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Lesions of the rat entopeduncular nucleus further deteriorate N-methyl-D-aspartate receptor antagonist-induced deficient prepulse inhibition.
Neurosci Lett. 2012 Feb 02; 508(1):27-30.NL

Abstract

Lesions of the rat entopeduncular nucleus (EPN), the equivalent to the human globus pallidus internus (GPi), have been shown to improve deficient prepulse inhibition (PPI) induced by the dopamine agonist apomorphine. We here tested the effect of EPN lesions on the PPI-disruptive effect of the non-competitive NMDA receptor antagonist dizocilpine in rats. Neurotoxic bilateral lesions of the EPN were induced by ibotenic acid (4 μg in 0.4 μl). Rats were tested for PPI and locomotor activity after systemic injection of dizocilpine (vehicle and 0.15 mg/kg). Bilateral EPN lesions further deteriorated the PPI deficit induced by dizocilpine, while locomotion was not affected. This work indicates that the EPN is an important brain region within the neuronal circuit responsible for NMDA receptor antagonist-induced PPI deficits.

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Authors+Show Affiliations

Lütjens G
Department of Neurosurgery, Medical University, MHH, Carl-Neuberg Str. 1, D-30625 Hannover, Germany.
Krauss JK
No affiliation info available
Schwabe K
No affiliation info available

MeSH

Acoustic StimulationAnimalsDisease Models, AnimalDizocilpine MaleateEntopeduncular NucleusExcitatory Amino Acid AntagonistsGait Disorders, NeurologicMaleMotor ActivityNeural InhibitionPsychoacousticsRatsRats, Sprague-DawleyReflex, Startle

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22178862

Citation

Lütjens, Götz, et al. "Lesions of the Rat Entopeduncular Nucleus Further Deteriorate N-methyl-D-aspartate Receptor Antagonist-induced Deficient Prepulse Inhibition." Neuroscience Letters, vol. 508, no. 1, 2012, pp. 27-30.
Lütjens G, Krauss JK, Schwabe K. Lesions of the rat entopeduncular nucleus further deteriorate N-methyl-D-aspartate receptor antagonist-induced deficient prepulse inhibition. Neurosci Lett. 2012;508(1):27-30.
Lütjens, G., Krauss, J. K., & Schwabe, K. (2012). Lesions of the rat entopeduncular nucleus further deteriorate N-methyl-D-aspartate receptor antagonist-induced deficient prepulse inhibition. Neuroscience Letters, 508(1), 27-30. https://doi.org/10.1016/j.neulet.2011.12.003
Lütjens G, Krauss JK, Schwabe K. Lesions of the Rat Entopeduncular Nucleus Further Deteriorate N-methyl-D-aspartate Receptor Antagonist-induced Deficient Prepulse Inhibition. Neurosci Lett. 2012 Feb 2;508(1):27-30. PubMed PMID: 22178862.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Lesions of the rat entopeduncular nucleus further deteriorate N-methyl-D-aspartate receptor antagonist-induced deficient prepulse inhibition. AU - Lütjens,Götz, AU - Krauss,Joachim K, AU - Schwabe,Kerstin, Y1 - 2011/12/13/ PY - 2011/09/26/received PY - 2011/11/30/revised PY - 2011/12/02/accepted PY - 2011/12/20/entrez PY - 2011/12/20/pubmed PY - 2012/5/9/medline SP - 27 EP - 30 JF - Neuroscience letters JO - Neurosci Lett VL - 508 IS - 1 N2 - Lesions of the rat entopeduncular nucleus (EPN), the equivalent to the human globus pallidus internus (GPi), have been shown to improve deficient prepulse inhibition (PPI) induced by the dopamine agonist apomorphine. We here tested the effect of EPN lesions on the PPI-disruptive effect of the non-competitive NMDA receptor antagonist dizocilpine in rats. Neurotoxic bilateral lesions of the EPN were induced by ibotenic acid (4 μg in 0.4 μl). Rats were tested for PPI and locomotor activity after systemic injection of dizocilpine (vehicle and 0.15 mg/kg). Bilateral EPN lesions further deteriorated the PPI deficit induced by dizocilpine, while locomotion was not affected. This work indicates that the EPN is an important brain region within the neuronal circuit responsible for NMDA receptor antagonist-induced PPI deficits. SN - 1872-7972 UR - https://www.unboundmedicine.com/medline/citation/22178862/Lesions_of_the_rat_entopeduncular_nucleus_further_deteriorate_N_methyl_D_aspartate_receptor_antagonist_induced_deficient_prepulse_inhibition_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0304-3940(11)01589-8 DB - PRIME DP - Unbound Medicine ER -