Chronic pain research is being conducted into neuroligin-2 as a cause exacerbating chronic pain, with the findings offering a potential new therapeutic direction to investigate.
Price’s research on the topic has recently been published online in Pain, the journal of the International Association for the Study of Pain.
The study focused on the body’s inhibitory networks — a series of biochemical reactions that decrease certain neurological activity, such as pain. When pain becomes chronic there is strong evidence that a process called GABAergic plasticity can cause GABA to lose its inhibitory activity, sometimes making the pain even worse.
The source of these excitatory actions in neuronal circuits has been broadly attributed to chloride ions, but Price’s research has found another potential cause of GABAergic plasticity: synaptic adhesion molecules called neuroligin-2.
Chronic pain may persist due to cells that hold “memories” of the pain according to this study
Some resources on back pain:
Neurology of Central Nervous System Injuries
Neurobiologists at UC San Diego have discovered how signals that orchestrate the construction of the nervous system also influence recovery after traumatic injury. They also found that manipulating these signals can enhance the return of function.
Most people who suffer traumatic injuries have incomplete lesions of neural circuits whose function can be partially restored from the reconfiguration of the spared circuits with rehabilitative training.