Swelling and ion uptake in cat cerebrocortical slices:

Abstract

Cat cerebrocortical slices incubating in medium containing normal K+ concentrations were exposed to a number of different transmitters. Norepinephrine, histamine and adenosine or 2-chloroadenosine caused increased swelling of the slices associated with an increased Na+ and Cl- content. These effects were seen only when both Cl- and HCO3- were present in the medium, and were inhibited by a number of anion transport inhibitors. These characteristics were identical to those of the HCO3(-)-dependent component of the swelling induced by high K+ levels in the medium. Other transmitters, namely 5-hydroxytryptamine, dopamine, and gamma-amino butyric acid, were ineffective. The effects of norepinephrine, histamine and 2-chloroadenosine were antagonised by propranolol and phentolamine, chlorpheniramine and diphenhydramine, and theophylline respectively. These antagonists also inhibited HCO3(-)-dependent, K+-stimulated swelling. The transmitters which induced swelling also stimulated the carbonic anhydrase activity of cerebrocortical slices. We conclude from these data that the HCO3(-)-dependent component of K+-stimulated swelling may be due to K+-stimulated release of transmitters. Furthermore, the fact that the transmitters which induce swelling have also been reported to be most effective in increasing cAMP content in both brain slices or cultured astrocytes is consistent with the swelling response being mediated via cAMP-induced changes and being predominantly localized to astrocytes.

Potassium Dependent Regulation of Astrocyte Water Permeability Is Mediated by cAMP Signaling

“…As a second messenger cAMP has been implicated in astrocyte signaling in the brain when exposed to high [K + ] o [17], [18]. When cells were exposed to 10mM [K + ] o , cAMP FRET ratio showed a significant change, indicating increased cAMP production, at 1min (1.9% ± 0.4%, p<0.001) and at 5min (2.5% ± 0.4%, p<0.001) in the astrocyte cell line (Figure 2B).…”

Rubidium Uptake and Accumulation in Peripheral Myelinated Internodal Axons and Schwann Cells

“…Studies involving electrical stimulation of peripheral and central nerves have demonstrated an activity-dependent transient rise in extraaxonal K~0 from resting levels of 3-4 to '-~12 mM (Kriz et al, 1974;Heinemann and Lux, 1977;Connors et al, 1982;Forstl et al, 1982;Bostock and Grafe, 1985;Hoppe et al, 1991). Axon injury associated with several neuropathic conditions (e.g., spinal cord trauma and nerve transection) is accompanied by significant increases in K~0to 50-60 mM (Bourke et al, 1983;Young and Koreh, 1986;Chesler et al, 1994). Maintenance of normal K~0concentrations is critical for conduction of axonal action potentials and membrane repolarization (Eidelberg et a!., 1975;Rasminsky, 1978;Brismar, 1981;Sykova, 1983).…”