Jul 12, 2007

Loss of high-affinity nicotinic receptors increases the vulnerability to excitotoxic lesion and decreases the positive effects of an enriched environment

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
Alessio ZanardiM Zoli


Pharmacological activation of nicotinic acetylcholine receptors (nAChRs) exerts neuroprotective effects in cultured neurons and the intact animal. Much less is known about a physiological protective role of nAChRs. To understand whether endogenous activation of beta2* nAChRs contributes to the maintenance of the functional and morphological integrity of neural tissue, adult beta2-/- mice were subjected to in vivo challenges that cause neurodegeneration and cognitive impairment (intrahippocampal injection of the excitotoxin quinolinic acid), or neuroprotection and cognitive potentiation (2-month exposure to an enriched environment). The excitotoxic insult caused an increased deficit in the Morris water maze learning curve and increased loss of hippocampal pyramidal cells in beta2-/- mice. Exposure to an enriched environment improved performance in contextual and cued fear conditioning and object recognition tests in beta2+/+, whereas the improvement was absent in beta2-/- mice. In addition, beta2+/+, but not beta2-/-, mice exposed to an enriched environment showed a significant hypertrophy of the CA1/3 regions. Thus, lack of beta2* nAChRs increased susceptibility to an excitotoxic insult and diminished the positive effects of an...Continue Reading

Mentioned in this Paper

Behavior, Animal
Quinolinic Acid
Nerve Degeneration

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