4.3 Article

Local Axon Collaterals of Area CA1 Support Spread of Epileptiform Discharges Within CA1, but Propagation is Unidirectional

期刊

HIPPOCAMPUS
卷 18, 期 10, 页码 1021-1033

出版社

WILEY-LISS
DOI: 10.1002/hipo.20460

关键词

hippocampus; trisynaptic pathway; intrinsic circuitry; seizure

资金

  1. NIH [NS045612]
  2. NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS045612] Funding Source: NIH RePORTER

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CA3 and subiculum are hippocampal formation regions that can initiate seizure activity because each has a substantial intrinsic excitatory connectivity. We studied the intrinsic connectivity of area CA1 by exploring the spread of synchronous population discharges in ventral hippocampal slices from rats using a recording chamber that permitted multiple simultaneous extracellular recordings along all laminae of CA1. Brief single stimulus pulses were applied to stratum oriens (SO) or stratum radiatum (SR) on the CA3 side or the subicular side of CA1. In disinhibited slices, events triggered with SO or SR stimulation on the CA3-side propagated over the proximo-distal extent of CA1 with a maximal conduction velocity of 0.4 m/s, comparable with antidromic conduction velocities within CA1. By contrast, SO or SR stimuli applied on the subicular side of CA1 triggered events that did not spread backward toward CA3. These events are rapidly decremented in amplitude and duration. Whereas antidromic responses were largest when stimuli were applied on the subicular side of CA1, such responses were not sufficient to trigger epileptiform discharges when excitatory transmission was intact. We conclude that the unidirectional spread of epileptiform activity in area CA1 is the result of an intrinsic axon collateral system where each pyramidal cell has a proportionally larger projection toward subiculum. Although this collateral system is sparse compared with other hippocampal formation regions, its unidirectionality protects against re-entrant activation of CA3 and may be physiologically significant as a relay from proximal CA1 to distal CA1. (C) 2008 Wiley-Liss, Inc.

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