Locomotion produced in mesencephalic cats by injections of putative transmitter substances and antagonists into the medial reticular formation and the pontomedullary locomotor strip

The purpose of this study was to determine the distribution of cells in the medial reticular formation (MRF) and the pontomedullary locomotor strip (PLS), which can induce locomotion when activated. Controlled microinjections of neuroactive substances (Goodchild et al., 1982) into the MRF or PLS were made in order to activate cell bodies in those areas. The ability of trigeminal receptive field stimulation to induce locomotion before and after drug infusion into the PLS was also assessed since the PLS and the spinal nucleus of the trigeminal nerve are similar in their anatomical distribution. Experiments were performed on precollicular-postmamillary decerebrate cats walking on a treadmill. Injections of glutamic acid (GA; 500 nmol) into the MRF produced locomotion that was antagonized by infusion of glutamic acid diethyl ester into the same spot. Decreases in the current threshold for locomotion produced by electrical stimulation of the MRF were observed when the MRF was infused with either GA (40-80 nmol), DL-homocysteic acid (DL-HCA; 200 nmol), or picrotoxin (PIC; 15 nmol). Injections of GA (100 nmol), DL-HCA (700 nmol), PIC (10-50 nmol), and substance P (2 nmol) into the PLS also produced locomotion. Locomotion produced by injections of PIC into the PLS was blocked by infusion of equal amounts of muscimol or GABA. Effective PLS injection sites were all confined to the trigeminal spinal nucleus or immediately ventral and medial to this in the adjacent lateral reticular formation. Trigeminal nerve peripheral field stimulation evoked locomotion after microinjection of PIC into the PLS, although this same facial stimulus was not effective prior to drug injection. We conclude that the MRF and PLS regions of the cat brain stem contain cells that produce locomotion when chemically stimulated, and we suggest that the PLS is closely related to or synonymous with the spinal nucleus of the trigeminal nerve. Furthermore, we suggest that stimulation of trigeminal afferents is analogous to stimulation of segmental afferent pathways in the production of locomotion (Sherrington, 1910; Jankowska et al., 1967; Afelt, 1970; Budakova, 1972; Grillner and Zangger, 1979).     

Role of joint afferents in relation to the initiation of forelimb stepping in thalamic cats

To analyze the roles of joint afferents in relation to initiation of forelimb stepping in thalamic cats, we recorded the unit spikes of the cervical dorsal roots, stimulated the joint afferents, and applied local anesthesia to the joint capsule. Almost all of the joint afferents of the shoulder, elbow, wrist and finger adapted slowly and exhibited alternating firing during forelimb stepping. About 45% of the afferents of each joint showed firings as the limb moved from forward to backward. About 44% of the afferents exhibited discharges as the limb moved from backward to forward. The remaining afferents showed firings as the limb moved in both directions. The application of local anesthesia to joints of the shoulder, elbow or wrist resulted in a marked reduction of forelimb stepping. Forelimb stepping was evoked by electric stimulation of the joint capsule, when excitabilities of flexor motoneurons were increased due to muscle stretching. Impulses originating in the joint afferents of the forelimb entered the spinal cord and ascended to the dorsolateral funiculus of the cervical cord, since forelimb stepping was abolished after bilateral transection of this part. Our results indicate that joint afferents may play an important role in the initiation of forelimb stepping in thalamic cats walking on a motor-driven treadmill.     

Analgesia produced by direct injection of morphine into the mesencephalic reticular formation

HAIGLER, H. J. AND R. S. MITTLEMAN. Analgesia produced by direct injection of morphine into the mesencephalicreticular formation. BRAIN RES. BULL. 3(6) 655–662, 1978.—Morphine administered intracerebrally (IC) (10 μg as the base on each side) into the MRF produced a significant dose dependent elevation of nociceptive threshold (i.e., analgesia) on the tail flick test and hemostat pinch test. However, morphine IC at lower doses had no analgesic effect. After morphine was injected IC (10 μg, bilaterally) into the MRF, naloxone, a specific narcotic antagonist, administered either IC at the same site (15 μg, bilaterally) or subcutaneously (10 mg/kg), antagonized the antinociceptive effects of morphine. Thirty percent of the animals given bilateral microinjection of 10 μg of morphine displayed hyperreactivity to mild stimuli. This hyperreactivity was not attenuated by large IC or systemic doses of naloxone. It was concluded that the MRF is a site where morphine may act to produce analgesia by a specific narcotic mechanism of action.