Official websites use. Share sensitive information only on official, secure websites. Email: doris. To evaluate their contribution to synaptic plasticity, we analyzed knock-out mice lacking either one of the GC isoforms. We found that LTP induced in the visual cortex is NO dependent in the wild-type mice, absent in either of the GC isoform-deficient mice, and restored with application of a cGMP analog in both strains.
The signaling molecule nitric oxide NO has been postulated to participate in long-term potentiation LTP , the use-dependent increase of transmission efficacy at synapses implicated in learning and memory for review, see Hawkins et al. Already, initial reports suggested NO as a retrograde messenger synthesized in response to NMDA receptor activation in the postsynaptic neuron and causing long-lasting increases of transmitter release in the presynaptic terminals Garthwaite et al.
Other studies performed mainly in hippocampal slices of the CA1 region revealed that NO is not involved in all forms of LTP but only in certain areas and under special experimental conditions Son et al. The isoforms appear to be very similar as they do not differ in regulatory or enzymatic properties.
The possible neuronal function of this isoform is supported by its high expression in the brain compared with other tissue. Here, we used knock-out KO mice deficient in either one of the GC isoforms to study the role of NO receptor GC in the enhancement of synaptic transmission.
In the experiments, either litter- or age-matched mice of the same sex were used wherever feasible. All experiments were performed in accordance with the guidelines of the local animal ethics commission and German laws. The animals were deeply anesthetized with ether and decapitated. Slices were placed in a holding chamber and incubated with oxygenated ACSF at room temperature.
