Ibotenic acid lesion of the ventral hippocampus differentially affects dopamine and its metabolites in the nucleus accumbens and prefrontal cortex in the rat

Lipska, Barbara K.; Jaskiw, George E.; Chrapusta, Stanisław J.; Karoum, Farouk; Weinberger, Daniel R.

doi:10.1016/0006-8993(92)91184-g

Cited by 204 publications

(98 citation statements)

References 53 publications

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“…Verification of lesions using Nissl-stained sections revealed cell loss and gliosis throughout the ventral hippocampus as previously reported (Lipska et al 1992;Lipska et al 1993;Khaing et al 2000). While the dorsal hippocampus was spared, there was neuronal loss, atrophy and cavitation in the ventral hippocampus with damage detected in portions of the subiculum and posterior dentate gyrus.…”

Section: Resultssupporting

confidence: 76%

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Neonatal Damage of the Ventral Hippocampus Impairs Working Memory in the Rat

Lipska

Aultman

Verma

et al. 2002

Neuropsychopharmacology

195

105

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Section: Resultssupporting

confidence: 76%

“…For experiments with the adult lesion, adult rats (Harlan Laboratories) (weighing 240-270 g, at approximately two months of age) were lesioned as previously described (Lipska et al 1992). Rats were anesthetized with Equithesin 3ml/kg (IP) and placed in a Kopf stereotaxic instrument using ear bars and a tooth bar ( Ϫ 2.5 mm).…”

Section: Surgerymentioning

confidence: 99%

Neonatal Damage of the Ventral Hippocampus Impairs Working Memory in the Rat

Lipska

Aultman

Verma

et al. 2002

Neuropsychopharmacology

195

105

View full text Add to dashboard Cite

show abstract

“…For example, neonatal lesions of the bilateral ventral hippocampus by ibotenate produced augmentation of amphetamine-induced locomotor activity in rats (Lipska et al, 1992(Lipska et al, , 1993Swerdlow et al, 2001). Bilateral hippocampal lesions induced by colchicine and kainate also produced the same effect, which was accompanied by an abnormal increase in amphetamine-induced DA release in the nucleus accumbens in adult rats (Wilkinson et al, 1993).…”

Section: Seizure-induced Hippocampal Damagementioning

confidence: 95%

Enhancement of Central Dopaminergic Activity in the Kainate Model of Temporal Lobe Epilepsy: Implication for the Mechanism of Epileptic Psychosis

Ando

Morimoto

Watanabe

et al. 2004

Neuropsychopharmacol

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There is an increased incidence of schizophrenia-like psychosis in temporal lobe epilepsy (TLE), and several risk factors have been implicated, including the duration of epilepsy and temporal lobe neuropathology. To investigate the biological mechanism of epileptic psychosis, we examined alterations of central dopaminergic systems in the kainate model of TLE. In adult rats, kainate was microinjected into the left amygdala to induce status epilepticus. An indirect dopamine agonist methamphetamine (MAP, 2 mg/kg, i.p.) was administered before and 1 month after the kainate treatment. MAP-induced locomotor activity was significantly enhanced in the kainate group compared with the baseline (pre-kainate) level, which was antagonized by pretreatment with haloperidol. The enhancement of locomotor activity in the kainate group was significantly correlated with the density of hippocampal CA1 neurons. Although the basal extracellular dopamine concentration was significantly lower in the striatum in the kainate group than in the control group (5.5 vs 39.2 fmol/20-min sample), the maximal concentration following MAP administration did not differ between the two groups. These results clearly demonstrate that hypersensitivity of the dopamine systems develops in the chronic phase of the kainate-induced TLE model, which may be responsible for the mechanism of epileptic psychosis.

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“…Young-adult VH lesions were performed on PD42 male Sprague-Dawley rats (weight 220-240 g) as described by Lipska et al (1992). Briefly, rats were anesthetized with Equithesin (3 ml/kg, i.p.)…”

Section: Young-adult Ventral Hippocampal Lesionsmentioning

confidence: 99%

Neonatal Ventral Hippocampal Lesions Produce an Elevation of ΔFosB-Like Protein(s) in the Rodent Neocortex

Powell

Binder

Hori

et al. 2005

Neuropsychopharmacol

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Rats that have sustained bilateral excitotoxic lesions of the ventral hippocampus (VH) as neonates develop behavioral abnormalities as adults (hyper-responsiveness to stress, diminished prepulse inhibition, and increased sensitivity to dopamine agonists), which resemble certain aspects of schizophrenia. Although this behavioral profile is thought to reflect dysregulation of the mesolimbic dopamine system, the precise neuroanatomical and neurochemical substrates that mediate the emergence of these abnormalities during brain maturation are unclear. In order to identify putative sites responsible for the development of behavioral abnormalities following neonatal lesions of the VH, we utilized the chronic neuronal activity marker DFosB. By comparison to sham lesioned animals, bilateral destruction of the VH elevated DFosB expression throughout the caudate putamen and neocortex of animals lesioned as neonates. These increases were not observed in rats lesioned as young-adults, suggesting that DFosB induction in the cortex of neonatally lesioned rats may be related to altered cortical neurodevelopment. Accumulating evidence implicates DFosB in mediation of the long-lasting effects of altered dopaminergic neurotransmission on behavior. The present findings are consistent with this proposal and suggest that elevated expression of DFosB identifies overactive neurons that may contribute to the enhanced sensitivity to stress and dopaminergic agonists of rats that have sustained bilateral ventral hippocampal lesions as neonates.

show abstract

Ibotenic acid lesion of the ventral hippocampus differentially affects dopamine and its metabolites in the nucleus accumbens and prefrontal cortex in the rat

Cited by 204 publications

References 53 publications

Neonatal Damage of the Ventral Hippocampus Impairs Working Memory in the Rat

Neonatal Damage of the Ventral Hippocampus Impairs Working Memory in the Rat

Enhancement of Central Dopaminergic Activity in the Kainate Model of Temporal Lobe Epilepsy: Implication for the Mechanism of Epileptic Psychosis

Neonatal Ventral Hippocampal Lesions Produce an Elevation of ΔFosB-Like Protein(s) in the Rodent Neocortex

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