Intranet

Inhibition effect of NAPE at spinal cord level


N-acylphosphatidylethanolamine (NAPE), as the precursor of anandamide, an endogenous agonist of TRPV1 and cannabinoid receptors, could play a role in modulation of nociceptive signalization in the spinal cord.

Modulation of synaptic transmission in the spinal cord dorsal horn plays a key role in nociceptive signalling. An important part in this process is thought to be mediated by presynaptic transient receptor potential vanilloid 1 (TRPV1) and cannabinoid (CB) receptors. TRPV1 receptors in the central nervous system may be activated by endogenous agonists. One of them, anandamide, has been first recognized as a potent CB receptor agonist and may activate both types of receptors on the presynaptic endings of primary afferents in the spinal cord. Anandamide is synthesized from N-acylphosphatidylethanolamine (NAPE) via NAPE-phospholipase D. NAPE might thus have a role in attenuation or amplification of nociceptive signalling at the spinal cord level.

 

The aim of our study is to determine the effect of NAPE on synaptic transmission using patch-clamp recordings of AMPA mediated mEPSC, sEPSC and eEPSC in the superficial dorsal horn neurons in acute spinal cord slices. The cooperation between TRPV1 and CB1 receptors may be important part of the spinal cord nociceptive signalling especially under pathological conditions.