Repeated high-frequency trains of stimuli induce long-term potentiation (LTP) in the CA1 region that persists for up to 8 hours in hippocampal slices and for days in intact animals. This long time course has made LTP an attractive model for certain forms of long-term memory in the mammalian brain. A hallmark of long-term memory in the intact animal is a requirement for transcription, and thus whether the late phase of LTP (L-LTP) requires transcription was investigated here. With the use of different inhibitors, it was found in rat hippocampal slices that the induction of L-LTP [produced either by tetanic stimulation or by application of the cyclic adenosine monophosphate (cAMP) analog Sp-cAMPS (Sp-cyclic adenosine 3',5'-monophosphorothioate)] was selectively prevented when transcription was blocked immediately after tetanization or during application of cAMP. As with behavioral memory, this requirement for transcription had a critical time window. Thus, the late phase of LTP in the CA1 region requires transcription during a critical period, perhaps because cAMP-inducible genes must be expressed during this period.

http://science.sciencemag.org/content/sci/265/5175/1104.full.pdf

Requirement of a Critical Period of Transcription for Induction of a Late Phase of LTP

Nerve growth is regulated by attractive and repulsive factors in the nervous system. Microscopic gradients of Collapsin-1/Semaphorin III/D (Sema III) and myelin-associated glycoprotein trigger repulsive turning responses by growth cones of cultured Xenopus spinal neurons; the repulsion can be converted to attraction by pharmacological activation of the guanosine 3',5'-monophosphate (cGMP) and adenosine 3',5'-monophosphate signaling pathways, respectively. Sema III also causes the collapse of cultured rat sensory growth cones, which can be inhibited by activation of the cGMP pathway. Thus cyclic nucleotides can regulate growth cone behaviors and may be targets for designing treatments to alleviate the inhibition of nerve regeneration by repulsive factors.

https://science.sciencemag.org/content/sci/281/5382/1515.full.pdf

Conversion of neuronal growth cone responses from repulsion to attraction by cyclic nucleotides.

The nitric oxide and cGMP signal transduction system: regulation and mechanism of action

https://www.cell.com/cell/pdf/0092-8674(94)90236-4.pdf

Cyclic GMP and Calcium Mediate Phytochrome Phototransduction

Regulation of cardiac contraction by neurotransmitters and hormones is often correlated with regulation of the L-type Ca2(+)-channel current (ICa) through the opposite actions of two second messengers, cyclic AMP and cyclic GMP. While cyclic AMP stimulation of ICa is mediated by the activation of cyclic AMP-dependent protein kinase, inhibition of ICa by cyclic GMP in frog heart is largely mediated by activation of cyclic AMP phosphodiesterase. The present patch-clamp study reveals that, in rat ventricular cells, cyclic GMP can also regulate ICa via activation of endogenous cyclic GMP-dependent protein kinase (cGMP-PK). Indeed, the effect of cyclic GMP on ICa was mimicked by intracellular perfusion with the proteolytic active fragment of purified cGMP-PK. Moreover, cGMP-PK immunoreactivity was detected in pure rat ventricular myocytes by using a specific polyclonal antibody. These results demonstrate a dual mechanism for the inhibitory action of cyclic GMP in heart, as well as a physiological role for cGMP-PK in the control of mammalian heart function.

Ca2+ current is regulated by cyclic GMP-dependent protein kinase in mammalian cardiac myocytes.

https://febs.onlinelibrary.wiley.com/doi/pdf/10.1016/0014-5793%2890%2980702-K

Inhibition of cGMP-dependent protein kinase by (Rp)-guanosine 3',5'-monophosphorothioates.

Starfish oocyte maturation: evidence for a cyclic AMP-dependent inhibitory pathway.

Synthesis of nucleoside-3',5'-cyclic phosphorothioates by cyclothiophosphorylation of unprotected nucleosides

Synthesis of the 3′,5′-Cyclic Phosphates from Unprotected Nucleosides

Derivatives of 1-β-d-ribofuranosylbenzimidazole 3′,5′-phosphate that mimic the actions of adenosine 3′,5′-phosphate (cAMP) and guanosine 3′,5′-phosphate (cGMP)

Elke Butt

Papers

Inhibition of cGMP-dependent protein kinase by (Rp)-guanosine 3',5'-monophosphorothioates.

Starfish oocyte maturation: evidence for a cyclic AMP-dependent inhibitory pathway.

Synthesis of nucleoside-3',5'-cyclic phosphorothioates by cyclothiophosphorylation of unprotected nucleosides

Synthesis of the 3′,5′-Cyclic Phosphates from Unprotected Nucleosides

Derivatives of 1-β-d-ribofuranosylbenzimidazole 3′,5′-phosphate that mimic the actions of adenosine 3′,5′-phosphate (cAMP) and guanosine 3′,5′-phosphate (cGMP)