ArticleSchizophrenia bulletin2015
Elevated Excitatory Input to the Nucleus Accumbens in Schizophrenia: A Postmortem Ultrastructural Study.
Article in Schizophrenia bulletin, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Synapse Pathology in Schizophrenia: A Meta-analysis of Postsynaptic Elements in Postmortem Brain Studies.Schizophrenia bulletin · 2020Pooled it
- A ventral hippocampus to nucleus accumbens pathway regulates impulsivity in male but not female rats.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Cellular and subcellular localization of the copper transporter CTR1 in human postmortem hippocampus and striatum.Scientific reports · 2026Article
- The Molecular Machinery of Synaptic Plasticity and Its Potential Role in the Aetiology of Schizophrenia.Molecular neurobiology · 2026Review
- A ventral hippocampus to nucleus accumbens pathway regulates impulsivity.bioRxiv : the preprint server for biology · 2025Article
- Activation of Metabotropic Glutamate Receptor 3 Modulates Thalamo-accumbal Transmission and Rescues Schizophrenia-Like Physiological and Behavioral Deficits.Biological psychiatry · 2024Article
- New clues for the role of cerebellum in schizophrenia and the associated cognitive impairment.Frontiers in cellular neuroscience · 2024Review
- Increased Metabolic Potential, Efficacy, and Safety of Emerging Treatments in Schizophrenia.CNS drugs · 2023Review
- Distinctive alterations in the mesocorticolimbic circuits in various psychiatric disorders.Psychiatry and clinical neurosciences · 2023Article
- Evidence for upregulation of excitatory synaptic transmission in the substantia nigra in Schizophrenia: a postmortem ultrastructural study.Journal of neural transmission (Vienna, Austria : 1996) · 2023Article
- Mitochondria DNA copy number, mitochondria DNA total somatic deletions, Complex I activity, synapse number, and synaptic mitochondria number are altered in schizophrenia and bipolar disorder.Translational psychiatry · 2022Article
- Abnormal synaptic plasticity and impaired cognition in schizophrenia.World journal of psychiatry · 2022Review
- Activity-State Dependent Reversal of Ketamine-Induced Resting State EEG Effects by Clozapine and Naltrexone in the Freely Moving Rat.Frontiers in psychiatry · 2022Article
- Mapping the serum proteome to neurological diseases using whole genome sequencing.Nature communications · 2021Article
- Decoding molecular and cellular heterogeneity of mouse nucleus accumbens.Nature neuroscience · 2021Article
- In vivo evidence of lower synaptic vesicle density in schizophrenia.Molecular psychiatry · 2021Article
- Increased glutamate transmission onto dorsal striatum spiny projection neurons in Pink1 knockout rats.Neurobiology of disease · 2021Article
- Mitochondrial dysfunction in schizophrenia: With a focus on postmortem studies.Mitochondrion · 2021Article
- Glutamatergic Dysfunction and Synaptic Ultrastructural Alterations in Schizophrenia and Autism Spectrum Disorder: Evidence from Human and Rodent Studies.International journal of molecular sciences · 2020Review
- Evidence for altered excitatory and inhibitory tone in the post-mortem substantia nigra in schizophrenia.The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The cause of schizophrenia (SZ) is unknown and no single region of the brain can be pinpointed as an area of primary pathology. Rather, SZ results from dysfunction of multiple neurotransmitter systems and miswiring between brain regions. It is necessary to elucidate how communication between regions is disrupted to advance our understanding of SZ pathology. The nucleus accumbens (NAcc) is a prime region of interest, where inputs from numerous brain areas altered in SZ are integrated. Aberrant signaling in the NAcc is hypothesized to cause symptoms of SZ, but it is unknown if these abnormalities are actually present. Electron microscopy was used to study the morphology of synaptic connections in SZ. The NAcc core and shell of 6 SZ subjects and 8 matched controls were compared in this pilot study. SZ subjects had a 19% increase in the density of asymmetric axospinous synapses (characteristic of excitatory inputs) in the core, but not the shell. Both groups had similar densities of symmetric synapses (characteristic of inhibitory inputs). The postsynaptic densities of asymmetric synapses had 22% smaller areas in the core, but not the shell. These results indicate that the core receives increased excitatory input in SZ, potentially leading to dysfunctional dopamine neurotransmission and cortico-striatal-thalamic stimulus processing. The reduced postsynaptic density size of asymmetric synapses suggests impaired signaling at these synapses. These findings enhance our understanding of the role the NAcc might play in SZ and the interaction of glutamatergic and dopaminergic abnormalities in SZ.
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