Repetitive Spreading Depolarization induces gene expression changes related to synaptic plasticity and neuroprotective pathways

Dell’Orco, Michela; Weisend, Jordan E; Perrone‐Bizzozero, Nora I.; Carlson, Andrew P.; Morton, Russell A.; Linsenbardt, David N.; Shuttleworth, C. William

doi:10.1101/2023.02.27.530317

Cited by 3 publications

(1 citation statement)

References 69 publications

(103 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…5 Synaptic plasticity is the activity-dependent change in neuronal connection strength. 6 In 1973, Bliss first reported the long-term potentiation (LTP) phenomenon during the synaptic transmission between performing fibers and hippocampal granule cells of rabbits, which was the prelude to the study of synaptic plasticity. 7 Then, the corresponding long-term depression (LTD) of synaptic plasticity was reported by Ito in 1982.…”

Section: Introductionmentioning

confidence: 99%

Regulatory Molecules of Synaptic Plasticity in Anxiety Disorder

Xu¹,

Xu²,

Li³

et al. 2023

IJGM

View full text Add to dashboard Cite

Synaptic plasticity is the capacity of synaptic transmission between neurons to be strengthened or weakened. There are many signal molecules accumulated in the presynaptic and postsynaptic membranes that can lead to the regulation of synaptic plasticity and involvement in numerous of neurological and psychiatric diseases, including anxiety disorder. However, the regulatory mechanisms of synaptic plasticity in the development of anxiety disorder have not been well summarized. This review mainly aims to discuss the biological functions and mechanisms of synaptic plasticity-related molecules in anxiety disorder, with a particular focus on the metabotropic glutamate receptors, brain-derived neurotrophic factor, hyperpolarization-activated cyclic nucleotide–gated channels, and postsynaptic density 95. The summarized functions and mechanisms of synaptic plasticity-related molecules in anxiety will provide insight into novel neuroplasticity modifications for targeted therapy for anxiety.

show abstract

Section: Introductionmentioning

confidence: 99%

Regulatory Molecules of Synaptic Plasticity in Anxiety Disorder

Xu¹,

Xu²,

Li³

et al. 2023

IJGM

View full text Add to dashboard Cite

show abstract

Seizure propagation triggers a protective contralesional spreading depolarization during focal hippocampal stroke predominantly in freely behaving female mice

Boyce,

Fouad,

Gom

et al. 2023

Preprint

View full text Add to dashboard Cite

Following stroke, women have worse functional outcomes than men, due in part to more frequent non-focal symptoms, leading to misdiagnosis and lack of treatment. Understanding changes in peri-stroke behavior is critical to improving outcomes. During an ischemic stroke, energy loss in tissue fed by a blocked cerebral vessel induces rapid neuronal death. Next, large depolarizing waves (spreading depolarization, SD) emanate from this ischemic core. While SD in nearby hypoperfused tissue is deleterious, its impact on remote structures is unclear. Behavioural and cognitive symptoms may mirror this biphasic nature of cell death. We present a model for delivering and monitoring focal stroke in awake freely behaving mice, using bilateral fiberoptic cannulas to induce hippocampal stroke (unilateral photothrombosis) and monitor both ipsi- and contralesional neuronal Ca2+dysregulation/dynamics via GCaMP6f photometry. Ipsilesional Ca2+dysregulation, which correlated with lesion size, was indistinguishable between sexes, yet females had larger, more frequent contralesional SD-associated Ca2+waves, with increased acute exploration. Hippocampal stroke generated retrograde and anterograde amnesia, yet anterograde amnesia was absent in mice that had SD-associated Ca2+waves. Fiber photothrombosis with paired photometry offers flexibility to induce and monitor stroke in any brain region in freely behaving mice, allowing interrogation of previously inaccessible stroke biology.

show abstract