Richard Norman <rsnorman at mediaone.net> wrote:
> On Wed, 05 Dec 2001 17:56:36 +1030, et_al at my-deja.com wrote:
>>On 2 Dec 2001 20:23:06 GMT, dag.stenberg at nospam.helsinki.fi wrote:
>>>2) increasing the permeability for Cl- will always cause inhibition, but
>>>this can occur without any change in membrane potential (because of
>>>"short-circuiting")
>>>>Um..no, not always. It depends on the concentration of Cl- in and
>>outside the cell. ...
Well, so much for "always".
See also:
Voipio J, Kaila K.
GABAergic excitation and K(+)-mediated volume
transmission in the hippocampus.
Prog Brain Res. 2000;125:329-38. Review.
Rivera C, Voipio J, Payne JA, Ruusuvuori E,
Lahtinen H, Lamsa K, Pirvola U, Saarma M, Kaila K.
The K+/Cl- co-transporter KCC2 renders GABA
hyperpolarizing during neuronal maturation.
Nature. 1999 Jan 21;397(6716):251-5.
Lamsa K, Palva JM, Ruusuvuori E, Kaila K, Taira T.
Synaptic GABA(A) activation inhibits AMPA-kainate
receptor-mediated bursting in the newborn
(P0-P2) rat hippocampus.
J Neurophysiol. 2000 Jan;83(1):359-66.
Kaila K, Lamsa K, Smirnov S, Taira T, Voipio J.
Long-lasting GABA-mediated depolarization evoked
by high-frequency stimulation in pyramidal
neurons of rat hippocampal slice is attributable
to a network-driven, bicarbonate-dependent K+ transient.
J Neurosci. 1997 Oct 15;17(20):7662-72.
Taira T, Lamsa K, Kaila K.
Posttetanic excitation mediated by GABA(A)
receptors in rat CA1 pyramidal neurons.
J Neurophysiol. 1997 Apr;77(4):2213-8.
--Dag Stenberg
