Supraspinal glycinergic neurotransmission in pain: A scoping review of current literature.

The neurotransmitter glycine is an agonist at the strychnine-sensitive glycine receptors. In addition, it has recently been discovered to act at two new receptors, the excitatory glycine receptor and metabotropic glycine receptor. Glycine's neurotransmitter roles have been most extensively investigated in the spinal cord, where it is known to play essential roles in pain, itch, and motor function.

Cannabis constituents for chronic neuropathic pain; reconciling the clinical and animal evidence.

Chronic neuropathic pain is a debilitating pain syndrome caused by damage to the nervous system that is poorly served by current medications. Given these problems, clinical studies have pursued extracts of the plant Cannabis sativa as alternative treatments for this condition. The vast majority of these studies have examined cannabinoids which contain the psychoactive constituent delta-9-tetrahydrocannabinol (THC).

Bidirectional Modulation of Nociception by GlyT2 Neurons in the Ventrolateral Periaqueductal Gray.

The midbrain periaqueductal gray (PAG), particularly its ventrolateral column (vlPAG), is part of a key descending pathway that modulates nociception, fear and anxiety behaviors in both humans and rodents. It has been previously demonstrated that inhibitory GABAergic neurons within the vlPAG have a major role in this nociceptive modulation. However, the PAG contains a diverse range of neuronal subtypes and the contribution of different subtypes of inhibitory neurons to nociceptive control has not been investigated.

Spinal glycinergic currents are reduced in a rat model of neuropathic pain following partial nerve ligation but not chronic constriction injury.

Animal models have consistently indicated that central sensitization and the development of chronic neuropathic pain are linked to changes to inhibitory signaling in the dorsal horn of the spinal cord. However, replication of data investigating the cellular mechanisms that underlie these changes remains a challenge and there is still a lack of understanding about what aspects of spinal inhibitory transmission most strongly contribute to the disease. Here, we compared the effect of two different sciatic nerve injuries commonly used to generate rodent models of neuropathic pain on spinal glycinergic signaling.