Learning performances, brain NGF distribution and NPY levels in transgenic mice expressing TNF-alpha

Marco Fiore, Francesco Angelucci, Enrico Alleva, Igor Branchi, Lesley Probert, Luigi Aloe

Research output: Contribution to journalArticle

Abstract

Tumor necrosis factor-alpha (TNF-α) is a cytokine involved in a variety of neurobiological activities including changing behavior and regulation of both neurotrophin and neuropeptide levels. In this study we used two lines of transgenic mice overexpressing brain TNF-α characterized by neurological deficits (line Tg6074) or phenotypically normal (line TgK3). We analyzed whether or not impairments in learning and memory processes due to TNF-α overexpression were associated with changes in endogenous brain NGF, NPY and β-amyloid. The results indicate that full TNF-α transgene expression disrupted the learning capabilities of transgenic mice (both Tg6074 and TgK3). NGF decreased in the hippocampus of both transgenic mice whereas hippocampal NPY slightly potentiated in Tg6074. The decrease in NGF is correlated with deficits in spatial learning and memory whereas inflammation in the brain of Tg6074 could be responsible of the hippocampal increase in NPY. As a whole, these results show that transgenic mice overexpressing TNF-α in the brain represent a useful model for studying neuronal degeneration and brain inflammatory processes.

Original languageEnglish
Pages (from-to)165-175
Number of pages11
JournalBehavioural Brain Research
Volume112
Issue number1-2
Publication statusPublished - 2000

Fingerprint

Nerve Growth Factor
Transgenic Mice
Tumor Necrosis Factor-alpha
Learning
Brain
Nerve Growth Factors
Encephalitis
Neuropeptides
Transgenes
Amyloid
Brain Neoplasms
Hippocampus
Cytokines

Keywords

  • Behaviour
  • Cytokine
  • Hippocampus
  • Inflammation
  • Neuropeptide
  • Neurotrophin
  • Water maze

ASJC Scopus subject areas

  • Behavioral Neuroscience

Cite this

Fiore, M., Angelucci, F., Alleva, E., Branchi, I., Probert, L., & Aloe, L. (2000). Learning performances, brain NGF distribution and NPY levels in transgenic mice expressing TNF-alpha. Behavioural Brain Research, 112(1-2), 165-175.

Learning performances, brain NGF distribution and NPY levels in transgenic mice expressing TNF-alpha. / Fiore, Marco; Angelucci, Francesco; Alleva, Enrico; Branchi, Igor; Probert, Lesley; Aloe, Luigi.

In: Behavioural Brain Research, Vol. 112, No. 1-2, 2000, p. 165-175.

Research output: Contribution to journalArticle

Fiore, M, Angelucci, F, Alleva, E, Branchi, I, Probert, L & Aloe, L 2000, 'Learning performances, brain NGF distribution and NPY levels in transgenic mice expressing TNF-alpha', Behavioural Brain Research, vol. 112, no. 1-2, pp. 165-175.
Fiore M, Angelucci F, Alleva E, Branchi I, Probert L, Aloe L. Learning performances, brain NGF distribution and NPY levels in transgenic mice expressing TNF-alpha. Behavioural Brain Research. 2000;112(1-2):165-175.
Fiore, Marco ; Angelucci, Francesco ; Alleva, Enrico ; Branchi, Igor ; Probert, Lesley ; Aloe, Luigi. / Learning performances, brain NGF distribution and NPY levels in transgenic mice expressing TNF-alpha. In: Behavioural Brain Research. 2000 ; Vol. 112, No. 1-2. pp. 165-175.
@article{260ac6d54054464dbf7b60537433e8a9,
title = "Learning performances, brain NGF distribution and NPY levels in transgenic mice expressing TNF-alpha",
abstract = "Tumor necrosis factor-alpha (TNF-α) is a cytokine involved in a variety of neurobiological activities including changing behavior and regulation of both neurotrophin and neuropeptide levels. In this study we used two lines of transgenic mice overexpressing brain TNF-α characterized by neurological deficits (line Tg6074) or phenotypically normal (line TgK3). We analyzed whether or not impairments in learning and memory processes due to TNF-α overexpression were associated with changes in endogenous brain NGF, NPY and β-amyloid. The results indicate that full TNF-α transgene expression disrupted the learning capabilities of transgenic mice (both Tg6074 and TgK3). NGF decreased in the hippocampus of both transgenic mice whereas hippocampal NPY slightly potentiated in Tg6074. The decrease in NGF is correlated with deficits in spatial learning and memory whereas inflammation in the brain of Tg6074 could be responsible of the hippocampal increase in NPY. As a whole, these results show that transgenic mice overexpressing TNF-α in the brain represent a useful model for studying neuronal degeneration and brain inflammatory processes.",
keywords = "Behaviour, Cytokine, Hippocampus, Inflammation, Neuropeptide, Neurotrophin, Water maze",
author = "Marco Fiore and Francesco Angelucci and Enrico Alleva and Igor Branchi and Lesley Probert and Luigi Aloe",
year = "2000",
language = "English",
volume = "112",
pages = "165--175",
journal = "Behavioural Brain Research",
issn = "0166-4328",
publisher = "Elsevier",
number = "1-2",

}

TY - JOUR

T1 - Learning performances, brain NGF distribution and NPY levels in transgenic mice expressing TNF-alpha

AU - Fiore, Marco

AU - Angelucci, Francesco

AU - Alleva, Enrico

AU - Branchi, Igor

AU - Probert, Lesley

AU - Aloe, Luigi

PY - 2000

Y1 - 2000

N2 - Tumor necrosis factor-alpha (TNF-α) is a cytokine involved in a variety of neurobiological activities including changing behavior and regulation of both neurotrophin and neuropeptide levels. In this study we used two lines of transgenic mice overexpressing brain TNF-α characterized by neurological deficits (line Tg6074) or phenotypically normal (line TgK3). We analyzed whether or not impairments in learning and memory processes due to TNF-α overexpression were associated with changes in endogenous brain NGF, NPY and β-amyloid. The results indicate that full TNF-α transgene expression disrupted the learning capabilities of transgenic mice (both Tg6074 and TgK3). NGF decreased in the hippocampus of both transgenic mice whereas hippocampal NPY slightly potentiated in Tg6074. The decrease in NGF is correlated with deficits in spatial learning and memory whereas inflammation in the brain of Tg6074 could be responsible of the hippocampal increase in NPY. As a whole, these results show that transgenic mice overexpressing TNF-α in the brain represent a useful model for studying neuronal degeneration and brain inflammatory processes.

AB - Tumor necrosis factor-alpha (TNF-α) is a cytokine involved in a variety of neurobiological activities including changing behavior and regulation of both neurotrophin and neuropeptide levels. In this study we used two lines of transgenic mice overexpressing brain TNF-α characterized by neurological deficits (line Tg6074) or phenotypically normal (line TgK3). We analyzed whether or not impairments in learning and memory processes due to TNF-α overexpression were associated with changes in endogenous brain NGF, NPY and β-amyloid. The results indicate that full TNF-α transgene expression disrupted the learning capabilities of transgenic mice (both Tg6074 and TgK3). NGF decreased in the hippocampus of both transgenic mice whereas hippocampal NPY slightly potentiated in Tg6074. The decrease in NGF is correlated with deficits in spatial learning and memory whereas inflammation in the brain of Tg6074 could be responsible of the hippocampal increase in NPY. As a whole, these results show that transgenic mice overexpressing TNF-α in the brain represent a useful model for studying neuronal degeneration and brain inflammatory processes.

KW - Behaviour

KW - Cytokine

KW - Hippocampus

KW - Inflammation

KW - Neuropeptide

KW - Neurotrophin

KW - Water maze

UR - http://www.scopus.com/inward/record.url?scp=0034219430&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034219430&partnerID=8YFLogxK

M3 - Article

C2 - 10862948

AN - SCOPUS:0034219430

VL - 112

SP - 165

EP - 175

JO - Behavioural Brain Research

JF - Behavioural Brain Research

SN - 0166-4328

IS - 1-2

ER -