The regulation of H+ in nervous systems is a function of several proce
sses, including H+ buffering, intracellular H+ sequestering, CO2 diffu
sion, Carbonic anhydrase activity and membrane transport of acid/base
equivalents across the cell membrane. Glial cells participate in all t
hese processes and therefore play a prominent role in shaping acid/bas
e shifts in nervous systems. Apart from B homeostatic function of H+-r
egulating mechanisms, pH transients occur in all three compartments of
nervous tissue, neurones, glial cells and extracellular spaces (ECS),
in response to neuronal stimulation, to neurotransmitters and hormone
s as well as secondary to metabolic activity and ionic membrane transp
ort. A pivotal role for H+ regulation and shaping these pH transients
must be assigned to the electrogenic and reversible Na+ - HCO3- membra
ne cotransport, which appears to be unique to glial cells in nervous s
ystems. Activation of this cotransporter results in the release and up
take of base equivalents by glial cells, processes which are dependent
on the glial membrane potential. Na+/H+ and Cl-/HCO3- exchange, and p
ossibly other membrane carriers, accomplish the set of tools in both g
lial cells and neurones to regulate their intracellular pH. Due to the
pH dependence of a great variety of processes, including ion channel
gating and conductances, synaptic transmission, intercellular communic
ation via gap junctions, metabolite exchange and neuronal excitability
, rapid and local pH transients may have signalling character for the
information processing in nervous tissue. The impact of H+ signalling
under both physiological and pathophysiological conditions will be dis
cussed for a variety of nervous system functions.