Acute stress is not acute: sustained enhancement of glutamate release after acute stress involves readily releasable pool size and synapsin I activation

@article{Musazzi2017AcuteSI,
  title={Acute stress is not acute: sustained enhancement of glutamate release after acute stress involves readily releasable pool size and synapsin I activation},
  author={Laura Musazzi and Paolo Tornese and Nathalie Sala and Maurizio Popoli},
  journal={Molecular Psychiatry},
  year={2017},
  volume={22},
  pages={1226-1227}
}
Acute stress is not acute: sustained enhancement of glutamate release after acute stress involves readily releasable pool size and synapsin I activation 

Multiomic profiling of the acute stress response in the mouse hippocampus

A brief swim exposure is used to trigger an acute stress response in mice, which transiently increases anxiety, without leading to lasting maladaptive changes, and characterize the acute stress-induced molecular events in the mouse hippocampus over time.

Acute Ketamine Facilitates Fear Memory Extinction in a Rat Model of PTSD Along With Restoring Glutamatergic Alterations and Dendritic Atrophy in the Prefrontal Cortex

The results show rapid effects of ketamine in animals subjected to acute FS, in line with previous studies suggesting a therapeutic action of the drug in PTSD models, and are consistent with a mechanism of ketamines involving re-establishment of synaptic homeostasis, through restoration of glutamate release, and structural remodeling of dendrites.

The Role of Stress-Induced Changes of Homer1 Expression in Stress Susceptibility.

The studies on animal models confirm that the HOMer1a-dependent remodeling most likely plays an important part in the stress susceptibility, whereas HOMER1a itself can be regarded as a neuroprotector.

Acute stress induces an aberrant increase of presynaptic release of glutamate and cellular activation in the hippocampus of BDNFVal/Met mice.

It is reported that the BDNF Val66Met SNP knock-in mice display an altered response to acute restraint stress in terms of hippocampal glutamate release, CREB phosphorylation, and neuronal activation, compared to wild-type animals.

Neurobiology of Stress Chronic mild stress induces anhedonic behavior and changes in glutamate release, BDNF tra ffi cking and dendrite morphology only in stress vulnerable rats. The rapid restorative action of ketamine

It is shown that the Chronic Mild Stress model of depression induces, only in stress-vulnerable rats, de- pressed-like anhedonic behavior, together with impairment of glutamate/GABA presynaptic release, BDNF mRNA levels reduced by chronic stress and dendritic morphology in hippocampus, and that a single administration of ketamine restores normal behavior and most of the cellular/molecular maladaptive changes in vulnerable rats.

Acute or Chronic? A Stressful Question

Acute Inescapable Stress Rapidly Increases Synaptic Energy Metabolism in Prefrontal Cortex and Alters Working Memory Performance.

The present data suggest that acute stress increases energy consumption at PFC synaptic terminals and alters working memory.

Molecular roadmap of the healthy stress response in the mouse hippocampus

The results unveil the complexity and specificity of the healthy stress response, with widespread changes in protein phosphorylation and gene transcription, but tightly regulated protein translation.

References

SHOWING 1-10 OF 14 REFERENCES

Stress and corticosterone increase the readily releasable pool of glutamate vesicles in synaptic terminals of prefrontal and frontal cortex

It is found that acute stress increases both the readily releasable pool (RRP) of vesicles and depolarization-evoked glutamate release, while application in vitro of corticosterone rapidly increases the RRP, an effect dependent on synaptic receptors for the hormone, but does not induce glutamate release for up to 20 min.

Chronic Desipramine Prevents Acute Stress-Induced Reorganization of Medial Prefrontal Cortex Architecture by Blocking Glutamate Vesicle Accumulation and Excitatory Synapse Increase

It is hypothesized that the preventing action of desipramine is located on pathways downstream of this process and/or other pathways, because enhancement of glutamate system remodeling may contribute to overexcitation dysfunctions, and this aspect could represent a crucial component in the pathophysiology of stress-related disorders.

The stressed synapse: the impact of stress and glucocorticoids on glutamate transmission

Understanding of the mechanisms by which stress and glucocorticoids affect glutamate transmission provides insights into normal brain functioning, as well as the pathophysiology and potential new treatments of stress-related neuropsychiatric disorders.

Mechanisms for acute stress-induced enhancement of glutamatergic transmission and working memory

It is suggested that acute stress, by activating glucocorticoid receptors, increases the trafficking and function of NMDARs and AMPARs through SGK/Rab4 signaling, which leads to the potentiated synaptic transmission, thereby facilitating cognitive processes mediated by the PFC.

The neuro-symphony of stress

Together, the effects of individual mediators on neuronal function and plasticity are integrated, and emerging evidence suggests that there is crosstalk between them that enables fine-tuned responses to diverse challenges.

Temporal Dynamics of Acute Stress‐Induced Dendritic Remodeling in Medial Prefrontal Cortex and the Protective Effect of Desipramine

Data demonstrate that 1) acute stressors may induce rapid and sustained changes of PL neurons; and 2) chronic DMI may protect neurons from rapid stress‐induced synaptic changes.

Correlated memory defects and hippocampal dendritic spine loss after acute stress involve corticotropin-releasing hormone signaling

It is concluded that acute, hours-long stress impairs learning and memory via mechanisms that disrupt the integrity of hippocampal dendritic spines through the mechanisms of CRH–CRFR1 signaling.

Glucocorticoids, depression, and mood disorders: structural remodeling in the brain.

  • B. McEwen
  • Psychology, Biology
    Metabolism: clinical and experimental
  • 2005

A hypothesized role for dendritic remodeling in the etiology of mood and anxiety disorders.

  • J. GormanJ. Docherty
  • Psychology, Biology
    The Journal of neuropsychiatry and clinical neurosciences
  • 2010
Drugs that reduce glutamatergic neurotransmission under these circumstances, many of which have already been shown helpful in treating mood and anxiety disorders, may prevent this dendritic retraction and thus protect synaptic connections throughout the brain.