Ionotropic glutamate receptor binding in the posterior cingulate cortex in schizophrenia patients

  title={Ionotropic glutamate receptor binding in the posterior cingulate cortex in schizophrenia patients},
  author={Kelly A Newell and Katerina Zavitsanou and Xu-Feng Huang},
Using quantitative autoradiography, the present study examined ionotropic glutamatergic receptor binding sites using [3H]dizocilpine, [3H]&agr;-amino-3-hydroxy-5-methylisoxazole-4-propionate, and [3H]kainate in the posterior cingulate cortex of schizophrenia patients and matched controls. We found a significant increase in [3H]dizocilpine binding in the superficial layers (41%, p<0.001) and deep layers (30%, p=0.004) of the posterior cingulate cortex in the schizophrenia group compared with… 

Alterations of muscarinic and GABA receptor binding in the posterior cingulate cortex in schizophrenia

Increased cannabinoid receptor density in the posterior cingulate cortex in schizophrenia

The posterior cingulate cortex (PCC) has recently been implicated in the pathophysiology of schizophrenia, through both animal and human studies. We have recently shown abnormal glutamate, GABA, and

Changes in cortical N-methyl-d-aspartate receptors and post-synaptic density protein 95 in schizophrenia, mood disorders and suicide

Differences in cortical NMDAR expression and post-synaptic density protein 95 are present in psychiatric disorders and suicide completion and may contribute to different responses to ketamine.

Neurotransmitter receptor binding in the posterior cingulate cortex in schizophrenia and in the phencyclidine mouse model: an exploration of the NMDA hypofunction hypothesis of schizophrenia

Results have shown for the first time that there are specific neurotransmitter imbalances in this region of the posterior cingulate cortex in schizophrenia, and it is possible that these changes stem from NMDA hypofunction.

Neuroscience research: related to the neuropathology of schizophrenia, neuroendocrinology of obesity, and brain map

The results suggest that aripiprazole has selective effects on the mesolimbic dopaminergic pathway, and is a possible therapeutic mechanism for the long-term efficacy of aripIPrazole in controlling schizophrenia symptoms with reduced extrapyramidal side-effects.

Excitatory and inhibitory neurotransmission is chronically altered following perinatal NMDA receptor blockade

Levels of Ionotropic Glutamate and Muscarinic Receptors in Three Animal Models of Schizophrenia

Data would suggest that different rodent paradigms cause variable changes in levels of CHRM3 and KAR in the rat CNS, and raises the possibility that such changes may, in part, modulate the behavioural differences that have been observed after isolation rearing, neonatal PCP treatment or sub-chronicPCP treatment.



Selective Alterations in Ionotropic Glutamate Receptors in the Anterior Cingulate Cortex in Schizophrenia

Increased density of glutamate/N-methyl-d-aspartate receptors in superior temporal cortex in schizophrenia

Glutamate receptor expression in schizophrenic brain

Regulation of ionotropic glutamate receptors following subchronic and chronic treatment with typical and atypical antipsychotics

Quantitative in vitro receptor autoradiography suggests that typical and atypical antipsychotics may exert some of their clinical effects by affecting NMDA receptors in the medial prefrontal cortex by producing minimal extrapyramidal side effects produced by clozapine.

Glutamate receptor dysfunction and schizophrenia.

It is proposed that since N-methyl-D-aspartate receptor hypofunction can cause psychosis in humans and corticolimbic neurodegenerative changes in the rat brain, and since these changes are prevented by certain antipsychotic drugs, including atypical neuroleptic agents, a better understanding of this mechanism may lead to improved pharmacotherapy in schizophrenia.

Cingulate gyrus volume and metabolism in the schizophrenia spectrum

Excessive cerebrocortical release of acetylcholine induced by NMDA antagonists is reduced by GABAergic and α2-adrenergic agonists

The microdialysis results are consistent with several aspects of the circuitry proposed to mediate the neurotoxic action of NMDA antagonists, including pentobarbital, diazepam and clonidine suppressed MK-801's effect on ACh release.