The effects of neonatal lesions in the amygdala or ventral hippocampus on social behaviour later in life

Daenen, E.W.P.M.; Wolterink, Gerrit; Gerrits, M.A.F.M.; Ree, Jan M. van

doi:10.1016/s0166-4328(02)00223-1

Cited by 94 publications

(78 citation statements)

References 55 publications

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“…Experimental studies that detail neural regions critical for peerdirected social interactions, especially under familiar, non-anxiogenic test conditions, are limited. However, recent research has revealed that frontal regions including medial prefrontal cortex, orbitofrontal cortex, amygdala, and ventral hippocampus, as well as dopamine input to these regions [6,9,11,19,24,26], play an important role in peer-directed social interactions. These brain regions are among those that undergo considerable remodeling during adolescence [1,15,16,18,35,37,48,49] and, hence are likely targets for contributing to the disruption in social preference following chronic adolescent exposure to ethanol.…”

Section: Discussionmentioning

confidence: 99%

Chronic tolerance to the social consequences of ethanol in adolescent and adult Sprague-Dawley rats

Varlinskaya

Spear

2007

Neurotoxicology and Teratology

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Section: Discussionmentioning

confidence: 99%

Chronic tolerance to the social consequences of ethanol in adolescent and adult Sprague-Dawley rats

Varlinskaya

Spear

2007

Neurotoxicology and Teratology

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“…However, not only early brain lesions but also subtle changes of brain development can have adverse effects on social behavior later in life. Capitalizing on the neurodevelopmental hypothesis of psychiatric disorders, several animal models were set up in the past decade, including neonatal excitotoxic lesions of the ventral hippocampus (Lipska et al, , 2002a, the amygdala (Wolterink et al, 2001;Daenen et al, 2002), and also the mPFC (Flores et al, 1996;Brake et al, 2000;Bennay et al, 2004;Schwabe et al, 2004). The study of neural systems involved in disturbances of social functioning in psychiatric disorders has become increasingly popular in recent years, since impaired social skills are among the hallmarks of psychiatric diseases (DSM IV, American Psychiatric Association, 1994).…”

Section: Discussionmentioning

confidence: 99%

“…Patterns of social play were displayed in a normal way, but lesioned animals responded inappropriately to play initiation and were easily distracted (Pellis et al, 1993). Input to these striatal structures comes inter alia from the amygdala (Kelley et al, 1982), lesions of which have also been shown to disrupt pinning in juvenile male rats (Wolterink et al, 2001;Daenen et al, 2002). Furthermore, lesions of the dorsomedial and parafascicular thalamus also decrease social play (Vanderschuren et al, 1997).…”

Section: Play Fightingmentioning

confidence: 99%

“…Likewise, social withdrawal and social isolation are among the key components of negative symptoms in schizophrenia (Daenen et al, 2002;DSM IV, American Psychiatric Association, 1994). Furthermore, it has been shown that limited social functions in childhood are precursors of impaired social function in adulthood (Goldberg and Schmidt, 2001).…”

Section: Social Behavior and Cpp For Social Contactmentioning

confidence: 99%

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Deficient Social and Play Behavior in Juvenile and Adult Rats after Neonatal Cortical Lesion: Effects of Chronic Pubertal Cannabinoid Treatment

Schneider

Koch

2004

Neuropsychopharmacol

142

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The aim of the present study was to investigate the effects of neonatal excitotoxic lesions of the medial prefrontal cortex (mPFC) on social play, social behavior unrelated to play, and self-grooming in juvenile and adult rats. We additionally examined the behavioral effects of chronic pubertal treatment with the cannabinoid agonist WIN 55,212-2 (WIN) in order to test the hypothesis that early lesions render the brain vulnerable to cannabinoid intake in later life. Neonatal mPFC lesions and pubertal WIN treatment disrupted social play, social behavior, and self-grooming in juvenile and adult rats. Additionally, we observed more social play behaviors during light cycle in WIN-treated than in vehicle-treated rats. Notably, the combination of surgery and WIN treatment disrupted social behavior in lesioned and sham-lesioned rats. The present data indicate that the mPFC is important for adequate juvenile response selection in the context of social play and might be involved in the development of adult social and nonsocial behavior. Moreover, our data add further evidence for an involvement of the cannabinoid system in anxiety and social behavior. Additive effects of neonatal surgery-induced stress or cortical lesions in combination with pubertal cannabinoid administration are also shown. The disturbances of social and nonsocial behavior in rats are comparable to symptoms of early frontal cortex damage, as well as neurodevelopmental disorders in humans, such as schizophrenia and autism. Therefore, we propose the combination of neonatal cortical lesions with chronic cannabinoid administration during puberty as an animal model for studying neuronal mechanisms of impaired social functioning in neuropsychiatric disorders.

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“…The disturbance in brain development can be caused either by genetic factors or by external factors, such as prenatal exposure to influenza virus, birth complications, etc. It has previously been shown in preclinical models that disturbance of neurodevelopment in rats can cause behavioral changes relevant to positive as well as negative symptoms of schizophrenia (Flagstad et al, 2004;Lipska et al, 1993;Sams-Dodd et al, 1997;Le Pen et al, 2002;Daenen et al, 2002;Talamini et al, 1999). One way of inducing prenatal disturbance is by treatment with the mitosis inhibitor methylazoxymethanol (MAM) during gestation (Johnston et al, 1988;Johnston and Coyle, 1982;Flagstad et al, 2004;Balduini et al, 1991;Virgili et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

Cognitive Deficits Caused by Late Gestational Disruption of Neurogenesis in Rats: a Preclinical Model of Schizophrenia

Flagstad

Glenthøj

Didriksen

2004

Neuropsychopharmacol

100

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Late gestational disruption of neurogenesis in rats has been shown to induce behavioral abnormalities thought to mimic aspects of positive and negative symptoms of schizophrenia. Furthermore, it has been shown that the morphological changes produced by the perturbation are relevant to schizophrenia with reduced thickness of the hippocampus, thalamus, and cortical regions. In addition to the positive and negative symptoms, schizophrenia is associated with deficits in a wide variety of cognitive domains. In the present studies, we assessed whether the cognitive deficits are modeled by disruption of neurogenesis late during gestation (gestational day 17) in the rat. In the battery of tests utilized, we describe that rats in which neurogenesis was disrupted have deficits in a reversal-learning paradigm of the Morris water maze and in object recognition, and that they exhibit perseveration in the Porsolt forced swimming test. Additionally, we found deficient associative learning in an acquisition of an active avoidance paradigm and deficits in latent inhibition. No deficits were observed in the reference memory version of the Morris water maze and in a non-match-to position experiment, showing that the deficits are limited to certain aspects of cognition.

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The effects of neonatal lesions in the amygdala or ventral hippocampus on social behaviour later in life

Cited by 94 publications

References 55 publications

Chronic tolerance to the social consequences of ethanol in adolescent and adult Sprague-Dawley rats

Chronic tolerance to the social consequences of ethanol in adolescent and adult Sprague-Dawley rats

Deficient Social and Play Behavior in Juvenile and Adult Rats after Neonatal Cortical Lesion: Effects of Chronic Pubertal Cannabinoid Treatment

Cognitive Deficits Caused by Late Gestational Disruption of Neurogenesis in Rats: a Preclinical Model of Schizophrenia

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