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Endocrinology Vol. 138, No. 10 4346-4350
Copyright © 1997 by The Endocrine Society

ARTICLES

Regulation of K+ Channels by Cell Contact in a Cloned Folliculo-Stellate Cell (TtT/GF)

Tomoko Yamasaki, Hiroko Fujita, Kinji Inoue, Toshiro Fujita and Naohide Yamashita

Fourth Department of Internal Medicine (T.Y., H.F., T.F., N.Y.), University of Tokyo School of Medicine, Tokyo 112 Japan; and Department of Regulation Biology (K.I.), Faculty of Science, University of Saitama, Saitama 338 Japan

Address all correspondence and requests for reprints to: Naohide Yamashita, M.D., Ph.D., Fourth Department of Internal Medicine, Tokyo University Branch Hospital, 3–28-6 Medjirodai, Bunkyo-ku, Tokyo 112 Japan.


   Abstract
Top
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Membrane currents in a folliculo-stellate cell line (TtT/GF) were examined using the whole-cell clamp technique. The cultured cells were morphologically categorized as isolated spread cells, isolated round cells, contact spread cells, and contact round cells. A distinct outward current was observed in isolated spread cells, contact round cells, and contact spread cells, whereas the outward current detected in isolated round cells was barely perceivable. The reversal potentials of the outward tail current obeyed the Nernst equation, indicating that the outward current was carried by K+ ions. The activation and deactivation processes of the K+ current could be fitted by single exponential curves. 4-aminopyridine, tetraethylammonium, and Ba2+ inhibited the K+ current. The concentrations for half-maximal inhibition of these agents to block the K+ current were 0.2 mM, 0.8 mM, and 8 mM, respectively. The biophysical and pharmacological characteristics of the K+ current in TtT/GF cells were similar to those of the K+ current in glial and Schwann cells. According to the results of the present study, it was concluded that TtT/GF cells possessed outward K+ channels, characteristics of which were similar to those of the K+ channels in glial and Schwann cells, and that the amplitude of the K+ current in TtT/GF cells seemed to be regulated by the condition of the cell contact.


   Introduction
Top
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
FOLLICULO-STELLATE cells (FS cells) are a specific subtype of cells in the anterior pituitary gland (1). These cells do not contain secretory granules and surround neighboring glandular cells with long-cell processes. Thus, it has been considered that FS cells serve in a supportive role in the anterior pituitaries. However, FS cells maintain trophic and catabolic activities in the anterior pituitary, and they also perform phagocytic activities (2). FS cells regulate hormone secretion from anterior pituitary cells through paracrine interactions (3). Therefore, FS cells are not simply supportive cells, but they also play important roles in the anterior pituitaries. Immunohistochemical studies demonstrated that FS cells are positive to S-100 protein and glial fibrillary acidic protein (4, 5), characteristics resembling those of glial cells in the central nervous system. Glial cells supply nutrition to the nerve cells, in addition to serving a supportive function in central nervous system. It recently has been demonstrated that glial cells possess various ionic channels on the cell membrane (6). These ionic channels have been considered to regulate the excitability of the nerve cells through changing the ionic environment of adjacent neurons. In addition, neurotransmitter receptors have also been noted (7). Therefore, the elucidation of the glial cell ion channels is necessary to understand the neuronal function.

The hormone-secreting cells in the anterior pituitary are known to be excitable in similar ways to neuronal cells, and Ca2+ influx through voltage-gated channels has been implicated for hormone secretion (8). Ca2+ influx through voltage-gated channels is regulated by Ca2+-dependent action potential firings. Therefore, it is necessary to investigate the ionic channels of FS cells in the anterior pituitary because these ionic channels may regulate the excitability of neighboring hormone-secreting cells. However, ionic channels in FS cells have not yet been investigated. Therefore, in the present study, we examined the ionic channels in FS cells using a clonal FS cell line, TtT/GF, which is derived from pituitary FS cells (9).


   Materials and Methods
Top
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Materials
GTP and ATP were purchased from Sigma (St. Louis, MO). HEPES, EGTA, tetramethylammonium (TMA), tetraethylammonium (TEA), and 4-aminopyridine (4AP) were purchased from Wako Junyaku (Tokyo, Japan). Dispase was purchased from Godo Syusei (Tokyo, Japan). Basic fibroblast growth factor was a thankful gift from the Takeda Pharmaceutical Company (Tokyo, Japan).

Cell culture
TtT/GF cells were cultured in DMEM supplemented with 10% FCS and basic fibroblast growth factor. Subculturing was performed twice a week. Experiments were carried out 3–4 days after subculture.

Electrophysiology
A whole-cell variation of the patch clamp technique was used. The standard patch electrode solution contained (in mM); 95 K aspartate, 47.5 KCl, 1 MgCl2, 5 EGTA [TMA salt], and 10 HEPES (TMA salt, pH 7.2). This solution also contained 2 mM ATP (Mg salt) and 100 µM GTP (Na salt). The standard external solution was (in mM); 128 NaCl, 5 KCl, 1 MgCl2, 2.5 CaCl2, and 10 HEPES (Na salt, pH 7.4). In high K+ media, K+ concentration was increased by the isosmotic replacement of Na+ ions. Liquid junction potential between the standard extracellular solution and other solutions used (internal and external) was directly measured using a 3-M KCl electrode as a reference. Liquid junctional potential value (-8 to -5 mV) was corrected in each experiment. A List L/M EPC-7 amplifier (List Electronic, Darmstadt, Germany) was used for recording the membrane currents. Application of voltage or current pulses, data acquisition, and analysis were done with a 486-based Gateway 2000 computer using the pCLAMP software package (Axon Instruments, Foster City, CA). Experiments were performed at room temperature (22–25 C). Glass capillaries of 1.5-mm diameter, with a filament, were used to fabricate electrodes. Patch electrode resistance ranged from 2–5 M{Omega}, and the access resistance under the whole cell clamp condition was 5–10 M{Omega}. Resistance compensation (70~90%) was used to reduce error in the clamped potential at which the cell was clamped. When necessary, membrane potential was corrected by the formula: Vc = V-Rs x I; where Vc is the corrected membrane potential; V, clamped potential; Rs, series resistance; and I, membrane current. Resting potential of TtT/GF cells ranged from -30 to -50 mV. Input resistance of TtT/GF cells, calculated from the membrane current between -78 to -108 mV, was 1–5 G{Omega} in most cells (>90%). Occasionally, we encountered leaky cells with an input resistance of less than 1 G{Omega}. Even though we were not sure whether these leaky cells represented a subclass of TtT/GF cells, we discarded the data for these cells because of their very low input resistance. Linear leakage calculated from the membrane current between -78 and -108 mV was subtracted in each record when necessary. Statistical analysis was determined using ANOVA.


   Results
Top
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
The outward current in FS cells
During the 3- to 4-day period succeeding cell culture, there were four types of cells that could be morphologically distinguished. These four types were: isolated round cells, isolated spread cells, contact (contact to other cells) round cells, and contact spread cells. Figure 1AGo shows the representative membrane current obtained in a round cell showing contact with other cells (contact round cell). When the membrane was depolarized at a step greater than -38 mV from the holding potential of -78 mV, the outward current with an activation process appeared. As the membrane depolarization grew stronger, the amplitude of the outward current increased. The current-voltage (I-V) relationship of the outward current is shown as circles in Fig. 1DGo. The I-V relationship showed an outward-going rectification. A well-developed outward current was observed irrespective of the shape (round or spread) of the contact cells. Figure 1BGo shows the representative membrane current that was obtained from an isolated round cell. In contrast to Fig. 1AGo, the outward current amplitude was much less than that of the contact cells. The I-V relationship of the cell in Fig. 1BGo is shown as triangles in Fig. 1DGo. The isolated spread cells showed an outward current similar to that in the case of the contact cells (Fig. 1CGo and squares in Fig. 1DGo).



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  		Figure 1. The membrane currents in TtT/GF cells. A, The membrane currents in a contact round cell. Current records at the test potentials of -28, -18, -8, and 2 mV are shown. B, The membrane currents in an isolated round cell. Current records at the test potentials of -28, -18, -8, and 2 mV are shown. C, The membrane currents in an isolated spread cell. Current records at the test potentials of -18, -8, and 2 mV are shown. D, I-V relationship of the membrane currents. Circles indicate the records in A; triangles, those in B; and squares, those in C. These data were obtained in the standard extracellular medium. The holding potential was -78 mV. The straight line indicates the zero current level. The patch electrode contained the standard intracellular solution.

 
The outward current amplitude was qualitatively compared among these cell types. The outward current amplitude was considerably large when the membrane was depolarized at greater than +10 mV, which interfered with obtaining the maximum conductance of the outward current. Therefore, a chord conductance between -40 mV and 0 mV was used to compare outward currents. Table 1Go summarizes the chord conductance of the outward current. It is clear that the amplitude of the outward current in isolated round cells was significantly smaller than those of isolated spread cells and contact cells, suggesting that the development of the outward current required contact with other cells or contact with the culture dish in a spread form. There was a possibility that the amplitude of the outward current in contact cells apparently increased because of their electrotonic coupling to other cells. To exclude this possibility, we treated cells with protease (Dispase) for several minutes. This procedure separated contact cells, which could be morphologically recognized. The amplitude of the outward current in acutely isolated cells was 16.5 ± 3.4 nanosiemens (nS) (n = 9). This value was virtually identical to that expressed previous to enzyme treatment. Therefore, it was improbable that the amplitude of the outward current apparently increased in contact cells as a result of electrotonic coupling.


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  		Table 1. Comparison of the conductance

 
Identification of the K+ current
To examine which ions were involved in the outward current, tail current was analyzed. In Fig. 2AGo, the membrane potential was shifted to various levels after it was depolarized to -8 mV, the extracellular K+ concentration being 5 mM. When the membrane was repolarized, a gradually deactivating tail current was observed. The amplitude of the tail current was calculated as an inset in Fig. 2Go, and it is plotted against the repolarized membrane potential (circles in Fig. 2CGo). The amplitude of the tail current showed a linear change against the membrane potential, and it became zero at approximately -84 mV, which was near the equilibrium potential for K+ ions. When the concentration of extracellular K+ ions was increased to 20 mM, the tail current’s reversal potential was approximately -52 mV (Fig. 2BGo and triangles in Fig. 2CGo). The reversal potential of the tail current is plotted against the extracellular K+ ion concentration in Fig. 2DGo, where the data in 40 mM K+ medium have been combined. The straight line was drawn according to the Nernst equation. The reversal potential of the tail current corresponded to the straight line, indicating that the outward current was carried through K+ channels.



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  		Figure 2. Tail currents of the outward current. A, Tail currents recorded in the standard extracellular medium. The holding potential was -78 mV, and the depolarizing potential was -8 mV. After membrane depolarization, the membrane potentials were repolarized at various levels, as depicted by the pulse protocol in the upper panel. Current records at the repolarizing potentials of -108, -88, -68, and -58 mV are shown. B, Tail currents recorded in 20 mM K+ medium. The holding potential was -75 mV, and the depolarizing potential was -5 mV. Current records at the repolarizing potentials of -75, -65, -55, and -45 mV are shown. C, The amplitude of tail currents plotted against the repolarizing potential. The amplitude of the tail current was calculated as an inset in A. Circles indicates the data obtained in the standard extracellular medium; and triangles, those in 20 mM K+ medium. D, Dependence of the reversal potentials on extracellular K+ ion concentrations. The ordinate indicates the reversal potential; and the abscissa, the concentration of extracellular K+ ions. Bar means SE. The numbers of examined cells were six in the standard extracellular medium, three in 20 mM K+ medium, and four in 40 mM K+ medium. Bars in the standard and 40-mM K+ medium were so small that they were hidden by symbols. The straight line was drawn according to the Nernst equation. The patch electrode contained the standard intracellular solution.

 
Activation and deactivation kinetics of the outward K+ current were examined as shown in Fig. 3Go. The time course of the activation was approximately fitted by single exponential (Fig. 3AGo) rather than the fourth power of an exponential described in the giant squid axon (10). The time course of deactivation kinetics also was corresponded to a single exponential (Fig. 3BGo). Time constants of activation and deactivation kinetics are plotted against the membrane potential in Fig. 4Go. The voltage dependency of activation and deactivation time constants of the K+ current in TtT/GF cells resembled that of the type II K+ current in Schwann cell (11).



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  		Figure 3. Activation and deactivation of the K+ current. A, Single exponential fit of the activation process. The holding potential was -78 mV. Current records at the test potentials of -28, -18, and -8 mV are shown. The broken line was drawn according to the formula: I = Imax [1 - exp(-t/{tau})]; where {tau} is the time constant and Imax, the maximum current at a given membrane potential. B, Single exponential fit of deactivation process. The holding potential was -80 mV and the depolarizing potential was 10 mV. Current records at the repolarizing potentials of -100, -90, -80, -70, and -60 mV are shown. The broken line was drawn according to the formula: I = I0 exp(-t/{tau}); where {tau} is the time constant and I0 is the tail current at t = 0. The extracellular and intracellular solutions were the standard.

 


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  		Figure 4. Plot of the activation and deactivation time constant ({tau}) against the membrane potential. The ordinate indicates the time constant; and the abscissa, the membrane potential. Closed symbols denote the deactivation time constants; and open symbols, the activation time constants. Each symbol indicates the data obtained from a separate cell. The broken line was drawn according to the formula: {tau} = 1/[A exp(V/B) + C exp(-V/D)]; where A is 0.188 sec-1; B, 7.4 mV; C, 7.3 x 10-3 sec-1; and D, 31.1 mV. The extracellular and intracellular solutions were the standard. The holding potential was approximately -78 to ~ -80 mV. In the case of obtaining a deactivation time constant, the depolarizing potential was fixed at approximately 8 ~ 10 mV.

 
Effects of 4AP, TEA, and Ba2+ on the K+ current
he application of TEA, 4AP, or Ba2+ inhibited the outward K+ current, as shown in Fig. 5Go. The extent of the K+ channel block was calculated by the changes in the chord conductance between -40 mV and 0 mV, and the dose dependency of these agents is depicted in Fig. 6Go. The concentrations for half-maximal inhibition (EC50s) of 4AP, TEA, and Ba2+ were about 0.2 mM, 0.8 mM, and 8 mM, respectively. Thus, the K+ channel of TtT/GF cells was less sensitive to Ba2+ than to 4AP and TEA. There was no apparent voltage dependency of the K+ current block by these agents (data not shown).



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  		Figure 5. Effects of 4AP, TEA, and Ba2+ on the K+ current. A, The effect of 2 mM 4AP; B, that of 20 mM TEA; and C, that of 20 mM Ba2+. The left panels indicate the control currents. The holding potential was -48 mV. Current records at -28 and -18 mV are shown in A; those at -38, -28, and -18 mV, in B; and those at -38 and -28 mV, in C. The straight line indicates a zero current level. Both extracellular and intracellular solutions were standard.

 


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  		Figure 6. Blocking the K+ current by 4AP, TEA, and Ba2+. The ordinate indicates the block (%) of the control chord conductance calculated from -40 to 0 mV, the control chord conductance being normalized as 100%. The abscissa indicates the concentration of these agents. The data are plotted by mean ± SE (bars). The numbers of examined cells were six in the case of 4AP, four in the case of TEA, and four in the case of Ba2+. The curves were drawn by the formula: A = Amax C/(C + EC50), where A denotes the block; Amax, the maximum attainable block; C, the concentration of the pharmacological agent; and EC50, the concentration of the pharmacological agents which exhibit a 50% block.

 
Other ionic channels
Figure 7AGo depicts the current records when the membrane was hyperpolarized, and their I-V relationship is shown in Fig. 7BGo. The inward rectifying K+ current reported in glial cells (6) was not observed in TtT/GF cells, and the I-V relationship exhibited only linear change along the voltage axis.



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  		Figure 7. Membrane currents at hyperpolarized membrane potentials in TtT/GF cells. A, The holding potential was -48 mV. Current records at -68, -88, -108, and -128 mV are shown. B, I-V relationship of the membrane currents. Both extracellular and intracellular solutions were standard. The straight line in A indicates a zero current level.

 

   Discussion
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
The results of the present study revealed the existence of voltage-gated K+ channels in a clonal FS cell (TtT/GF). A distinct K+ current was observed either when cells contacted each other or when the cell attached to the culture dishes with prominent cell processes. In ovine oligodendrocytes, K+ currents are not observed in the cells without cell processes (12). In TtT/GF cells, round cells without cell contact exhibited a little amount of the K+ current, whereas round cells with cell contact showed a substantial amount of the K+ current. Therefore, K+ channel expression in TtT/GF cells could not be ascribed to the presence of cell processes. It is reasonable to deduce that the expression of the K+ current was dependent on cell contact. Round cells may possess a weak contact, which explains their negligible K+ current. However, the amount of K+ current for contact round cells was virtually identical to that of isolated or contact spread cells. One explanation for the present results may be that the expression of K+ channels was regulated by adhesion molecules, which govern the conditions of cell contact. In neuroblastoma cells, integrin (an adhesion molecule) activates the inward rectifying K+ current, and an integrin-induced neurite outgrowth is inhibited by blocking this K+ conductance (13). In renal epitheloid MDCK cells (14), cell-cell contact regulates the expression of K+ channels. Because the adhesion molecules for cell-cell contact and those for contact to culture dish are different (15), the expression of K+ channels in TtT/GF cells may be attributed to the manifestation of different adhesion molecules occurring in different contact conditions. An influence of soluble factors on the expression of K+ channels also may be possible. In chick parasympathetic neurons (16), A-type K+ current is regulated by cell-cell interaction through some soluble growth factors. Owing to the fact that several cytokines, including IL-6, are secreted from FS cells (17, 18), some soluble factor(s) in combination with the cell contact condition may affect the expression of K+ channels.

K+ channels expressed in TtT/GF cells were sensitive to 4AP, TEA, and Ba2+. EC50s for 4AP, TEA, and Ba2+ were 0.2 mM, 0.8 mM, and 8 mM, respectively. The I-V relationship of the K+ current in TtT/GF cells showed an outward-going rectification, and this K+ current did not show a prominent inactivation process, which was different from the A-type K+ current. Because A-type K+ channels are TEA-insensitive (19), pharmacological characteristics of K+ channels in TtT/GF cells also differ from those of A-type K+ channels. The Ca2+-activated K+ current shows the outward-going rectification, but it is much less sensitive to 4AP, as compared with the K+ current in TtT/GF cells (19). In addition, in the present study, intracellular Ca2+ ions were chelated by internally applied EGTA (5 mM). Therefore, it was improbable that the K+ current in TtT/GF cells was the Ca2+-activated K+ current. From these reasons, it was concluded that the K+ channels in TtT/GF cells belong to the delayed rectifier K+ channels. Voltage dependency and the values of activation and deactivation time constants of K+ channels in TtT/GF cells were different from those of delayed rectifier K+ channels in rat suprachiasmatic nucleus neurons (20), rat hippocampal astrocytes (21), and rabbit Schwann cells (type I K+ channel) (11). Overall characteristics of K+ channels in TtT/GF cells, including the threshold for the channel activation, time constants for activation and deactivation processes, and the pharmacological characteristics, were similar to those of K+ channels in rod bipolar cells (22) and type II K+ channels in rabbit Schwann cells (11). In rod bipolar cells, these K+ channels have been revealed to be Shaker-like channels Kv1.1 by using the RT-PCR method. Hormone-secreting anterior pituitary GH3 cells express three kinds of voltage-gated K+ channels (Kv1.4, Kv1.5, and Kv2.1) and shal gene homologue (23). Although we cannot rule out the possibility that the K+ channels in TtT/GF cells are derived from the assembly of a heteromeric structure involving varied proportions of monomers of different K+ channel subtypes, it seems that K+ channels expressed in TtT/GF cells were different from those in hormone-secreting anterior pituitary cells.

The resting potential of TtT/GF cells was about -30 to -50 mV, which was in close proximity to the threshold for K+ channels. Some change in the resting potential can alter the permeability of K+ channels, and K+ ions that escape through the K+ channel in FS cells accumulate in the extracellular space of adjacent hormone-secreting cells. This mechanism may alter the excitability of these cells. TtT/GF cells possess several characteristics similar to glial cells. The present study revealed that existence of K+ channels also was relevant in this case. In glial cells, the existence of several classes of K+ channels, including delayed K+ channels and A channels, have been reported (6, 7). Delayed K+ channels are implicated in the proliferation and lineage progression of oligodendrocyte (24). It also has been revealed that the density and activity of delayed K+ channels tend to be closely related to the proliferation of Schwann cells (25). Therefore, it is conceivable that delayed K+ channels may play a role in the proliferation of TtT/GF cells.

Received March 27, 1997.


   References
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

  1. Rinehart JF, Farquhar MG 1953 Electron microscopic studies of the anterior pituitary gland. J Histochem Cytochem 1:93–113[Abstract]
  2. Allaerts W, Carmeliet P, Denef C 1990 New perspectives in the function of pituitary folliculo-stellate cells. Mol Cell Endocrinol 71:73–81[CrossRef][Medline]
  3. Jones TH, Brown BL, Dobson PRM 1990 Paracrine control of anterior pituitary hormone secretion. J Endocrinol 127:5–13[Abstract/Free Full Text]
  4. Cocchia D, Miani N 1980 Immunohistocytochemical localization of the brain-specific S-100 protein in the pituitary gland of adult rat. J Neurocytol 9:771–782[CrossRef][Medline]
  5. Velasco ME, Roessmann U, Gambetti P 1982 The presence of glial fibrillary acidic protein in the human pituitary gland. J Neuropathol Exp Neurol 41:150–163[Medline]
  6. Barres BA 1990 Glial ion channels. Curr Opin Neurobiol 1:354–359
  7. Barres BA, Chun LLY, Corey DP 1990 Ion channels in vertebrate glia. Annu Rev Neurosci 13:441–474[CrossRef][Medline]
  8. Ozawa S, Sand O 1986 Electrophysiology of excitable endocrine cells. Physiol Rev 66:887–952[Free Full Text]
  9. Inoue K, Matsumoto H, Koyama C, Shibata K, Nakazato Y, Ito A 1992 Establishment of a folliculo-stellate-loke cell line from a murine thyrotropic pituitary tumor. Endocrinology 131:3110–3116[Abstract]
  10. Hodgkin AL, Huxley AF 1952 A quantitative description of membrane current and its application to conduction and excitation in nerve. J Physiol (London) 117:500–544
  11. Baker M, Howe JR, Ritchie JM 1993 Two types of 4-aminopyridine-sensitive potassium current in rabbit Schwann cells. J Physiol (London) 464:321–342[Abstract/Free Full Text]
  12. Soliven B, Szuchet S, Arnason BGW, Nelson DJ 1988 Voltage-gated potassium currents in cultured ovine oligodendrocytes. J Neurosci 8:2131–2141[Abstract]
  13. Arcangeli A, Becchetti A, Mannini A, Mugnai G, Defilippi P, Tarone G, DelBene MR, Barletta E, Wanke E, Olivotti M 1993 Integrin-mediated neurite outgrowth in neuroblastoma cells depends on the activation of potassium channels. J Cell Biol 122:1131–1143[Abstract/Free Full Text]
  14. Talavera D, Ponce A, Fiorentino R, Gonzalez-Mariscal L, Contreras RG, Sanchez SH, Garcia-Villegas MR, Valdes J, Cereijido M 1995 Expression of potassium channels in epithelial cells depends on calcium-activated cell-cell contacts. J Membr Biol 143:219–226[Medline]
  15. Albelda SM, Buck CA 1990 Integrins and other cell adhesion molecules. FASEB J 4:2868–2880[Abstract]
  16. Dourado M, Dryer SE 1994 Regulation of A-currents by cell-cell interactions and neurotrophic factors in developing chick parasympathetic neurones. J Physiol (London) 474:367–377[Abstract/Free Full Text]
  17. Tatsuno I, Somogyvari-Vigh A, Mizuno K, Gottschalll PE, Hidaka H, Arimura A 1991 Neuropeptide regulation of interleukin-6 production from the pituitary: stimulation by pituitary adenylate cyclase activating polypeptide and calcitonin gene-related peptide. Endocrinology 129:1797–1804[Abstract]
  18. Matsumoto H, Koyama C, Sawada T, Koike K, Hirota K, Miyake A, Arimura A, Inoue K 1993 Pituitary folliculo-stellate like cell line (TtT/GF) responds to novel hypophysiotrophic peptide (pituitary adenylate cyclase-activating peptide), showing increased adenosine 3',5'-monophosphate and interleukin-6 secretion and cell proliferation. Endocrinology 133:2150–2155[Abstract]
  19. Nelson MT, Quayle JM 1995 Physiological properties of potassium channels in arterial smooth muscle. Am J Physiol 268:C799–C822
  20. Bouskila Y, Dudek FE 1995 A rapidly activating type of outward rectifier K+ current and A-current in rat suprachiasmatic nucleus neurones. J Physiol (London) 488:339–350[Medline]
  21. Tse FW, Fraser DD, Duffy S, MacVicar BA 1992 Voltage-activated K+ currents in acutely isolated hippocampal astrocytes. J Neurosci 12:1781–1788[Abstract]
  22. Klumpp DJ, Song EJ, Ito S, Sheng MH, Jan LY, Pinto LH 1995 The Shaker-like potassium channels of the mouse rod bipolar cell and their contributions to the membrane current. J Neurosci 15:5004–5013[Abstract]
  23. Meyehof W, Schwartz JR, Bauer CK, Hubel A, Richer D 1992 A rat pituitary tumor K+ channel expressed in frog oocytes induces a transient K+ current indistinguishable from that recorded in native cells. J Neuroendocrinol 4:245–253
  24. Gallo V, Zhou JM, McBain CJ, Wright P, Knutson PL, Armstrong RC 1996 Oligodendrocyte progenitor cell proliferation and lineage progression are regulated by glutamate receptor-mediated K+ channel block. J Neurosci 16:2659–2670[Abstract/Free Full Text]
  25. Chiu SY, Wilson GF 1989 The role of potassium channels in Schwann cell proliferation in Wallerian degeneration of explant rabbit sciatic nerves. J Physiol (London) 408:199–222[Abstract/Free Full Text]



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Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals