pends on innervation from the eye. In the absence of 
retinal innervation, aduk flies entirely lack the first 
optic ganglion, the lamina, which receives direct 
synaptic input from the outer photoreceptor cells 
Rl-6. 
Dr. Steller's group has found that the birth of lam- 
ina neurons is controlled by innervation from the 
developing eye. The neurons are produced by a 
wave of mitotic activity induced by the arrival of 
photoreceptor axons in the brain. These results sug- 
gest a novel mechanism for matching the number of 
target neurons in the first optic ganglion to the num- 
ber of incoming photoreceptor axons, and they ex- 
plain how developmental synchrony between the 
Drosopbila retina and the first optic ganglion is 
achieved. 
More recently Dr. Steller and his colleagues have 
found that the differentiation, but not the birth, of 
glial cells in the lamina depends on retinal innerva- 
tion. Several different approaches are now being 
used to elucidate the detailed cellular and molecu- 
lar mechanisms underlying this process. 
Although the importance of retinal innervation on 
the development of the adult optic ganglia of Dro- 
sopbila is well documented, little is known about 
retrograde effects of the brain on photoreceptor 
cells in the compound eye. Dr. Steller and his col- 
leagues have recently discovered the first evidence 
for the existence of such retrograde effects in the 
Drosopbila visual system. Although photoreceptor 
cells develop normally in the absence of connec- 
tions to the optic ganglia, their continued survival 
requires these connections. This situation is reminis- 
cent of trophic interactions that are commonly 
found in invertebrates. 
Genetic Control of Cell Death 
Dr. Steller's group is interested in isolating genes 
required for the initiation or execution of pro- 
grammed cell death in Drosopbila. They have found 
that the ultrastructural characteristics of cell deaths 
seen in the Drosopbila embryo are strikingly similar 
to apoptotic deaths described in mammalian sys- 
tems. Techniques have been developed that permit 
the rapid and reliable visualization of apoptotic 
cells in live embryos. 
These methods have been used to screen for cell 
death-defective mutants. A complex genetic locus 
on the third chromosome is required for either the 
commitment to, or the execution of, a cell death 
program. The DNA encompassing this locus has 
been cloned, and the molecular characterization of 
this interval is in progress. 
Dr. Steller is also Associate Professor of Neurobi- 
ology at the Massachusetts Institute of Technology 
and Adjunct Assistant Neurobiologist at Massa- 
chusetts General Hospital, Boston. 
Articles 
Abrams, J., Lux, A., Steller, H., and Kreiger, M. 
1992. Macrophages in Drosopbila embryos and 
L2 cells exhibit scavenger receptor-mediated en- 
docytosis. Proc Natl Acad Sci USA 89:10375- 
10379. 
Campos, A.R., Fischbach, K.-F., and Steller, H. 
1992. Survival of photoreceptor neurons in the 
compound eye of Drosopbila depends on con- 
nections with the optic ganglia. Development 
114:355-366. 
Winberg, M.L., Perez, S.E., and Steller, H. 1992. 
Generation and early differentiation of glial cells 
in the first optic ganglion of Drosopbila melano- 
gaster. Development 115:903-911- 
STUDIES ON A MOUSE MUTANT SUPPORT THE CONNECTION 
BETWEEN LONG-TERM POTENTIATION AND LEARNING 
Charles F. Stevens, M.D., Ph.D., Investigator 
Most neurobiologists have accepted the notion 
that long-term potentiation (LTP) — the enduring in- 
crease in synaptic strength that occurs with certain 
types of synaptic use — is the cellular basis for stor- 
ing memories in the hippocampus. This acceptance 
is based mainly on three lines of evidence: first, LTP 
has the properties required for a memory mecha- 
nism (it is associative, synapse specific, rapidly es- 
tablished, and long lasting); second, LTP is promi- 
nent in the hippocampus, a brain region known to 
be involved in storing memories; and third, several 
drugs that block LTP, by interfering with the func- 
tion of A'-methyl-D-aspartate (NMDA) receptors 
(APV [aminophosphono valerate], for example), 
440 
