Premium
All thalamocortical neurones possess a T‐type Ca 2+ ‘window’ current that enables the expression of bistability‐mediated activities
Author(s) -
Hughes Stuart W.,
Cope David W.,
Tóth Tibor I.,
Williams Stephen R.,
Crunelli Vincenzo
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.1469-7793.1999.0805s.x
Subject(s) - bistability , conductance , biophysics , endogeny , membrane potential , chemistry , inhibitory postsynaptic potential , neuroscience , physics , biological system , biology , biochemistry , optoelectronics , condensed matter physics
1 The existence of a non‐negligible steady‐state (‘window’) component of the low threshold, T‐type Ca 2+ current ( I T ) and an appropriately large ratio of I T to I Leak conductance (i.e. g T / g Leak ) have been shown to underlie a novel form of intrinsic bistability that is present in about 15 % of thalamocortical (TC) neurones. 2 In the present experiments, the dynamic clamp technique was used to introduce into mammalian TC neurones in vitro either an artificial, i.e. computer‐generated, I T in order to enhance endogenous I T , or an artificial inward I Leak to decrease endogenous I Leak . Using this method, we were able to investigate directly whether the majority of TC neurones appear non‐bistable because their intrinsic ionic membrane properties are essentially different (i.e. presence of a negligible I T ‘window’ component), or simply because they possess a g T or g Leak conductance that is insufficiently large or small, respectively. 3 The validity of the dynamic clamp arrangement and the accuracy of artificial I T were confirmed by (i) recreating the low threshold calcium potential (LTCP) with artificial I T following its block by Ni 2+ (0.5–1 mM), and (ii) blocking endogenous LTCPs with an artificial outward I T . 4 Augmentation of endogenous I T by an artificial analog or introduction of an artificial inward I Leak transformed all non‐bistable TC neurones to bistable cells that expressed the full array of bistability‐mediated behaviours, i.e. input signal amplification, slow oscillatory activity and membrane potential bistability. 5 These results demonstrate the existence of a non‐negligible I T ‘window’ component in all TC neurones and suggest that rather than being a novel group of neurones, bistable cells are merely representative of an interesting region of dynamical modes in the ( g T , g Leak ) parameter space that may be expressed under certain physiological or pathological conditions by all TC neurones and other types of excitable cells that possess an I T ‘window’ component with similar biophysical properties.