Hyperactivity, decreased startle reactivity, and disrupted prepulse inhibition following disinhibition of the rat ventral hippocampus by the GABAA receptor antagonist picrotoxin

Bast, Tobias; Zhang, Weining; Feldon, Joram

doi:10.1007/s002130100775

Cited by 71 publications

(43 citation statements)

References 74 publications

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“…In addition, mice with functional disruption of PV-IR FSI in the entire hippocampus are hypoactive, while GCLM Ϫ/Ϫ mice show strong novelty-induced exploration. Such hyperactivity can be induced by a decreased GABA inhibition in the VH (Bast et al, 2001a). The altered behavior of GCLM Ϫ/Ϫ mice under mild stress (in elevated plus maze and light/dark box) is also in line with a specific functional disruption of the VH but not DH (Bannerman et al, 2004).…”

Section: Discussionmentioning

confidence: 71%

Redox Dysregulation Affects the Ventral But Not Dorsal Hippocampus: Impairment of Parvalbumin Neurons, Gamma Oscillations, and Related Behaviors

Steullet¹,

Cabungcal²,

Kulak³

et al. 2010

J. Neurosci.

185

171

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Elevated oxidative stress and alteration in antioxidant systems, including glutathione (GSH) decrease, are observed in schizophrenia. Genetic and functional data indicate that impaired GSH synthesis represents a susceptibility factor for the disorder. Here, we show that a genetically compromised GSH synthesis affects the morphological and functional integrity of hippocampal parvalbumin-immunoreactive (PV-IR) interneurons, known to be affected in schizophrenia. A GSH deficit causes a selective decrease of PV-IR interneurons in CA3 and dendate gyrus (DG) of the ventral but not dorsal hippocampus and a concomitant reduction of ␤/␥ oscillations. Impairment of PV-IR interneurons emerges at the end of adolescence/early adulthood as oxidative stress increases or cumulates selectively in CA3 and DG of the ventral hippocampus. Such redox dysregulation alters stress and emotion-related behaviors but leaves spatial abilities intact, indicating functional disruption of the ventral but not dorsal hippocampus. Thus, a GSH deficit affects PV-IR interneuron's integrity and neuronal synchrony in a region-and time-specific manner, leading to behavioral phenotypes related to psychiatric disorders.

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Section: Discussionmentioning

confidence: 71%

Redox Dysregulation Affects the Ventral But Not Dorsal Hippocampus: Impairment of Parvalbumin Neurons, Gamma Oscillations, and Related Behaviors

Steullet¹,

Cabungcal²,

Kulak³

et al. 2010

J. Neurosci.

185

171

View full text Add to dashboard Cite

show abstract

“…In addition, amygdala kindling has been found to increase the density of dopamine receptors in the nucleus accumbens (Csernansky et al, 1988) and produce significant PPI deficits in rats (Koch and Ebert, 1998). Moreover, a number of theories have proposed that an increase of excitatory activity entering the hippocampus from the amygdala via both direct and indirect pathways may significantly contribute to the pathophysiology of schizophrenia (Bast and Feldon, 2003;Bast et al, 2001;Benes and Berretta, 2000;Berretta et al, 2001). Taken together, these observations and views support the hypothesis that hyperactivation of the amygdala may be involved in the induction of neurochemical and behavioral abnormalities found in schizophrenia.…”

Section: Discussionmentioning

confidence: 99%

Prepulse Inhibition Deficits in GAD65 Knockout Mice and the Effect of Antipsychotic Treatment

Heldt

Green

Ressler

2004

Neuropsychopharmacol

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Recent postmortem studies in humans suggest that defects in GABAergic neurotransmission might contribute to the neuropathology associated with schizophrenia. Disturbances in GABAergic systems may also contribute to the sensorimotor gating deficits classically observed in schizophrenic patients, including deficits in prepulse inhibition (PPI). To explore the relationship, the current study examined the integrity of PPI and startle habituation in knockout (KO) mice that lack the GABA synthesizing enzyme glutamic acid decarboxylase 65 (GAD 65). GAD65 KO mice displayed normal baseline and habituated startle responses, which did not differ from GAD65 wild-type (WT) or heterozygous (HET) mice. However, GAD65 KO mice showed robust deficits in PPI which were reversed by the atypical antipsychotic agent clozapine. These results lend support to the view that abnormalities in GABAergic systems might contribute to the basic pathophysiological mechanisms in schizophrenia.

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“…Therefore, we determined the expression of GR, GAP-43 and RC3 in the amygdala, frontal cortex and hippocampus of our euthyroid, hypothyroid and hyperthyroid B6 and TRα o/o mice. These three brain regions are involved in the behaviors tested in this study [7,8,26,30].…”

Section: Differential Decreased Expression Of Gr Gap-43 and Rc3 In Rmentioning

confidence: 95%

Behavioral inhibition and impaired spatial learning and memory in hypothyroid mice lacking thyroid hormone receptor α

Wilcoxon

Nadolski

Samarut

et al. 2007

Behavioural Brain Research

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Thyroid hormone insufficiency leads to impaired neurogenesis, behavioral alterations and cognitive deficits. Thyroid hormone receptors, expressed in brain regions involved in these behaviors, mediate the effects of thyroid hormone deficiency or excess. To determine the contribution of thyroid hormone receptor alpha (TRα) in these behaviors, we examined the behavior of euthyroid as well as hypo-and hyperthyroid mice lacking all isoforms of the TRα (TRα o/o ). The hypothyroxinemic TRα o/o mice demonstrated behavioral inhibition, manifested in decreased activity and increased anxiety/fear in the open field test (OFT) and increased immobility in the forced swim test (FST) compared to C57BL/6J mice. TRα o/o mice also showed learning and recall impairments in the Morris water maze (MWM), which were exaggerated by hypothyroidism in TRα o/o mice. These impairments were concurrent with increased thigmotaxis, suggesting an increased anxiety-like state of the TRα o/o mice in the MWM. Expression of genes, known to be involved in processes modulating learning and memory, such as glucocorticoid receptor (GR), growth-associated protein 43 (GAP-43) and neurogranin (RC3), were significantly decreased in the hippocampus of TRα o/o mice. GR expression was also decreased in the frontal cortex and amygdala of TRα o/o mice, indicating that expression of GR is regulated, probably developmentally, by one or more isoforms of TRα in the mouse brain. Taken together these data demonstrate behavioral alterations in the TRα o/o mice, indicating the functional role of TRα, and a delicate interaction between TRα and TRβ-regulated genes in these behaviors. Thyroid hormone-regulated genes potentially responsible for the learning deficit found in TRα o/o mice include GR, RC3 and GAP-43.

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Hyperactivity, decreased startle reactivity, and disrupted prepulse inhibition following disinhibition of the rat ventral hippocampus by the GABAA receptor antagonist picrotoxin

Cited by 71 publications

References 74 publications

Redox Dysregulation Affects the Ventral But Not Dorsal Hippocampus: Impairment of Parvalbumin Neurons, Gamma Oscillations, and Related Behaviors

Redox Dysregulation Affects the Ventral But Not Dorsal Hippocampus: Impairment of Parvalbumin Neurons, Gamma Oscillations, and Related Behaviors

Prepulse Inhibition Deficits in GAD65 Knockout Mice and the Effect of Antipsychotic Treatment

Behavioral inhibition and impaired spatial learning and memory in hypothyroid mice lacking thyroid hormone receptor α

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