Effects of lesions to the glutamatergic afferents to the nucleus accumbens in the modulation of reactivity to spatial and non-spatial novelty in mice.
The purpose of this study was to compare the effects of selective lesions of the three main sources of limbic afferents to the nucleus accumbens-fornix, prelimbic cortex and amygdala-with those induced by N-methyl-D-aspartate receptor blockage in this structure, in a non-associative task designed to estimate the ability of rodents to encode spatial and non-spatial relationships between discrete stimuli. The task consists of placing mice in an open field containing five objects and, after three sessions of habituation, examining their reactivity to object displacement (spatial novelty) and object substitution (object novelty). Focal administrations of the competitive N-methyl-D-aspartate antagonist DL-2-amino-5-phosphonopentanoic acid (0.1 microg/side) induced a selective impairment in the ability of mice to react to the spatial change. Lesions to the different structures affect the response of mice to spatial and non-spatial novelty in different ways. In particular, while fornix lesions induced a decrease in re-exploration of the displaced objects, prelimbic cortex lesions enhanced the exploration of both displaced and non-displaced objects. Finally, the basolateral amygdala lesions did not induce any impairment in the detection of the displaced objects but decreased the latencies to approach novel objects. It is concluded that N-methyl-D-aspartate receptor blockage in the nucleus accumbens subsumes the effects of the three lesions. Some hypotheses on the role of glutamatergic transmission in the accumbens on information processing are briefly discussed.
Sargolini
F
F
Dipartimento di Genetica e Biologia Molecolare, Università di Roma La Sapienza, Rome, Italy.
Roullet
P
P
Oliverio
A
A
Mele
A
A
D000344:Afferent Pathways / Q000293:injuries / Q000503:physiopathology; D000679:Amygdala / Q000293:injuries / Q000502:physiology*; D000818:Animals; D018690:Excitatory Amino Acid Agonists / Q000633:toxicity; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology* / Q000633:toxicity; D005106:Exploratory Behavior / Q000187:drug effects* / Q000502:physiology; D018698:Glutamic Acid / Q000502:physiology*; D006624:Hippocampus / Q000293:injuries / Q000502:physiology*; D007051:Ibotenic Acid / Q000633:toxicity; D007267:Injections; D008032:Limbic System / Q000293:injuries / Q000502:physiology*; D051379:Mice; D008959:Models, Neurological; D009043:Motor Activity / Q000502:physiology; D016202:N-Methylaspartate / Q000037:antagonists & inhibitors*; D009714:Nucleus Accumbens / Q000502:physiology* / Q000648:ultrastructure; D013037:Spatial Behavior / Q000187:drug effects*; D014633:Valine / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000633:toxicity
D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D007051:Ibotenic Acid; D018698:Glutamic Acid; D016202:N-Methylaspartate; C056639:2-amino-5-phosphopentanoic acid; D014633:Valine