Glial cells respond to various electrical, mechanical, and chemical stimuli, including neurotransmitters, neuromodulators, and hormones, with an increase in intracellular Ca2+ concentration ([Ca2+]i). The increases exhibit a variety of temporal and spatial patterns. These [Ca2+]i responses result from the coordinated activity of a number of molecular cascades responsible for Ca2+ movement into or out of the cytoplasm either by way of the extracellular space or intracellular stores. Transplasmalemmal Ca2+ movements may be controlled by several types of voltage- and ligand-gated Ca(2+)-permeable channels as well as Ca2+ pumps and a Na+/Ca2+ exchanger. In addition, glial cells express various metabotropic receptors coupled to intracellular Ca2+ stores through the intracellular messenger inositol 1,4,5-triphosphate. The interplay of different molecular cascades enables the development of agonist-specific patterns of Ca2+ responses. Such agonist specificity may provide a means for intracellular and intercellular information coding. Calcium signals can traverse gap junctions between glial cells without decrement. These waves can serve as a substrate for integration of glial activity. By controlling gap junction conductance, Ca2+ waves may define the limits of functional glial networks. Neuronal activity can trigger [Ca2+]i signals in apposed glial cells, and moreover, there is some evidence that glial [Ca2+]i waves can affect neurons. Glial Ca2+ signaling can be regarded as a form of glial excitability.

SUMMARY1. Membrane potential, tension and membrane current were simultaneously recorded from frog ventricular strips in a modified sucrose-gap which enabled control of membrane potential by voltage clamp.2. Shortening the frog ventricular action potential by repolarizing the membrane to the resting potential terminates contraction. 3. Depolarization to the level of the normal action potential plateau for longer than about 80-100 msec (up to 30 sec) produces and maintains tension for the duration of the depolarization.4. Depolarizations less than about 80 msec in duration generate no tension but can facilitate the tension response to subsequent depolarizations. The facilitating effect of a short depolarizing pulse persists for no longer than 0 5 sec.5. The mechanical threshold is about -50 mV; the relation between membrane potential and tension is fairly linear from about + 5 to + 80 mV.6. Variation of holding potential, below the mechanical threshold, has no effect on the tension-voltage relation. The absolute membrane potential rather than pulse amplitude determines the developed tension.7. Increasing external calcium increases the slope of the voltage-tension relation.8. Contraction of the frog ventricle is directly controlled by the electrical activity of the surface membrane.

SUMMARY1. Using ventricle strips of the frog's heart stimulated at the low rate of about 1 shock/min intracellular action potentials were recorded under conditions of varying calcium concentrations.2. Overshoots of action potentials were increased by about 18*3 mV as a result of a 10-fold increase, within the range of 0-1-5 mm, of the calcium concentration.3. A similar effect was obtained by strontium, but magnesium was ineffective.4. The increase of the overshoot by high calcium was associated with an increased rate of rise of the potential during the later part of its ascending phase. The initial fast upstroke remained unaltered.5. Another effect, a depression of the overshoot, developed during periods of repetitive stimulation, at the rate of 20/min, and this was followed by a gradual recovery during subsequent periods of rest.6. The depression of the overshoot increased with increasing calcium concentrations reaching values of over 40 mV.7. High concentrations of strontium and low concentrations of sodium also induced depression of the overshoot, but high magnesium was ineffective.8. A tentative hypothesis has been proposed attributing these two effects: (a) to an entry of calcium through the excitable membrane thus contributing to the ionic inward current, and (b) to a resulting accumulation of calcium in some cellular store.

Membrane currents induced by noxious heat (Iheat) were studied in cultured dorsal root ganglion (DRG) neurones from newborn rats using ramps of increasing temperature of superfusing solutions. I heat was observed in about 70 % of small (< 25 μm) DRG neurones. At ‐60 mV, Iheat exhibited a threshold at about 43 °C and reached its maximum, sometimes exceeding 1 nA, at 52 °C (716 ± 121 pA; n= 39). I heat exhibited a strong temperature sensitivity (temperature coefficient over a 10 °C temperature range (Q10) = 17·8 ± 2·1, mean ± s.d., in the range 47‐51 °C; n= 41), distinguishing it from the currents induced by capsaicin (1 μM), bradykinin (5 μM) and weak acid (pH 6·1 or 6·3), which exhibited Q10 values of 1·6‐2·8 over the whole temperature range (23‐52 °C). Repeated heat ramps resulted in a decrease of the maximum Iheat and the current was evoked at lower temperatures. A single ramp exceeding 57 °C resulted in an irreversible change in Iheat. In a subsequent trial, maximum Iheat was decreased to less than 50 %, its threshold was lowered to a temperature just above that in the bath and its maximum Q10 was markedly lower (5·6 ± 0·8; n= 8). DRG neurones that exhibited Iheat were sensitive to capsaicin. However, four capsaicin‐sensitive neurones out of 41 were insensitive to noxious heat. There was no correlation between the amplitude of capsaicin‐induced responses and Iheat. In the absence of extracellular Ca2+, Q10 for Iheat was lowered from 25·3 ± 7·5 to 4·2 ± 0·4 (n= 7) in the range 41‐50 °C. The tachyphylaxis, however, was still observed. A high Q10 of Iheat suggests a profound, rapid and reversible change in a protein structure in the plasma membrane of heat‐sensitive nociceptors. It is hypothesized that this protein complex possesses a high net free energy of stabilization (possibly due to ionic bonds) and undergoes disassembly when exposed to noxious heat. The liberated components activate distinct cationic channels to generate Iheat. Their affinity to form the complex at low temperatures irreversibly decreases after one exposure to excessive heat.