Abstract Details

Title Early Synaptic Composition Changes after Global Cerebral Ischemia

Topic Cerebrovascular Disease and Interventional Neurology

Presentation(s) P05 - (-)

Poster/Presentation
Number 225

Objective

Background BACKGROUND: Neurological impairment from oxygen deprivation after cardiac arrest (CA) hinders synaptic transmission and cellular action potential firing of the neurons in the brain.

Design/Methods DESIGN/METHODS: Thirteen male adult Wistar rats underwent 7-minute asphyxial CA, with 2 additional rats as shams. Multiunit activity (MUA) was continuously recorded from the primary somatosensory forelimb area during baseline, injury, and early recovery. We characterized the recovery of electrophysiological signals by analyzing the neural firing rate and short-latency responses of evoked neural activities. After CA, the animals were euthanized (1) 5 minutes after resuscitation (Pre-spike Group, n=3), (2) immediately after early recovery of spontaneous multiunit spike (Early Group, n=5), or (3) upon later recovery of multiunit spike when SSEP N10 amplitude recovered to 50% of its baseline or 60 minutes after resuscitation (Late Group, n=5). Total and activated CaMKII in the synaptosomal fractions of brains were quantified using Western Blot analysis.

Results RESULTS: The Late Group had significant MUA firing rate (37.6 ±12.9%) normalized to baseline, compared to the Early Group (2.0±1.7%, p=0.01) and the Pre-spike Group (0.2±0.1%, p=0.01). An increase in total CaMKII was found in synaptosomal fractions of the Pre-spike Group, compared to shams (p=0.003) and the Late Group (p=0.014). A strong activation of CaMKII was found in the Pre-spike Group (p=0.011) compared to the Late group, with no significant difference between the Early Group and the Late Group.

Conclusions CONCLUSIONS: Early CaMKII change is associated with early burst recovery of neuron spike activity after global cerebral ischemia. Activation of CaMKII may be associated with the recovery of synaptic protein regulation and responsible for or coincident with recovery of neural spike activity. Further studies may elucidate the mechanistic link between synaptic proteins, synaptic strength recovery, and restoration of electrical brain function.

Authors/Disclosures
PRESENTER	No disclosure on file
Manuel M. Buitrago Blanco, MD, PhD (University of California Los Angeles)	No disclosure on file
	No disclosure on file
	No disclosure on file
	No disclosure on file
	No disclosure on file
Nitish Thakor	No disclosure on file
	No disclosure on file
Romergryko G. Geocadin, MD, FAAN (Johns Hopkins University School of Medicine)	Dr. Geocadin has received personal compensation in the range of $5,000-$9,999 for serving as an Expert Witness for Medicolegal Consulting.

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