2. ELECTROPHYSIOLOGY OF THE RETINA
39
following release from the inhibitory PIII. The following observations
(Motokawa et al., 1959, 1961) also support Granit. The carp retina,
detached from the pigment epithelium and mounted receptor side up
on the indifferent electrode, gives a characteristic pattern of local ERG
(Fig. 4 ) to a micropipette electrode placed on the distal retinal surface
when a spot of light is scanned across the site of recording. When the
light spot is on the recording site, a positive or PIII-dominant ERG is
obtained, but as the spot is moved away from the recording site, the local
ERG becomes negative or PII-dominant. In this PII-dominant zone,
ganglion cells responding to light with on discharge outnumber those
inhibited during light, whereas in the PIII-dominant zone the relation
is just the reverse. Meanwhile, the characteristic pattern of local ERG
shown in Fig. 4 was recently analyzed by Murakami and Sasaki (1968a,b)
in terms of spatial distribution of ERG components, using the carp retina.
Concerning the significance of the ERG in the chain of events evoked
by light in the retina, however, much remains to be studied. Hamasaki
and Bridges (1965) report, for instance, that a second light flash applied
within 5 sec after the first to a dark-adapted retina (elasmobranches)
fails to elicit an ERG, but the evoked responses at the optic tectum to
these two successive light flashes are about the same.
C. Localization of Electroretinogram Components
It is generally agreed that the PI1 originates from some cell type in
the inner nuclear layer (Granit, 1947). This has been confirmed by the
observation that the polarity of the b-wave is reversed after the recording microelectrode has penetrated through this layer ( Tomita, 1950;
Brown and Wiesel, 1961). Recent work on the carp retina with intracellular micropipettes (Kaneko and Hashimoto, 1969) shows that some
cells in the inner nuclear layer are depolarized during light while some
others are hyperpolarized ( cf. Fig. 12). Although their cell types have not
yet been identified, it is possible that those depolarized by light are
related to the PII.
The PI is localized in the outermost retinal structures (Tomita, 1950;
Brown and Wiesel, 1961). This localization is also based on the finding
from depth recording of the ERG with penetrating microelectrodes. After
the retina is detached from the pigment epithelium, the PI is lost both
in the retina proper and in the remaining part of the eye covered by the
pigment epithelium. Tomita (1950) assumes on this basis that the PI
is a phenomenon associated with some metabolic interaction between
the receptors and pigment epithelium cells. Noell (1954) and Brown and
Wiesel (1961) consider the pigment epithelium cells as the origin of PI.
39
following release from the inhibitory PIII. The following observations
(Motokawa et al., 1959, 1961) also support Granit. The carp retina,
detached from the pigment epithelium and mounted receptor side up
on the indifferent electrode, gives a characteristic pattern of local ERG
(Fig. 4 ) to a micropipette electrode placed on the distal retinal surface
when a spot of light is scanned across the site of recording. When the
light spot is on the recording site, a positive or PIII-dominant ERG is
obtained, but as the spot is moved away from the recording site, the local
ERG becomes negative or PII-dominant. In this PII-dominant zone,
ganglion cells responding to light with on discharge outnumber those
inhibited during light, whereas in the PIII-dominant zone the relation
is just the reverse. Meanwhile, the characteristic pattern of local ERG
shown in Fig. 4 was recently analyzed by Murakami and Sasaki (1968a,b)
in terms of spatial distribution of ERG components, using the carp retina.
Concerning the significance of the ERG in the chain of events evoked
by light in the retina, however, much remains to be studied. Hamasaki
and Bridges (1965) report, for instance, that a second light flash applied
within 5 sec after the first to a dark-adapted retina (elasmobranches)
fails to elicit an ERG, but the evoked responses at the optic tectum to
these two successive light flashes are about the same.
C. Localization of Electroretinogram Components
It is generally agreed that the PI1 originates from some cell type in
the inner nuclear layer (Granit, 1947). This has been confirmed by the
observation that the polarity of the b-wave is reversed after the recording microelectrode has penetrated through this layer ( Tomita, 1950;
Brown and Wiesel, 1961). Recent work on the carp retina with intracellular micropipettes (Kaneko and Hashimoto, 1969) shows that some
cells in the inner nuclear layer are depolarized during light while some
others are hyperpolarized ( cf. Fig. 12). Although their cell types have not
yet been identified, it is possible that those depolarized by light are
related to the PII.
The PI is localized in the outermost retinal structures (Tomita, 1950;
Brown and Wiesel, 1961). This localization is also based on the finding
from depth recording of the ERG with penetrating microelectrodes. After
the retina is detached from the pigment epithelium, the PI is lost both
in the retina proper and in the remaining part of the eye covered by the
pigment epithelium. Tomita (1950) assumes on this basis that the PI
is a phenomenon associated with some metabolic interaction between
the receptors and pigment epithelium cells. Noell (1954) and Brown and
Wiesel (1961) consider the pigment epithelium cells as the origin of PI.