Evidence for an intracellular calcium store releasable by surface stimuli ifibroblasts (L cells)

نویسندگان

  • M P Henkart
  • P G Nelson
چکیده

A spontaneously occurring or electrically elicited hyperpolarizing activation (HA) in L cells was previously shown to be due to a specific increase in the membrane K+ permeability (Nelson et at. 1972. J. Gen. Physiol. 60:58--71). Intracellular injection of Ca++ elicits an identical hyperpolarizing response which suggests that the increased K+ permeability associated with the HA is mediated by an increase in cytoplasmic Ca++. In zero-Ca, EGTA-containing saline the proportion of cells in which HA's can be evoked decreases, but the amplitude of those HA's that are produced is comparable to that of HA's in normal Ca saline. Co++ does block the HA but only after a period of 2 h or longer; D-600 does not affect the HA. The observations, with others, suggest that the primary source of the Ca mediating the HA response is intracellular. In L cells the endoplasmic reticulum forms morphologically specialized appositions with the surface membrane which resemble structures at the triads of muscle that are thought to mediate coupling between surface membrane electrical activity and contraction via Ca release from the sarcoplasmic reticulum. The similar structures in L cells may mediate coupling between surface membrane electrical, mechanical, or chemical stimuli and the HA response via release of Ca from the endoplasmic reticulum. Surface-coupled release of Ca from intracellular stores might also regulate a number of other intracellular functions in nonmuscle cells.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Discrimination of intracellular calcium store subcompartments using TRPV1 (transient receptor potential channel, vanilloid subfamily member 1) release channel activity.

The store-operated calcium-release-activated calcium current, I (CRAC), is a major mechanism for calcium entry into non-excitable cells. I (CRAC) refills calcium stores and permits sustained calcium signalling. The relationship between inositol 1,4,5-trisphosphate receptor (InsP(3)R)-containing stores and I (CRAC) is not understood. A model of global InsP(3)R store depletion coupling with I (CR...

متن کامل

Current by Muscarinic Receptors in Neuroblastoma Cells

A B S TRACT The relationship between the deplet ion of IP3-releasable intracellular Ca z+ stores and the activation of Ca2+-selective membrane current was determined dur ing the st imulation of M1 muscarinic receptors in N1E-115 neuroblastoma cells. External Ca 2+ is required for refilling Ca 2+ stores and the voltage-independent , receptor-regulated Ca 2+ current represents a significant Ca 2+...

متن کامل

Heat shock protein 70 protects motor neuronal cells expressing mutant Cu/Zn superoxide dismutase (SOD1) against altered calcium homeostasis

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder characterized by the progressive loss of motor neurons leading to paralysis and death. Mutations of the human Cu/Zn superoxide dismutase (SOD1) are found in some cases of familial ALS (fALS). Recent evidences suggest the accumulation of intracellular calcium is one of the primary mechanisms of motor neuronal degeneration. In th...

متن کامل

The relationship between depletion of intracellular Ca2+ stores and activation of Ca2+ current by muscarinic receptors in neuroblastoma cells

The relationship between the depletion of IP3-releasable intracellular Ca2+ stores and the activation of Ca(2+)-selective membrane current was determined during the stimulation of M1 muscarinic receptors in N1E-115 neuroblastoma cells. External Ca2+ is required for refilling Ca2+ stores and the voltage-independent, receptor-regulated Ca2+ current represents a significant Ca2+ source for refilli...

متن کامل

Heat shock protein 70 protects motor neuronal cells expressing mutant Cu/Zn superoxide dismutase (SOD1) against altered calcium homeostasis

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder characterized by the progressive loss of motor neurons leading to paralysis and death. Mutations of the human Cu/Zn superoxide dismutase (SOD1) are found in some cases of familial ALS (fALS). Recent evidences suggest the accumulation of intracellular calcium is one of the primary mechanisms of motor neuronal degeneration. In th...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:
  • The Journal of General Physiology

دوره 73  شماره 

صفحات  -

تاریخ انتشار 1979