(2001) Presynaptic inhibition caused by retrograde signal from metabotropic glutamate to cannabinoid receptors.
(2001) Endogenous cannabinoids mediate retrograde signals from depolarized postsynaptic neurons to presynaptic terminals.
Although the capture of 24-h LTF is independent of protein synthesis, the initiation of LTF by synaptic application of 5-HT is dependent on protein synthesis, suggesting that the newly synthesized local proteins may serve as, or help generate, the presumed retrograde signal to the nucleus.
If the retrograde signal induced expression (or repression) of new macromolecules in the soma that were subsequently shipped to the synapse, additional time might be required for these intermediate steps.
However, if in our experiments LTF triggered by synaptic application of 5-HT to distal terminals requires retrograde transport to the soma and subsequent somatic protein synthesis, then one might have expected that protein synthesis in the soma could have returned to normal by the time the retrograde signal arrived, and hence LTF blockade might not have occurred.
In cases where the retrograde messenger is not sufficient, pairing the other factor(s) with the retrograde signal
should mimic the phenomenon.
This result implies that a retrograde signal is necessary for the long-term presynaptic morphological changes.
Given this situation, it is clear that these changes must be mediated by some, as yet unknown, retrograde signal. An apparent counterexample to the idea that long-term presynaptic changes depend on retrograde signals, however, is non-NMDA receptor-dependent LTP of the mossy fiber [right arrow] CA3 pyramidal cell synapse.
We cannot rule out the possibility that other retrograde signals
may promote activation of local procaspase-8 in the cell body and along the axon of SC projecting neurons.