Reticulospinal systems mediate atonia with short and long latencies.
|Reticulospinal systems mediate atonia with short and long latencies.
|Year of Publication
|Kohyama J, Lai YY, Siegel JM
|Animals, Cats, Electric Stimulation, Electromyography, Hindlimb, Medulla Oblongata, Muscle Tonus, Muscle, Skeletal, Neck Muscles, Neural Conduction, Pons, Reaction Time, Time Factors
The pontomedullary region is responsible for both the tonic and phasic reduction of muscle activity in rapid-eye-movement sleep and contributes to the control of muscle tone in waking. This study focused on determining the time course of activity in the pontomedullary systems mediating atonia. Short-train stimulations (3 0.2-ms pulses at 330 Hz) of the pons and medulla suppressed neck and hindlimb muscle activity in decerebrate cats. We identified two distinct phases of suppression, early and late. The anatomic sites that produced each suppression were intermixed. We estimated the dividing value of the conduction velocity for reticulospinal projections responsible for early and late phases of hindlimb muscle tone suppression to be 22.8 m/s. In the medial medulla, 238 reticulospinal units, which send axons to the L1 level of the spinal cord, were identified. Pontine stimulation that suppressed hindlimb muscle tone increased the firing rate of 138 units (type I). Sixteen type I units showed a delayed response to the pontine stimulation with a latency of 10 ms or longer (type Id), whereas 122 type I units exhibited an earlier response (type Ie). Seven type Ie units had an axonal conduction velocity of <22.8 m/s, whereas the remaining 115 conducted at faster than 22.8 m/s. Early and late hindlimb muscle tone suppressions were hypothesized to be mediated through fast and slow conducting type Ie reticulospinal units. The activity of type Id neurons may contribute to the cessation of the early-phase suppression as well as to the induction, maintenance, or cessation of the late-phase suppression.
|HL-41370 / HL / NHLBI NIH HHS / United States
NS-14610 / NS / NINDS NIH HHS / United States