Table 3.
Pharmacological mediators of respiratory plasticity post-SCI
| Molecule | Receptor | Expression post-injury | Anatomical location of expression | Effect on plasticity |
|---|---|---|---|---|
| Serotonin | 5HT-1A | Increased | Dorsal horn [62,64] | Enhancing |
| PhMN [64] | ||||
| 5HT-2A | Increased | Medulla [99] | Enhancing | |
| Spinal cord [99], PhMN [63] | Enhancing | |||
| Glutamate | AMPA-GluR1 | Increased [66] | PhMN [66] | Enhancing |
| AMPA-GluR2 | Decreased [66] | PhMN [66] | Enhancing | |
| NMDA–2A | Increased [66] | PhMN [66] | Enhancing | |
| GABA | GABA-A | – | Dorsal horn [71] | Inhibiting |
| GABA-B | – | Inhibiting | ||
| Adenosine | Adenosine–A1 | – | Carotid bodies [69] | Inhibiting |
| Adenosine–A2a | – | Carotid bodies [69] | Enhancing | |
| PhMN [33] |
Summary of some of the reported molecules and receptors that can influence the onset and extent of respiratory plasticity following spinal cord injury. Identification of these neuromodulators, and an increasing interest in their role following injury, has led to the development of several therapeutic approaches to improving respiratory function post-SCI.