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Somatic amplification of distally generated subthreshold EPSPs in rat hippocampal pyramidal neurones
Author(s) -
Andreasen Mogens,
Lambert John D. C.
Publication year - 1999
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1999.0085o.x
Subject(s) - excitatory postsynaptic potential , membrane potential , somatic cell , tetrodotoxin , biophysics , subthreshold conduction , stimulation , chemistry , intracellular , electrophysiology , biology , neuroscience , inhibitory postsynaptic potential , microbiology and biotechnology , biochemistry , physics , transistor , quantum mechanics , voltage , gene
1 Intracellular recordings from hippocampal CA1 pyramidal neurones revealed that EPSPs evoked by selective stimulation of the isolated afferent input to the distal third of the apical dendrites were relatively insensitive to changes in dendritic membrane potential ( V m ) but amplified by depolarizations of the somatic V m . The amplification was present at potentials depolarized from resting membrane potential (RMP) but was most marked when the EPSPs were close to threshold for action potential generation. The amplification consisted of a uniform component and a variable component which was only present when the EPSPs were threshold straddling. 2 The somatic amplification was caused by an intrinsic membrane current which was blocked by somatic application of tetrodotoxin (TTX, 10 μ m ), but was insensitive to bath application of NiCl 2 (100–200 μ m ). We therefore suggest that the amplification of the subthreshold EPSP is due primarily to the activation of a non‐inactivating Na + current ( I NaP ). 3 Injection of 4‐aminopyridine (4‐AP, 25–50 mM) during intradendritic recordings resulted in amplification of the EPSPs in 37 % of the dendrites, which was similar to that observed in somatic recordings. However, in the one case in which somatic application of TTX was tested, dendritic amplification was blocked, suggesting that it is a reflection of the somatic amplification. 4 Because the shift to variable amplification was very abrupt and it is present in only a very narrow voltage range close to threshold, we suggest that the variable component is caused by the regenerative activation of I NaP . The variability itself is probably due to the simultaneous activation of different outward K + currents. 5 The present results indicate that the somatic region of CA1 pyramidal neurones can function as a voltage‐dependent amplifier of distally evoked EPSPs and that this is due to the activation of a somatic I NaP . The presence of this amplifying mechanism will have important functional consequences for the way in which distally generated EPSPs are integrated.