Rhythmic synaptic activity induced by mechanical injury of rat CA3 hippocampal area.

Abegg, Mathias (2007). Rhythmic synaptic activity induced by mechanical injury of rat CA3 hippocampal area. Journal of neurotrauma, 24(9), pp. 1536-1542. M.A. Liebert 10.1089/neu.2005.360

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Mechanical injury of the CNS frequently results from accidents but also occurs in the course of neurosurgical interventions. A great variety of anatomical and physiological changes have been described to evolve after a brain trauma yet only little is known about processes that occur during a trauma. In the present study, I obtained whole-cell patch clamp recordings from pyramidal cells in hippocampal slice cultures while mechanically lesioning the CA3 area. Electrophysiological analysis revealed that traumatic injury massively increased excitatory and inhibitory synaptic activity in the entire CA3 region. Cutting the CA3 region induced highly rhythmic excitatory postsynaptic currents (EPSCs) that reached frequencies of around 70 Hz. Blocking voltage-dependent sodium channels with tetrodotoxin prevented the increase in synaptic activity and injury-induced neurotransmitter release in CA3 remote from the lesion site. With fast synaptic transmission blocked only neurons in the immediate vicinity of a lesion depolarized and fired action potentials upon mechanical damage. I hence suggest that mechanical injury damages the membrane and induces action potential firing in only a small population of neurons. This activity is then propagated throughout the undamaged CA3 network inducing highly rhythmic discharges. Thus mechanical brain injury initiates immediate functional changes that exceed the lesion site.

Item Type:	Journal Article (Original Article)
Division/Institute:	04 Faculty of Medicine > Department of Head Organs and Neurology (DKNS) > Clinic of Ophthalmology
UniBE Contributor:	Abegg, Mathias
Subjects:	600 Technology > 610 Medicine & health
ISSN:	0897-7151
Publisher:	M.A. Liebert
Language:	English
Submitter:	Mathias Abegg
Date Deposited:	01 May 2015 11:45
Last Modified:	05 Dec 2022 14:45
Publisher DOI:	10.1089/neu.2005.360
PubMed ID:	17892414
URI:	https://boris.unibe.ch/id/eprint/67690