Molecular mechanisms that underlie structural and functional changes atthe postsynaptic membrane duringsynaptic plasticity
Abstract
The synaptic plasticity that is addressed in this review follows neurodegeneration in the brain and thus has both structural as well as functional components. The model of neurodegeneration that has been selected is the kainic acid lesioned hippocampus. Degeneration of the CA3 pyramidal cells results in a loss of the Schaffer collateral afferents innervating the CA1 pyramidal cells. This is followed by a period of structural plasticity where new synapses are formed. These are associated with changes in the numbers and shapes of spines as well as changes in the morphometry of the dendrites. It is suggested that this synaptogenesis is responsible for an increase in the ratio of NMDA to AMPA receptors mediating excitatory synaptic transmission at these synapses. Changes in the temporal and spatial properties of these synapses resulted in an altered balance between LTP and LTD. These properties together with a reduction in the inhibitory drive increased the excitability of the surviving CA1 pyramidal cells which in turn triggered epileptiform bursting activity. In this review we discuss the insights that may be gained from studies of the underlying molecular machinery. Developments in one of the collections of the cogs in this machinery has been summarized through recent studies characterizing the roles of neural recognition molecules in synaptic plasticity in the adult nervous systems of vertebrates and invertebrates. Such investigations of neural cell adhesion molecules, cadher…
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Glycine receptors mediate synaptic inhibition, particularly in the brainstem and spinal cord.
“Glycine receptors (GlyRs) also mediate synaptic inhibition, particularly in the brainstem and spinal cord [56].”
From Molecular Physiology of the Neuronal Synapse (2026) · cites this paper as [56]
Gephyrin binds with high affinity to the large cytoplasmic loop of the GlyR β-subunit, anchoring the receptor to the subsynaptic cytoskeleton and forming postsynaptic clusters.
“Gephyrin binds with high affinity to the large cytoplasmic loop of the GlyR β-subunit (GlyRβ), anchoring the receptor to the subsynaptic cytoskeleton and forming postsynaptic clusters [56].”
From Molecular Physiology of the Neuronal Synapse (2026) · cites this paper as [56]
Dysfunction of MAGUK family scaffold proteins is a convergent factor in neuropsychiatric disorders such as autism and schizophrenia.
“MAGUK family scaffold proteins are central to this architecture, linking receptors to signaling cascades; their dysfunction is a convergent factor in neuropsychiatric disorders such as autism and schizophrenia [56,85].”
From Molecular Physiology of the Neuronal Synapse (2026) · cites this paper as [56]
MAGUK family scaffold proteins are central to synaptic architecture, linking receptors to signaling cascades.
“MAGUK family scaffold proteins are central to this architecture, linking receptors to signaling cascades; their dysfunction is a convergent factor in neuropsychiatric disorders such as autism and schizophrenia [56,85].”
From Molecular Physiology of the Neuronal Synapse (2026) · cites this paper as [56]
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Molecular Physiology of the Neuronal Synapse
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“Gephyrin binds with high affinity to the large cytoplasmic loop of the GlyR β -subunit (GlyR β ), anchoring the receptor to the subsynaptic cytoskeleton and forming postsynaptic clusters [56].”
- Authors
- Wheal, H. V., Chen, Y., Mitchell, J., Schachner, M., Maerz, W., Wieland, H., van Rossum, D., & Kirsch, J.
- Affiliations
- University of Southampton (GB)
- Universität Hamburg (DE)
- University of Freiburg (DE)
- Max Planck Institute for Brain Research (DE)
- Corresponding author
- Wheal, Howard V
- Venue
- Progress in Neurobiology
- Publisher
- Elsevier BV
- Published
- 1998-08
- Volume
- 55
- Issue
- 6
- Pages
- 611-640
- ISSN
- 0301-0082 (ISSN-L)
- OpenAlex
- W2039503157
- Cited by
- 93
- References
- 7
- Citations by year
- 2026: 2 · 2022: 2 · 2021: 3 · 2020: 1 · 2018: 1 · 2016: 1 · 2015: 2 · 2014: 5 · 2013: 1 · 2012: 5
- FWCI
- 4.32
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Progress in Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- Rutgers University Community Repository (Rutgers University) (submittedVersion)
- Open Research (University of Surrey) (submittedVersion)
- Surrey Research Insight Open Access (The University of Surrey) (submittedVersion)
- FreiDok plus (Universitätsbibliothek Freiburg) (submittedVersion)
- Funders
- Wellcome Trust
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- synaptic plasticity, postsynaptic membrane, neurodegeneration, kainic acid lesion, hippocampus, CA1 pyramidal neurons, Schaffer collaterals, synaptogenesis, dendritic spine morphology, NMDA receptor, AMPA receptors, long-term potentiation, long-term depression, excitability, epileptiform bursting, CD56, cadherins, amyloid precursor protein, LDL receptor, receptor clustering, postsynaptic density, MAGUK proteins, calcium/calmodulin-dependent protein kinase II, Alzheimer's disease, signal transduction, cognitive function
- MeSH terms
- Animals, Multigene Family, Hippocampus, Humans, Kainic Acid, Nerve Degeneration, Neuronal Plasticity, Receptors, LDL, Synaptic Membranes, Neural Cell Adhesion Molecules
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