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Interactions of light and of tetraethylammonium-chloride (TEA) on action potentials in identified neurons of Helix Pomatia
Neuroscience Letters, 32 0982) 143-148 Elsevier ,%-ientific Publishers IreLand Ltd o
~e.j
L~C£ERACTIONS OF LIGHT AND OF T E T P ~ E T H Y L . ~ f ~ O ~ q ~ M C ~ O R I D E (TEA)ON ACTION POTENTIALS IN IDENTIFIED NE"~5~ONS OF HELIX POMATIA . . . . . . .
H. SCHULZE and E.-J, SPECKMANN
Physiologisches Instimt I tier Universitiit~ Domagkstr. 6, D-4400 Miinste~r (F.R.G.) (Received March !8th, 1982; Revised version received July 6th, 1982; Accepted July 14th, ~982)
Key words: Helix pomatia - identified neurons tetraethylammonium
-
light response
-
actior,
potent.,-'.ab: -
In neurons BI, B2 and B3 of Helixpomatia an illumination elicited: (1) a reduction of the width of ac,:ion poteatials ~ ",P) in control bath quid; (2) an acceleration of the deve!opment of tetraeth/lamm~mium (TEA) action on AP; and (3) a diminution of the full established effe;:t of "IEA. The short~ ning of the AP I~y light was augmented with ~ncreasing prolongation of the AP, regardless o:" whether it was evoked by externaJ or internal TEA or by depolarization of the cells. The effect.~; may b : interpreted on the basis of ~ single mechanism.
Illumination has been found to change bioe;ectric activity of neur)us i~~ Hefix ¢.~mati~. In identified cells of the buccal gangli~ exposure to light elic ted a hypc~rpolarizat:ion with the input resistaltce beiltg simultaneously re:lucec~. '~'~ equilibrium potential of this light response was ca. -- 50 m (ref. 12, cf. refs. 3 a rvl 4). Furthermore, the shape of action potentials was ii,,fluenced by Ii~ght {11]. In connectior with the analysis of the latter effect, the interactions of light and of tetraethylammonium ¢hlaride (TEA) were examine(!. The investigations were carried out on neurons B!, B2 and B3 of the buccal ganglion of H e l i x p o m a t i a [12]. Tb.: experiments were perforraed o~ 120 neurons° As bath fluid, snail saline solution was used (Meng's solution ;! [8]: N~.CI 130, KCi 4.5, CaCI2 9 retool/l). The saline was buffered with 5 mmol/l Tris-C~ to adju.~t the pH to values between 7.35 and 7.45. The chamber containing the p~'el~aratio~ had a capacilty of 0.2 rrd and was continuously perfused with a flow of 6 ml/min. The. tempera,Lure of the fluid was kept constant by t~: servo-syste~ v.t 20~: ~ C . Fo ~ intraceilular potential recording and current injection two s e p ~ . t e g~t~:~; r~F.:~°o~;ec-. trodes were inserted into the neurons. The micrc~eiectrodes were fil!e~ with 3 ~o!/! KCI, I moI/l potassium acetate or 3 rnot/l Tris-propionate. TEA was aO.ded tc~ th~ bath fluid to give concentrations of 5, 10, 20, 30, 50 and !0~9_rr~r~o1/~o T o ~eei3 ~:hG solutiot~ isotonic, the sodium was reduced by an appropriate amount. Suc~ re&~c0 3 0 4 . ' - ~ 9 ~ / 8 2 / ( J ( K ~ - ~ / $ 02.75 © 1982 Elsevier Scientific Publishe;'~ Irelar..;:I Ltd.
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Fig. I. Actions of light and of tetra:'thylarnw.onium chloride (TEA) on action potentials (APs) of identiffed ne~;,-ons of Helix ~omatia. A: AP and their slope of rise and decay (dU/dt) in neurons BI, B2 and B3 during dark (D) and ~,ight (L) in control conditions. Resting membrane potential was adjusted by currein inject,,'on to a constant value of - g 5 inV. APs were lriggered by a short depolarizing current pul~;e. "l'l~,eAPs labeled L were elicited 1 rain after light was switchea on, B and C: development of the effect of extracelIularly applied TEA on AP with continuous dark (a) and with interposed illumination (b) in nearon B2. B: original recordings of AP, The recordings of the derivatives (dU/dt) oi AP were shifted to fl:e right, CTRL, control solution. Time after TEA app.lication is indicated. C: plot of the AP-width (AP-W) of the experiment in B. AP-W was determined from the distance between maximal slope cf rise avd decay of the AP. D: development of the effect of imr.aeelIularly applied TEA (1 mol/l TEA; 50 hA; ! rain} on AP-W Mth continuous dark in neuron B2.
~45
tions in sodium concentration were frequently found to ha~,e no effect on action poter~ials of snail neurons 3~]. In some experiments TEA was injected iontophoretical|y into the cells th:ough a third intracetlular microelectrode filled with I tool/I TEA. The neurons wer.~ illuminated by a tungsten tamp having a broad spectral emission and a peak intenslty at a wavelength of 550 nm. Infrared radiation was removed by filters. From light to dark the illumination of the preparation was changed from about IlXJ0 to 0.1 !ux. In neurons BI, B2 and B3, light enhanced the slope of rise and decay on action pol:entials (AP), decreased their duration and frequently increased the hyperpo[arizing afterpotentials (Fig. IA). This effect was more pronounced in neurons B t and B3 than in neuron B2. Addition of T E A to the bath fluid (50 retool/l) exerted the commonl7 known effects [5, 7, 10]. As shown in Fig. IB, the duration of the AP was increased and the slope of decay reduced. The slope of rise was transier.,tly increased by a small amount. In all experimems it was found that depolarizations a~d hyperpolar:izations even of only a few mV increased and decreased, respectively, ~:he TEA-elicited prolongation of the AP to a great exzent (Fig. 2C). To obtain a comparable measure of the TEA effects the res~:ing membrane potential (MP) was therefore adjusted precisely to a constant value by current injection. The maximal TEA effect was reached after ca. 15 rain when the preparation was kept in dark (Fig. I Ba and C). The development of the TEA action was markedly changed when, after systemic application of the drug, dark was interrupted by a sh~r~ illu~ination. As v~hown ir~ Fig. IBb m~d C, TEA was applied in dark. After a shc~rt period of TEA appticatio~:~ dark was replaced by transient illumination (horizontal bars). Dt~ring this period ~:h(: duration of AP was reduced, with the slope of rise and decas, bd~.~_g~,i~u!~anco~t~+ly increased. When dark was re-established the development of the TEA effect was accelerated compared with experiments in continuous dark. A similar abrupt appearance of the maximal TEA effect was observed after intracellu[a~ injection:~ of TEA (Fig. 1D i~. Washing the preparation in normal bath fluid after a systemic application of TEA , o time course, whether or not the neurons had abolished the drug effect in the ...am,. been transiently illuminated (Fig. IC). After intracellular injection of TEA, however, a decline of the TEA action could not be observed within ca. I h. The maximal, steady-state effect of TEA on AP was also influenced by illumination of the neurons. As shown in Fig. 2A, TEA caused a do~-dep,.~,.d~nt I.~rolor~galion of the AP in dark. When the maximal effe<~ of the actu~! TEA conce~tra'(io~ was reached light was switched on for I rnin. Tt~e A P triggered at ~ c end of ti~i~ period of illumination demonstrated that Iigh.; changed :I~e AP proiongatF)~ 57 TEA application in the same way as i~ untreated ~e~_~ro~s. "~'hi:~ ~ffcct wa:; ai~o observed with intraceitular "~'EA. Furthermore, with increasing proioaga~ior~ o~~i ae AP, the shortening of ~he AP by ~ight ,,,as augmer~,~:ed .(~; ~'~" ~ .....' ~ .... ~""....... of illumination was touna when, at a constant TEA concentration. ~a~ ~.,-,,~,,~,~.i~-~,
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Fig. 2. Steady,-~tate effect of tetraethdammonium chloride (TEA) on action potentials (APs) in dark (D) and light (L). A: original recordings of APs and their slope of rise and decay (dU/dt) in ne~ron B2 in ~:ontrol so|ution d,-'T~,, ~ . . ~ . ~ and afte~ e=~tracellular applic:~{ion of TEA in different concentrations. Retting ~nembrane potential (MP) was adjus-:ed by currea: inj~tion to a constant value of -,~,5 inV. APs were triggered by a short depolarizing current pulse. The APs labeled L were elicited I minafter light was .~witched on. B: plot of the relative A?-wi,~th against the concentration of extracellular TEAusing the dam in A. AP-width was determined f:ol~ the distance between maximal slope of rise and decay of the: AP. The numbers correspond to the one; i~ A. C: plot of A P - ~ d t h against the ac~uai r~tin$ MP in CTRL and in a so|ution with constant con:entration of extracellular TEA (5 mn,ol/l), Neuron BI.
14'7
of the AP was further increased by a depoIarlzaticn of the neurons (Fig. 2C). These findings demonstrate that the absolute value of tke light effect corresponds with the absolute width of the AP. T'._ae ef~c~: of illumination on the shape of the AP has as yet on~y been stud~ed in neurons B1,B3 of Hetixpomatia [i ;'.]. The present in;'estigation showed that ta~ shortening of the A P was the more pronounce, d, ti~e greater the initial width of th.. AP was. This effect proved to be independent of ~he actual origin of the prolongation (Fig. 2). Theref~re~ it may be suggested ~i.hat illumination elicits an unspecific acceleration of channel activation [4, 611.On tt~e basis of such an activating light effe~, the hastening of the development of TE,\ action on AP by illumination may be interpreted by assuming the following mo l..q: the TEA receptor is located at the inner end of the ionic channel [I, 2]. In consequence, the drug can easily approac!~ the blocking site from within the cell [1]. Therefore, a full TEA effect can be expected to occur immediately after intracellular application (Fig. I D). According to the model a 'passage' is necessary for TEA. after extracetiular app!ic:':tion [! ]. Thi:-; should lead to a delayed onset of the drug action in this case (Fig..~C). As pointed out, light elicits a channel activation. This permits externa'~ TEA to reach the blocking site faste~ and thereby accelerates the development of the TEA action. The effect of intracellularly applied TEA was irreversible. Ar~ explanation of this finding may be that the efflux of the drug is blocked by a complex of the receptor and the interna! TEA [5, 101. From the phenomenological point of view, light exerts a synergistic acfio~, o~. the development of the TEA effect and an antagonistic one on the fuHy-estabH~imd ei'o feet of the drug, with the suggested mechanis~qas being ident;cal. •
a,
1 Armstrong, C.M., Potassium pr, r, s of nerve and rm, sde membranes. Irl G. Eismnmn (Ed). Mer.'~branes, Vol. 3, Lipid Bilayers ant Biological Membranes Marcd Dekker, ~ c New Yo~k, ~')v5 2 Armstrong, C.M. and Hille, B., The inner cuarternary ammonium ion receptor in p~tassium channel,; of the node of Ranvier. J. gen. P;~ysiol., 59 (I972) 388-4(]0. 3 Arvanitaki, A. and Chalazonitis, N., Excitv.tory and inhibitory processes initiated by light and infrared radiatiops in single identifi ~ble nerve cells (giant ganglion cells of Aplysia). In E.F. Florey (Ed.), Nervous Inhibition, Pergamon Press, Oxford, 1961. 4 Brown, A.M, and Brown, H.M., Light response of a giant Aplysia neuron, J. gen. Physiol., 62 (~973) 239-254. 5 Hermann, A, and German, A . L F . , Effects of tetraethy~ammonium on potassium currents in a molluscan r~euron, J, ~gen. Physio:., 78 ([981) 87-!10. 6 Lux, H.D. and Heinemann, U., Co.~lsequznces of calcium-e!ectrogenesis for t~e generation of paro×ysmal depolarization shift. In E.-2. Speckm~nn and C.E. E!ger (Eds.), Epilepsy and Motor Sy,~tem, Urban and ~chwarzenberg, Mfinc:aen, 1982. 7 Meech, R.W., intracel!ular calcivm injection causes u'~crea~ed pota:,sim~ cond~cta~c.~: i~ Aoedy'4a' nerve cells, Comp. Biochem. Phy;v~l., 42A (~J~) ~ "
14.~;
i0 Neh¢~,, E. and Lux, H.D., Differerai~ a¢fic~n of TEA +. Two K*-cu~em corrv~ments of a molluscan neurcne, Pfl~g~s Arc[~., 336 (1972) 87-100. I I Schulze, I-~. and Specknmnn, E.-J.. ~..~tagorisfic effects of light and of tctx~_-ethylamn~oniumchlorkle on the action potential:~ of identif:~l neurc,~s in the buccal gangli.~n of Helix pomatia, Proc. Int. Cong~'. Physiol. Sci., ~voL XIII, 1977 p. 20~1. |2 Schulze, H., Spcckmana, E.-J., Kuhlmann, D. and Caspers, H., Topography and biodectrical pro= perties of identifiable r~eurons in the l~u¢~al ganglion of Hetixpomatia, N e u r o n . L ~ . , 1 (1975) 277-281.
~e.j
L~C£ERACTIONS OF LIGHT AND OF T E T P ~ E T H Y L . ~ f ~ O ~ q ~ M C ~ O R I D E (TEA)ON ACTION POTENTIALS IN IDENTIFIED NE"~5~ONS OF HELIX POMATIA . . . . . . .
H. SCHULZE and E.-J, SPECKMANN
Physiologisches Instimt I tier Universitiit~ Domagkstr. 6, D-4400 Miinste~r (F.R.G.) (Received March !8th, 1982; Revised version received July 6th, 1982; Accepted July 14th, ~982)
Key words: Helix pomatia - identified neurons tetraethylammonium
-
light response
-
actior,
potent.,-'.ab: -
In neurons BI, B2 and B3 of Helixpomatia an illumination elicited: (1) a reduction of the width of ac,:ion poteatials ~ ",P) in control bath quid; (2) an acceleration of the deve!opment of tetraeth/lamm~mium (TEA) action on AP; and (3) a diminution of the full established effe;:t of "IEA. The short~ ning of the AP I~y light was augmented with ~ncreasing prolongation of the AP, regardless o:" whether it was evoked by externaJ or internal TEA or by depolarization of the cells. The effect.~; may b : interpreted on the basis of ~ single mechanism.
Illumination has been found to change bioe;ectric activity of neur)us i~~ Hefix ¢.~mati~. In identified cells of the buccal gangli~ exposure to light elic ted a hypc~rpolarizat:ion with the input resistaltce beiltg simultaneously re:lucec~. '~'~ equilibrium potential of this light response was ca. -- 50 m (ref. 12, cf. refs. 3 a rvl 4). Furthermore, the shape of action potentials was ii,,fluenced by Ii~ght {11]. In connectior with the analysis of the latter effect, the interactions of light and of tetraethylammonium ¢hlaride (TEA) were examine(!. The investigations were carried out on neurons B!, B2 and B3 of the buccal ganglion of H e l i x p o m a t i a [12]. Tb.: experiments were perforraed o~ 120 neurons° As bath fluid, snail saline solution was used (Meng's solution ;! [8]: N~.CI 130, KCi 4.5, CaCI2 9 retool/l). The saline was buffered with 5 mmol/l Tris-C~ to adju.~t the pH to values between 7.35 and 7.45. The chamber containing the p~'el~aratio~ had a capacilty of 0.2 rrd and was continuously perfused with a flow of 6 ml/min. The. tempera,Lure of the fluid was kept constant by t~: servo-syste~ v.t 20~: ~ C . Fo ~ intraceilular potential recording and current injection two s e p ~ . t e g~t~:~; r~F.:~°o~;ec-. trodes were inserted into the neurons. The micrc~eiectrodes were fil!e~ with 3 ~o!/! KCI, I moI/l potassium acetate or 3 rnot/l Tris-propionate. TEA was aO.ded tc~ th~ bath fluid to give concentrations of 5, 10, 20, 30, 50 and !0~9_rr~r~o1/~o T o ~eei3 ~:hG solutiot~ isotonic, the sodium was reduced by an appropriate amount. Suc~ re&~c0 3 0 4 . ' - ~ 9 ~ / 8 2 / ( J ( K ~ - ~ / $ 02.75 © 1982 Elsevier Scientific Publishe;'~ Irelar..;:I Ltd.
144
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TEA - IN T,RACEL L
Fig. I. Actions of light and of tetra:'thylarnw.onium chloride (TEA) on action potentials (APs) of identiffed ne~;,-ons of Helix ~omatia. A: AP and their slope of rise and decay (dU/dt) in neurons BI, B2 and B3 during dark (D) and ~,ight (L) in control conditions. Resting membrane potential was adjusted by currein inject,,'on to a constant value of - g 5 inV. APs were lriggered by a short depolarizing current pul~;e. "l'l~,eAPs labeled L were elicited 1 rain after light was switchea on, B and C: development of the effect of extracelIularly applied TEA on AP with continuous dark (a) and with interposed illumination (b) in nearon B2. B: original recordings of AP, The recordings of the derivatives (dU/dt) oi AP were shifted to fl:e right, CTRL, control solution. Time after TEA app.lication is indicated. C: plot of the AP-width (AP-W) of the experiment in B. AP-W was determined from the distance between maximal slope cf rise avd decay of the AP. D: development of the effect of imr.aeelIularly applied TEA (1 mol/l TEA; 50 hA; ! rain} on AP-W Mth continuous dark in neuron B2.
~45
tions in sodium concentration were frequently found to ha~,e no effect on action poter~ials of snail neurons 3~]. In some experiments TEA was injected iontophoretical|y into the cells th:ough a third intracetlular microelectrode filled with I tool/I TEA. The neurons wer.~ illuminated by a tungsten tamp having a broad spectral emission and a peak intenslty at a wavelength of 550 nm. Infrared radiation was removed by filters. From light to dark the illumination of the preparation was changed from about IlXJ0 to 0.1 !ux. In neurons BI, B2 and B3, light enhanced the slope of rise and decay on action pol:entials (AP), decreased their duration and frequently increased the hyperpo[arizing afterpotentials (Fig. IA). This effect was more pronounced in neurons B t and B3 than in neuron B2. Addition of T E A to the bath fluid (50 retool/l) exerted the commonl7 known effects [5, 7, 10]. As shown in Fig. IB, the duration of the AP was increased and the slope of decay reduced. The slope of rise was transier.,tly increased by a small amount. In all experimems it was found that depolarizations a~d hyperpolar:izations even of only a few mV increased and decreased, respectively, ~:he TEA-elicited prolongation of the AP to a great exzent (Fig. 2C). To obtain a comparable measure of the TEA effects the res~:ing membrane potential (MP) was therefore adjusted precisely to a constant value by current injection. The maximal TEA effect was reached after ca. 15 rain when the preparation was kept in dark (Fig. I Ba and C). The development of the TEA action was markedly changed when, after systemic application of the drug, dark was interrupted by a sh~r~ illu~ination. As v~hown ir~ Fig. IBb m~d C, TEA was applied in dark. After a shc~rt period of TEA appticatio~:~ dark was replaced by transient illumination (horizontal bars). Dt~ring this period ~:h(: duration of AP was reduced, with the slope of rise and decas, bd~.~_g~,i~u!~anco~t~+ly increased. When dark was re-established the development of the TEA effect was accelerated compared with experiments in continuous dark. A similar abrupt appearance of the maximal TEA effect was observed after intracellu[a~ injection:~ of TEA (Fig. 1D i~. Washing the preparation in normal bath fluid after a systemic application of TEA , o time course, whether or not the neurons had abolished the drug effect in the ...am,. been transiently illuminated (Fig. IC). After intracellular injection of TEA, however, a decline of the TEA action could not be observed within ca. I h. The maximal, steady-state effect of TEA on AP was also influenced by illumination of the neurons. As shown in Fig. 2A, TEA caused a do~-dep,.~,.d~nt I.~rolor~galion of the AP in dark. When the maximal effe<~ of the actu~! TEA conce~tra'(io~ was reached light was switched on for I rnin. Tt~e A P triggered at ~ c end of ti~i~ period of illumination demonstrated that Iigh.; changed :I~e AP proiongatF)~ 57 TEA application in the same way as i~ untreated ~e~_~ro~s. "~'hi:~ ~ffcct wa:; ai~o observed with intraceitular "~'EA. Furthermore, with increasing proioaga~ior~ o~~i ae AP, the shortening of ~he AP by ~ight ,,,as augmer~,~:ed .(~; ~'~" ~ .....' ~ .... ~""....... of illumination was touna when, at a constant TEA concentration. ~a~ ~.,-,,~,,~,~.i~-~,
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60
Fig. 2. Steady,-~tate effect of tetraethdammonium chloride (TEA) on action potentials (APs) in dark (D) and light (L). A: original recordings of APs and their slope of rise and decay (dU/dt) in ne~ron B2 in ~:ontrol so|ution d,-'T~,, ~ . . ~ . ~ and afte~ e=~tracellular applic:~{ion of TEA in different concentrations. Retting ~nembrane potential (MP) was adjus-:ed by currea: inj~tion to a constant value of -,~,5 inV. APs were triggered by a short depolarizing current pulse. The APs labeled L were elicited I minafter light was .~witched on. B: plot of the relative A?-wi,~th against the concentration of extracellular TEAusing the dam in A. AP-width was determined f:ol~ the distance between maximal slope of rise and decay of the: AP. The numbers correspond to the one; i~ A. C: plot of A P - ~ d t h against the ac~uai r~tin$ MP in CTRL and in a so|ution with constant con:entration of extracellular TEA (5 mn,ol/l), Neuron BI.
14'7
of the AP was further increased by a depoIarlzaticn of the neurons (Fig. 2C). These findings demonstrate that the absolute value of tke light effect corresponds with the absolute width of the AP. T'._ae ef~c~: of illumination on the shape of the AP has as yet on~y been stud~ed in neurons B1,B3 of Hetixpomatia [i ;'.]. The present in;'estigation showed that ta~ shortening of the A P was the more pronounce, d, ti~e greater the initial width of th.. AP was. This effect proved to be independent of ~he actual origin of the prolongation (Fig. 2). Theref~re~ it may be suggested ~i.hat illumination elicits an unspecific acceleration of channel activation [4, 611.On tt~e basis of such an activating light effe~, the hastening of the development of TE,\ action on AP by illumination may be interpreted by assuming the following mo l..q: the TEA receptor is located at the inner end of the ionic channel [I, 2]. In consequence, the drug can easily approac!~ the blocking site from within the cell [1]. Therefore, a full TEA effect can be expected to occur immediately after intracellular application (Fig. I D). According to the model a 'passage' is necessary for TEA. after extracetiular app!ic:':tion [! ]. Thi:-; should lead to a delayed onset of the drug action in this case (Fig..~C). As pointed out, light elicits a channel activation. This permits externa'~ TEA to reach the blocking site faste~ and thereby accelerates the development of the TEA action. The effect of intracellularly applied TEA was irreversible. Ar~ explanation of this finding may be that the efflux of the drug is blocked by a complex of the receptor and the interna! TEA [5, 101. From the phenomenological point of view, light exerts a synergistic acfio~, o~. the development of the TEA effect and an antagonistic one on the fuHy-estabH~imd ei'o feet of the drug, with the suggested mechanis~qas being ident;cal. •
a,
1 Armstrong, C.M., Potassium pr, r, s of nerve and rm, sde membranes. Irl G. Eismnmn (Ed). Mer.'~branes, Vol. 3, Lipid Bilayers ant Biological Membranes Marcd Dekker, ~ c New Yo~k, ~')v5 2 Armstrong, C.M. and Hille, B., The inner cuarternary ammonium ion receptor in p~tassium channel,; of the node of Ranvier. J. gen. P;~ysiol., 59 (I972) 388-4(]0. 3 Arvanitaki, A. and Chalazonitis, N., Excitv.tory and inhibitory processes initiated by light and infrared radiatiops in single identifi ~ble nerve cells (giant ganglion cells of Aplysia). In E.F. Florey (Ed.), Nervous Inhibition, Pergamon Press, Oxford, 1961. 4 Brown, A.M, and Brown, H.M., Light response of a giant Aplysia neuron, J. gen. Physiol., 62 (~973) 239-254. 5 Hermann, A, and German, A . L F . , Effects of tetraethy~ammonium on potassium currents in a molluscan r~euron, J, ~gen. Physio:., 78 ([981) 87-!10. 6 Lux, H.D. and Heinemann, U., Co.~lsequznces of calcium-e!ectrogenesis for t~e generation of paro×ysmal depolarization shift. In E.-2. Speckm~nn and C.E. E!ger (Eds.), Epilepsy and Motor Sy,~tem, Urban and ~chwarzenberg, Mfinc:aen, 1982. 7 Meech, R.W., intracel!ular calcivm injection causes u'~crea~ed pota:,sim~ cond~cta~c.~: i~ Aoedy'4a' nerve cells, Comp. Biochem. Phy;v~l., 42A (~J~) ~ "
14.~;
i0 Neh¢~,, E. and Lux, H.D., Differerai~ a¢fic~n of TEA +. Two K*-cu~em corrv~ments of a molluscan neurcne, Pfl~g~s Arc[~., 336 (1972) 87-100. I I Schulze, I-~. and Specknmnn, E.-J.. ~..~tagorisfic effects of light and of tctx~_-ethylamn~oniumchlorkle on the action potential:~ of identif:~l neurc,~s in the buccal gangli.~n of Helix pomatia, Proc. Int. Cong~'. Physiol. Sci., ~voL XIII, 1977 p. 20~1. |2 Schulze, H., Spcckmana, E.-J., Kuhlmann, D. and Caspers, H., Topography and biodectrical pro= perties of identifiable r~eurons in the l~u¢~al ganglion of Hetixpomatia, N e u r o n . L ~ . , 1 (1975) 277-281.