Research article summary (published 30 Dec 2000):

Selective immunolesioning of cholinergic neurons in nucleus basalis magnocellularis impairs prepulse inhibition of acoustic startle.

Full Abstract

Information processing and attentional abnormalities are prominent in neuropsychiatric disorders. Since the cholinergic neurons located in the nucleus basalis magnocellularis have been shown to be involved in attentional performance and information processing, recent efforts to analyze the significance of the basal forebrain in the context of schizophrenia have focused on this nucleus and its projections to the cerebral cortex. We report here that bilateral selective immunolesioning of the cholinergic neurons in the nucleus basalis magnocellularis is followed by significant deficits in sensorimotor gating measured by prepulse inhibition of the startle reflex in adult rats. This behavioral approach is used in both humans and rodents and has been proposed as a valuable model contributing to the understanding of the neurobiological substrates of schizophrenia. The disruption of prepulse inhibition persisted over repeated testing. The selective lesions were induced by bilateral intraparenchymal infusions of 192 IgG saporin at a concentration having minimal diffusion into adjacent nuclei of the basal forebrain. The infusions were followed by extensive loss of choline acetyltransferase-immunopositive neurons. Our results show that the cholinergic neurons of the nucleus basalis magnocellularis represent a critical station of the startle gating circuitry and suggest that dysfunction of these neurons may result in impaired sensorimotor gating characteristic of schizophrenia.

Author information

Author/s: Ballmaier, M (M); Casamenti, F (F); Zoli, M (M); Pepeu, G (G); Spano, P (P);

Affiliation: Department of Biomedical Sciences and Biotechnologies, Brescia University Mecial School, Italy. mballm(-atsign-)med.unibs.it

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

Journal: Neuroscience (Neuroscience), published in United States. (Language: eng)

Reference: 2001-; vol 108 (issue 2) : pp 299-305

Dates: Created 2001/12/05; Completed 2002/03/05; Revised 2007/11/15;

PMID: 11734362, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Acetylcholine - metabolism Animals Antibodies, Monoclonal - pharmacology Basal Nucleus of Meynert - drug effects; pathology; physiopathology Behavior, Animal - drug effects; physiology Cerebral Cortex - physiopathology Choline O-Acetyltransferase - metabolism Cholinergic Agents - pharmacology Cholinergic Fibers - drug effects; metabolism; pathology Immunohistochemistry Immunotoxins - pharmacology

Male N-Glycosyl Hydrolases Nerve Degeneration - chemically induced; pathology; physiopathology Neural Inhibition - drug effects; physiology Neural Pathways - drug effects; pathology; physiopathology Neurons - drug effects; metabolism; pathology Rats Rats, Sprague-Dawley Ribosome Inactivating Proteins, Type 1 Schizophrenia - metabolism; pathology; physiopathology Startle Reaction - drug effects; physiology

Associated Chemicals: 192 IgG-saporin (0) ; Antibodies, Monoclonal (0) ; Cholinergic Agents (0) ; Immunotoxins (0) ; Ribosome Inactivating Proteins, Type 1 (0) ; Acetylcholine (51-84-3) ; Choline O-Acetyltransferase (EC 2.3.1.6) ; N-Glycosyl Hydrolases (EC 3.2.2.-)

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