Interaction of anaesthetics with electrical synapses

Abstract

Studies of the interaction of anaesthetics with various preparations, from whole animals to organic solvents, have been continuing since Overton and Meyer found a correlation between anaesthetic potency and solubility in olive oil. Although the physiological basis of anaesthesia is far from clear, one popular hypothesis is that anaesthetics act primarily by interfering with the normal functioning of chemical synapses. This hypothesis is supported by experiments showing that these synapses are more sensitive to both local and general anaesthetics than are axons. The effects of anaesthetics on electrical synapses (gap-junctions or nexus) have not previously been studied. These ubiquitous structures, presumably responsible for cell-to-cell communication, are found in most vertebrate and invertebrate tissues. We report here the effects of several anaesthetics on electronic coupling between nerve cells, and show that electrical synapses are less sensitive to most anaesthetics than are chemical synapses and axonal membranes.

Synchronized Spontaneous Ca2+ Transients in Acute Anterior Pituitary Slices

“…The extent of dye coupling, however, did not usually exceed five to six cells, as seen by three-dimensional reconstruction of optical slices (data not shown). Similar experiments were further conducted in presence of the gap junction blocker halothane (33,34). In pituitary slices bathed for 15-60 min in Ringer's saline saturated with 3 mM halothane, the appearance of dye-coupled cells was reduced to 17.8% (Fig.…”

P2X7Receptors Mediate ATP Release and Amplification of Astrocytic Intercellular Ca2+Signaling

“…CBX is a glycyrrhetinic acid derivate that requires long exposure time and concentrations above 50 M to block gap junctional communication (Davidson et al, 1986;Spray et al, 2002) and also affects other ion channels (Rouach et al, 2003;Vessey et al, 2004). Long chain alkanols (halothene) and alcohols (octanol and heptanol) have long been known to close gap junctions (Johnston et al, 1980) and also to reduce neuronal excitability probably by affecting membrane fluidity (Takens-Kwak et al, 1992).…”

Intracellular acidification reduced gap junction coupling between immature rat neocortical pyramidal neurones.

“…Effects of 1-octanol on input resistance and synaptic transmission 1-Octanol, one of the best characterized pharmacological agents known to reduce gap junctional conductance (Johnston, Simon & Ramon, 1980;Burt & Spray, 1988), applied at a concentration of 2 mm, increased input resistance in only four out of twelve neurones tested (by 47-33 + 19 76%) between P2 and P9 (Fig. 12A).…”