Alterations in dendritic morphology of prefrontal cortical and nucleus accumbens neurons in post-pubertal rats after neonatal excitotoxic lesions of the ventral hippocampus

Flores, Gonzalo; Alquicer, Glenda; Silva-Gómez, Adriana B.; Zaldivar, G. Alvarado; Stewart, Jane; Quirion, Rémi; Srivastava, Lalit K.

doi:10.1016/j.neuroscience.2005.02.021

Cited by 203 publications

(212 citation statements)

References 75 publications

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“…Such abnormality at sites with diminished spine density has been reported in a neonatally-inflicted ventral hippocampus damage model for the hypothesis of developmental disorders associated with NMDA receptor hypofunction. 33) Parvalbumin-positive GABA interneurons in the dorsolateral prefrontal cortex express NMDA receptors, and the neuronal activity of GABA interneurons is strongly modulated by glutamatergic neural input from the cerebral cortex, hippocampus, and thalamus, while GABA interneurons per se play a role in inhibiting glutamatergic neural activity. 34) It has been hypothesized that excessive liberation of glutamic acid might occur in the brains of patients with schizophrenia on the grounds that NMDA receptor blockade gives rise to glutamate release in the frontal cortex and that parvalbuminpositive GABA interneurons are decreased in patients with schizophrenia.…”

Section: Discussionmentioning

confidence: 99%

Neonatal Phencyclidine Treatment in Mice Induces Behavioral, Histological and Neurochemical Abnormalities in Adulthood

Nakatani-Pawlak

Yamaguchi²,

Tatsumi

et al. 2009

Biological & Pharmaceutical Bulletin

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N-Methyl-D-aspartate (NMDA)-type glutamic acid receptors play a critical role in excitatory synaptic transmission, synaptic plasticity and neuronal development in the central nervous system. During the developmental stage from week 25 of gestation to birth in humans, elongation and branching of axons and dendrites of nerve cells, synapse formation, myelination and realignment of nerve pathways (neural circuits) for acquiring higher neural function actively proceed, and this stage corresponds to postnatal weeks 1 through 2 in mice.1) It is generally recognized that non-synapse-mediated intercellular glutamic acid is largely involved in this process of nerve development. Stimulation of NMDA receptors facilitated radial migration of the cortical plate of excitatory nerve cells 2) and the selective blockade of NMDA receptors disturbed neuronal migration in the cerebral cortex.3)It has been reported that rats injected subcutaneously (s.c.) with phencyclidine (PCP), a noncompetitive NMDA receptor antagonist, at 10 mg/kg once a day during the postnatal development stage (postnatal days 7, 9 and 11) exhibit an increase in spontaneous motor activity, impairment of prepulse inhibition and behavioral changes in respect of learning and cognition after attaining maturation.4-7) When rats neonatally administered PCP were examined for any changes in the binding capacity of NMDA receptors and g-aminobutyrate A (GABA A ) receptors at maturity by autoradiography using In the present study, we investigated brain function from the behavioral, anatomical and neurochemical viewpoints in mice injected with PCP at 10 mg/kg on postnatal days 7, 9 and 11. Especially, we focused on changes in social interaction in PCP-treated mice, and examined the effects of clozapine, an atypical antipsychotic drug, D-cycloserine, an NMDA receptor partial agonist, flumazenil, a benzodiazepine receptor antagonist, and SHC50911, a GABA B receptor antagonist on social interaction deficits in PCP-treated mice. Of note, as far as we are aware, this is the first experimental demonstration that neonatal PCP treatment in mice results in increased sensitivity to PCP, and impaired social interaction behaviors in adulthood, which are accompanied by a decrease in the number of GABAergic interneurons and spine density in the frontal cortex and hippocampus, and abnormal monoamine metabolism in the brain. Neonatal PCP treatment in mice could be regarded as a neurodevelopmental animal model for schizophrenia. MATERIALS AND METHODSMethods. Animals Male mice aged 13 weeks old and female mice aged 13 weeks old Crlj:CD1 (ICR) were mated, and male offspring were used on postnatal day 7. Animals were maintained in a room controlled at 23°C and 55% humidity with a 12-h lighting cycle (lights on: 6:00 a.m.), and 12 ventilations/h. Animals had free access to solid feed (CRF-1; Oriental Yeast Co., Ltd., Tokyo, Japan) from feed- Kakuma-machi, Kanazawa 920-1192, Japan: b Nihon Bioresearch Inc.; 6-104 Majima, Fukuju-cho, Hashima, Gifu 501-6251, Japan: c Narabyouri Research Co.,...

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Section: Discussionmentioning

confidence: 99%

Neonatal Phencyclidine Treatment in Mice Induces Behavioral, Histological and Neurochemical Abnormalities in Adulthood

Nakatani-Pawlak

Yamaguchi²,

Tatsumi

et al. 2009

Biological & Pharmaceutical Bulletin

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“…Esto puede afectar la integración sináptica y la neurotransmisión (5,6). Se requiere ensayar otras fórmulas de impregnación argéntica, como la versión más reciente del método de Golgi-Cox (30), para incrementar la cantidad de neuronas impregnadas, y acudir a métodos que permitan evaluar cuantitativamente las modificaciones de la arborización dendrítica, tales como el método de Sholl, utilizado en estudios recientes (31)(32)(33). Lo anterior combinado con el análisis de la expresión de proteínas del citoesqueleto (MAP-2, NF y otras) contribuirán a determinar qué tan importante puede ser la patología dendrítica como componente de la patogénesis de la rabia.…”

Section: Discussionunclassified

Alteraciones de la morfología dendrítica neuronal en la corteza cerebral de ratones infectados con rabia: un estudio con la técnica de Golgi

2007

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Introducción. Los signos neurológicos de la rabia son impresionantes; no obstante, el cerebro infectado sufre apenas cambios histológicos muy sutiles. Objetivo. Estudiar la morfología neuronal mediante la técnica de Golgi, en la corteza cerebral de ratones infectados con el virus de la rabia. Materiales y métodos. Se inocularon ratones con virus silvestre de la rabia (virus 'calle') de origen canino o con virus adaptado (virus 'fijo') de la cepa CVS (challenge virus standard). Los animales se sacrificaron en la fase terminal de la enfermedad y se fijaron por perfusión con paraformaldehído. Los cerebros se procesaron con la técnica de Golgi, se obtuvieron cortes coronales de la corteza, se contaron las neuronas impregnadas en un área de 1 mm 2 , se midió el tamaño de sus cuerpos celulares y se tomaron fotografías en diferentes planos de profundidad. Resultados. Se observaron alteraciones morfológicas notables en el soma y las dendritas de neuronas piramidales, con pérdida acentuada de espinas, en 12,9% de neuronas corticales de animales infectados con virus 'calle' por vía intracerebral; en 8,2% de neuronas de ratones inoculados con este mismo virus por la ruta intramuscular y en 31,8% de neuronas en los animales inoculados con virus 'fijo' por vía intramuscular. Además, en las muestras de material infectado el número de neuronas impregnadas por la técnica de Golgi fue considerablemente menor al observado en las muestras no infectadas. Conclusiones. Estos resultados son evidencia de que el virus de la rabia sí puede inducir daño neuronal estructural. Además, esta infección aparentemente interfiere con los mecanismos de impregnación argéntica del método de Golgi.Palabras clave: rabia, virus de la rabia, corteza cerebral, neuronas, neuroanatomía, técnicas histológicas. Neuronal dentritic morphology alterations in the cerebral cortex of rabies-infected mice: a Golgi studyIntroduction. The neurological signs of rabies are very dramatic. Nevertheless, the infected brain manifests only very subtle histological changes. Objective. The neuronal morphology in the cerebral cortex of rabies-infected mice was examined by means the Golgi technique for detection of neuropathy. Materials and methods. Two groups of mice were inoculated with rabies-one with street virus isolated from an infected dog and the second with fixed CVS (challenge virus standard) virus. At the terminal phase of illness, the animals were sacrificed and fixed for histological staining by perfusion with paraformaldehyde. Next, the brains were treated by the Golgi technique and coronal sections were obtained. Neurons enclosed within 1 mm 2 frames of the frontal cortex sections were counted and the sizes of the cellular bodies were measured. Photographs of several depth levels from the sections were obtained. Results. Cortical pyramidal neurons showed distinctive morphological alterations in the soma and dendrites (including loss of dendritic spines) in 12.9% of cells from intracerebral infectedmice with street virus; in 8.2% of neurons from intramuscular inf...

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“…The nVHLX model, which involves permanent excitotoxic damage to the VH during a sensitive period in early postnatal development, results in a wide range of neuronal abnormalities hypothesized to contribute to the development of SZ, including: decreases in dendritic spine density in NAC and PFC (Flores et al, 2005); abnormal activation of PFC and NAC neurons in response to mesocorticolimbic stimulation (Goto and O'Donnell, 2002;O'Donnell et al, 2002); and altered regulation of cortical cholinergic activity (Alexander et al, 2009;Brooks et al, 2011;Laplante et al, 2004). The nVHLX model also reveals a range of SZ-like cognitive impairments, including: reductions in prepulse inhibition (Le Pen and Moreau, 2002) and latent inhibition (Grecksch et al, 1999); deficits in working memory (Lipska et al, 2002a;Brady et al, 2010) and cognitive flexibility (Marquis et al, 2008;Brady, 2009) tasks, which are known to be heavily reliant on appropriate hippocampal-PFC-NAC interactions (Chambers et al, 1996;Floresco et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Transient Inactivation of the Neonatal Ventral Hippocampus Impairs Attentional Set-Shifting Behavior: Reversal with an α7 Nicotinic Agonist

Brooks

Pershing

Thomsen

et al. 2012

Neuropsychopharmacol

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Cognitive deficits represent a core symptom cluster in schizophrenia that are thought to reflect developmental dysregulations within a neural system involving the ventral hippocampus (VH), nucleus accumbens (NAC), and prefrontal cortex (PFC). The present experiments determined the cognitive effects of transiently inactivating VH in rats during a sensitive period of development. Neonatal (postnatal day 7, PD7) and adolescent (PD32) male rats received a single bilateral infusion of saline or tetrodotoxin (TTX) within the VH to transiently inactivate local circuitry and efferent outflow. Rats were tested as adults on an attentional set-shifting task. Performance in this task depends upon the integrity of the PFC and NAC. TTX infusions did not affect the initial acquisition or ability to learn an intradimensional shift. However, TTX rats required a greater number of trials than did controls to acquire the first reversal and extradimensional shift (ED) stages. These impairments were age and region-specific as rats infused with TTX into the VH at PD32, or into the dorsal hippocampus at PD7, exhibited performance in the task similar to that of controls. Finally, acute systemic administration of the partial a7 nicotinic acetylcholine receptor (nAChR) agonist SSR 180711 (3.0 mg/kg) eliminated the TTX-induced performance deficits. Given that patients with schizophrenia exhibit hippocampal pathophysiology and deficits in the ED stages of set-shifting tasks, our results support the significance of transient hippocampal inactivation as an animal model for studying the cognitive impairments in schizophrenia as well as the pro-cognitive therapeutic potential of a7 nAChR agonists.

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Alterations in dendritic morphology of prefrontal cortical and nucleus accumbens neurons in post-pubertal rats after neonatal excitotoxic lesions of the ventral hippocampus

Cited by 203 publications

References 75 publications

Neonatal Phencyclidine Treatment in Mice Induces Behavioral, Histological and Neurochemical Abnormalities in Adulthood

Neonatal Phencyclidine Treatment in Mice Induces Behavioral, Histological and Neurochemical Abnormalities in Adulthood

Alteraciones de la morfología dendrítica neuronal en la corteza cerebral de ratones infectados con rabia: un estudio con la técnica de Golgi

Transient Inactivation of the Neonatal Ventral Hippocampus Impairs Attentional Set-Shifting Behavior: Reversal with an α7 Nicotinic Agonist

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