Immunohistochemical localization of γ-aminobutyric acidB receptor in the hippocampus of subjects with schizophrenia

Sasaki, Megumi; Ishikawa, Masanori; Iwakiri, Masahiko; Hidaka, Shin; Shiraishi, Hiroyasu; Iritani, Shyuji

doi:10.1016/s0304-3940(00)00939-3

Cited by 64 publications

(54 citation statements)

References 16 publications

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“…We simulated a presynaptic mechanism for GABA B -R activation on CA3 pyramidal cells. This is consistent with recent data (Mizukami et al 2000) showing a relatively larger loss of GABA B -R immunoreactivtity on pyramidal cells when compared to interneurons within the hippocampus of subjects with schizophrenia.…”

Section: Mechanism For Presynaptic Gaba B -Receptor Activationsupporting

confidence: 93%

“…This model also predicts that direct pharmacological manipulation of the presynaptic GABA B -R alone may not be an appropriate method of restoring normal gating. However, since recent data (Mizukami et al 2000) have shown a reduction of GABA B -Rs on hippocampal pyramidal cells, patients with schizophrenia not responding to traditional medication may benefit from both Ach-R and GABA B -R activation. Such a suggestion is consistent with recent hypotheses that have proposed a role for altered GABAergic transmission in the etiology of several mental illnesses, including schizophrenia, and cannot be explained by previous models.…”

Section: Discussionmentioning

confidence: 99%

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Inhibitory control of sensory gating in a computer model of the CA3 region of the hippocampus

Moxon

Gerhardt

Gulinello

et al. 2003

Biological Cybernetics

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A model of the CA3 region of the hippocampus was used to simulate the P50 auditory-evoked potential response to repeated stimuli in order to study the neuronal circuits involved in a sensoryprocessing deficit associated with schizophrenia. Normal subjects have a reduced P50 auditoryevoked potential amplitude in response to the second of two paired auditory click stimuli spaced 0.5 s apart. However, schizophrenic patients do not gate or reduce their response to the second click. They have equal auditory-evoked response amplitudes to both clicks. When schizophrenic patients were medicated with traditional neuroleptics, the evoked potential amplitude to both clicks increased, but gating of the second response was not restored or improved. Animal studies suggest a role for septohippocampal cholinergic activity in sensory gating. We used a computational model of this system in order to study the relative contributions of local processing and afferent activity in sensory gating. We first compared the effect of information representation as average firing rate to information representation as cell assemblies in order to evaluate the best method to represent the response of hippocampal neurons to the auditory click. We then studied the effects of nicotinic cholinergic input on the response of the network and the effect of GABA B receptor activation on the ability of the local network to suppress the test response. The results of our model showed that nicotinic cholinergic input from the septum to the hippocampus can control the flow of sensory information from the cortex into the hippocampus. In addition, postsynaptic GABA B receptor activation was not sufficient to suppress the test response when the interstimulus interval was 500 ms. However, presynaptic GABA B receptor activity may be responsible for the suppression of the test response at this interstimulus interval.

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Section: Mechanism For Presynaptic Gaba B -Receptor Activationsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Inhibitory control of sensory gating in a computer model of the CA3 region of the hippocampus

Moxon

Gerhardt

Gulinello

et al. 2003

Biological Cybernetics

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show abstract

“…62 Previous studies have suggested that the CA2/3 region of the hippocampus may be particularly vulnerable to neuropathological changes in psychosis. 18,[63][64][65][66][67][68] This is particularly evident in relation to the pathology of GABAergic interneurons in schizophrenia 15,18,[69][70][71][72] but is less clear in relation to markers of synaptic and glutamatergic function 72,73 and in relation to mood disorders. 7,65,72,74,75 Using an unbiased proteomic approach to assess protein changes within different hippocampal fields, we have shown an excess of differential protein expression in disease within CA2/3 compared with the other regions.…”

Section: Commentmentioning

confidence: 99%

Common Proteomic Changes in the Hippocampus in Schizophrenia and Bipolar Disorder and Particular Evidence for Involvement of Cornu Ammonis Regions 2 and 3

Föcking

Dicker²,

English³

et al. 2011

Arch Gen Psychiatry

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“…Previous studies have indicated that the reduction of GABAergic interneurons in schizophrenia is paralleled by increased GABA A receptor binding in the prefrontal cortex (Benes et al, 1996). In contrast, a marked reduction of GABA B receptors was reported in the hippocampus and prefrontal cortex (Mizukami et al, 2000;Ishikawa et al, 2005). Although the role of GABA B receptors in schizophrenia and related disorders is still poorly understood, recent pharmacologic studies have demonstrated that baclofen, a GABA B receptor agonist, prevents PPI deficits in rodents (Bortolato et al, 2004(Bortolato et al, , 2007.…”

Section: Introductionmentioning

confidence: 99%

Involvement of Pallidotegmental Neurons in Methamphetamine- and MK-801-Induced Impairment of Prepulse Inhibition of the Acoustic Startle Reflex in Mice: Reversal by GABAB Receptor Agonist Baclofen

Arai

Takuma

Mizoguchi

et al. 2008

Neuropsychopharmacol

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We have previously demonstrated that pallidotegmental GABAergic neurons play a crucial role in prepulse inhibition (PPI) of the startle reflex in mice through the activation of GABA B receptors in pedunculopontine tegmental neurons. In this study, we investigated whether PPI disruption induced by methamphetamine (METH) or MK-801 is associated with the dysfunction of pallidotegmental neurons. Furthermore, we examined the effects of baclofen, a GABA B receptor agonist, on METH-and MK-801-induced PPI impairment. Acute treatment with METH (3 mg/kg, subcutaneouly (s.c.)) and MK-801 (40.3 mg/kg, s.c.) significantly disrupted PPI, accompanied by the suppression of c-Fos expression in lateral globus pallidus induced by PPI. Furthermore, acute treatment with METH and MK-801 stimulated c-Fos expression in the caudal pontine reticular nucleus (PnC) in mice subjected to the PPT test, although PPI alone had no effect on c-Fos expression. Repeated treatment with 1 mg/kg METH for 7 days, which did not affect PPI acutely, showed similar effects on PPI and c-Fos expression to acute treatment with METH (3 mg/kg). Baclofen dose-dependently ameliorated PPI impairment induced by acute treatment with METH (3 mg/kg) and MK-801 (1 mg/kg), and decreased METH-and MK-801-stimulated c-Fos expression in PnC to the basal level. These results suggest that dysfunction of pallidotegmental neurons is involved in PPI disruption caused by METH and MK-801 in mice. GABA B receptor may constitute a putative target in treating neuropsychiatric disorders with sensorimotor gating deficits, such as schizophrenia and METH psychosis.

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Immunohistochemical localization of γ-aminobutyric acidB receptor in the hippocampus of subjects with schizophrenia

Cited by 64 publications

References 16 publications

Inhibitory control of sensory gating in a computer model of the CA3 region of the hippocampus

Inhibitory control of sensory gating in a computer model of the CA3 region of the hippocampus

Common Proteomic Changes in the Hippocampus in Schizophrenia and Bipolar Disorder and Particular Evidence for Involvement of Cornu Ammonis Regions 2 and 3

Involvement of Pallidotegmental Neurons in Methamphetamine- and MK-801-Induced Impairment of Prepulse Inhibition of the Acoustic Startle Reflex in Mice: Reversal by GABAB Receptor Agonist Baclofen

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