Role of descending aminergic pathways in the development of locomotion.
- Edouard Pearlstein
- Current pharmaceutical design
We detected changes in the gene c-fos expression induced by activation of muscle afferents in the rat spinal cord after systemic introduction of reserpine (irreversible suppressor of vesicular transporter of monoamines, 1.5 mg/kg, intraperitoneally) and with no action of this agent. Numbers of Fosimmunoreactive (Fos-ir) neurons were calculated in the gray matter of the lumbar spinal segments after unilateral vibrational stimulation (VS) of the Achilles tendon of the mm. gastrocnemius–soleus. In the spinal cord of rats preliminarily injected with reserpine, greater numbers of Fos-ir neurons were observed; these units were localized mostly in layers 4–7 and in the nucl. intermediolateralis (35.4 ± 1.6 and 16.7 ± 0.9 positive neurons per 40 μm-thick slice) of segments L1–L2, and also in layers 4–7 and layer 9 (Fos-ir motoneurons) of segments L4–L5 (51.7 ± 3.4 and 11.4 ± 1.5 labeled units, respectively). The numbers of activated cells in the above structures of the spinal cord after VS but without preliminary injections of reserpine were, on average, 25.6 ± 1.4 and 3.5 ± 0.5, 27.8 ± ± 0.9 and 6.9 ± 0.3 units, respectively. Most ipsilateral Fos-ir motoneurons (86%) were localized in the lateral pool of layer 9, and only 14% of labeled motoneurons were localized in its medial regions. The results obtained show that weakening of monoaminergic influences resulting from administration of reserpine is accompanied by increase in the activity of intraspinal neuronal networks activated by proprioceptive afferent volleys, and the effects of the above inputs on spinal motoneurons and sympathetic preganglionic neurons are intensified. Weakening of inhibitory control, realized by inhibitory interneurons in the pathways of transmission of excitatory influences from muscle afferents to motoneurons, which was observed in our experiments after suppression of monoaminergic modulatory systems, can be considered a significant factor responsible for the development of rigidity/spasticity of the limb muscles manifested in neurodegenerative diseases and after traumas of the spinal cord.