Introduction
Along their entire length from the inner to the
outer limiting membrane of the retina each Müller
cell (MC) makes contact with all types of retinal
neurones.
1
These cells must, therefore, be highly
adapted to very different environmental demands.
For instance, to meet the needs of the different
neurones they are serving, their K
+
channels are
differentially distributed along the length of the cell.
2
This feature seems to facilitate the K
+
homeostasis of
the retina by the so-called spatial buffering process,
3,4
which involves mainly the inwardly rectifying K
+
currents.
5
Although we have an idea about the func-
tion of inwardly rectifying K
+
currents in MC, we
do not know why they express delayed rectifier K
+
channels
6
and the recently described transient Na
+
channels
7
, as well as the -aminobutyric acid A
(GABA
A
) receptors that have been described in
baboon
8
and skate.
9
Whereas the delayed rectifier K
+
currents have been found in all species, Na
+
currents
are found in only some species, including mouse,
man, horse and zebra, but are not present in rat,
rabbit and guinea pig. Among mammals, expression
of GABA
A
receptors seems to be restricted to
primates.
8
This short survey provides an impression
of the numerous species differences regarding MC
membrane characteristics.
This study was aimed at basic determination of the
main voltage-dependent ion conductances and phar-
macological characterization of the GABA
A
recep-
tors of baboon MC.
Material and Methods
Whole-cell voltage-clamp recordings were per-
formed on MC acutely isolated from seven baboons
(Papio cynocephalus) which had been infected with
Schistosoma mansoni during a series of experiments.
8
Eyes were enucleated immediately after the animals
had been sacrificed, the retinas were prepared within
the next half hour and stored in Ames’ media
(Sigma) on ice until they are used for isolating of MC
every 2–3 h during the next 24 h. MC were prepared
according to the method described earlier.
8
In
brief, retinal pieces were immersed in Ca
2+
/Mg
2+
-free
recording solution (see below) containing 1 mg ml
–1
papain (Boehringer Mannheim, Germany) for 30 min
at 37ºC in 5% CO
2
/95% air. The tissue was
then washed four times with recording solution,
Membrane and Cellular Biophysics and Biochemistry
1
1
1
1
1
p
© Rapid Science Publishers Vol 8 No 2 20 January 1997 541
THE electrophysiological features of isolated baboon
Müller cells was investigated using the whole-cell
voltage-clamp technique. Application of depolarizing
voltage steps evoked transient inward and delayed
outward currents. The transient currents disappeared
when extracellular Na
+
was replaced by choline
+
and
were substantially decreased by application of tetro-
dotoxin (1 M). The outward currents were strongly
diminished by extracellular Ba
2+
(1 mM), and the hyper-
polarization-generated inward currents disappeared
following application of Ba
2+
. The recently described -
aminobutyric acid A (GABA
A
) receptor currents were
increased by flunitrazepam, nordiazepam, pentobarbital
and Zn
2+
, as well as by the inverse agonist DMCM. These
results suggest that the baboon Müller cells possess the
same voltage-dependent current pattern as those from
other species, e.g. humans, whereas their GABA
A
recep-
tors react in an uncharacteristic manner to DMCM and
Zn
2+
, when compared with neuronal GABA
A
receptors.
Key words: Barbiturates; Benzodiazepines; GABA
A
recep-
tor; Müller cells; Potassium currents; Primates; Retina
currents; Sodium; Zinc
Voltage- and GABA-
evoked currents from
Müller glial cells of the
baboon retina
Winfried Reichelt,
CA
Miguel Hernandez,
1
Raymond T. Damian,
2
William S. Kisaalita
1
and
Berry L. Jordan
3
Paul-Flechsig-Institute for Brain Research,
Department of Neurophysiology, University of
Leipzig, Jahnallee 59, 04109 Leipzig, Germany;
Departments of
1
Biological and Agricultural
Engineering and
2
Cellular Biology, University
of Georgia, Athens, GA 30602;
3
Department of
Ophthalmology, College of Medicine,
University of Florida, Gainesville, FL 32610,
USA
CA
Corresponding Author
NeuroReport 8, 541–544 (1997)