Somatic amplification of distally generated subthreshold EPSPs in rat hippocampal pyramidal neurones.
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 (Vm) but amplified by depolarizations of the somatic Vm. 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 microM), but was insensitive to bath application of NiCl2 (100-200 microM). We therefore suggest that the amplification of the subthreshold EPSP is due primarily to the activation of a non-inactivating Na+ current (INaP). 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 INaP. 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 INaP. The presence of this amplifying mechanism will have important functional consequences for the way in which distally generated EPSPs are integrated.
Andreasen
M
M
Department of Physiology, University of Aarhus, DK-8000 Arhus C, Denmark. ma@fi.au.dk
Lambert
J D
JD
D000344:Afferent Pathways / Q000502:physiology; D000818:Animals; D002462:Cell Membrane / Q000502:physiology; D003712:Dendrites / Q000502:physiology; D004558:Electric Stimulation; D004594:Electrophysiology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology*; D006624:Hippocampus / Q000502:physiology*; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009532:Nickel / Q000494:pharmacology; D015221:Potassium Channels / Q000502:physiology; D017966:Pyramidal Cells / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D015222:Sodium Channels / Q000502:physiology; D013779:Tetrodotoxin / Q000494:pharmacology; D014741:Video Recording
D015221:Potassium Channels; D015222:Sodium Channels; D013779:Tetrodotoxin; C022838:nickel chloride; D009532:Nickel