

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“…The /3-amyloid protein was dissolved in 35% acetonitrile/0.1% trifluoacetic acid (TFA). Continuous infusion of the f3-amyloid protein (0, 3, 30, 300 pmol/day) was maintained for two weeks by attachment of a cannula to a modified miniosmotic pump (Alzet 2002; Alza, Palo Alto, CA, USA) (Nabeshima et al 1991). Each group consisted of seven rats.…”

Section: Surgery and Experimental Designmentioning

confidence: 99%

Memory Impairment and Neuronal Dysfunction Induced by .BETA.-Amyloid Protein in Rats.

Nabeshima

Nitta

1994

Tohoku J. Exp. Med.

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Memory impairment and morphological changes in rats induced by active fragment of anti-nerve growth factor-antibody

Cited by 28 publications

References 11 publications

Disruption of a Single Allele of the Nerve Growth Factor Gene Results in Atrophy of Basal Forebrain Cholinergic Neurons and Memory Deficits

Disruption of a Single Allele of the Nerve Growth Factor Gene Results in Atrophy of Basal Forebrain Cholinergic Neurons and Memory Deficits

Increased Phospholipase A2 Activity and Inflammatory Response But Decreased Nerve Growth Factor Expression in the Olfactory Bulbectomized Rat Model of Depression: Effects of Chronic Ethyl-Eicosapentaenoate Treatment

Memory Impairment and Neuronal Dysfunction Induced by .BETA.-Amyloid Protein in Rats.

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