STUART, D. G. 
with 400 ju A/pulse, 50 pulses/sec and 3 msec pulse duration sup- 
pressed shivering in the cat anesthetized with pentobarbital sodium 
(35 mg/kg I. ?.)• Shivering returned after 10 minutes and was again 
suppressed in the process of destroying tissue at locus A electro- 
lytically. Shivering was depressed for 10 minutes but was repro- 
duced by stimulating locus C at 1600 /; A/pulse with 25 1 msec/ 
pulse/sec. Following locus C stimulation, spontaneous shivering 
returned on the right hindlimb, but was suppressed by locus B 
stimulation with a 30- second stimulus of 200 m A/pulse and 50 3 
msec pulses/sec. Shivering was then reproduced by stimulation of 
locus C (not shown in Figure 7) but suppressed by electrolytic 
destruction of locus B. Following bilateral ventrolateral posterior 
hypothalamic destruction, shivering did not reoccur while the 
animal was anesthetized, but thirty-one days after surgery it was 
immediately apparent on exposure of the cat to cold, the VO shiv- 
ering/resting being 3 .2 . The failure of shivering to occur immediate- 
ly after bilateral ventrolateral posterior hypothalamic destruction 
may have been due to an unmeasured cardio-vascular depression, 
in that Fuster and Weinberg (1960) have shown that stimulation of 
the regions destroyed in this particular experiment increases 
myocardial contractility. The main aspect of this experiment is the 
demonstration of Birzis and Hemingway's result in an experiment 
that also illustrates seemingly conflicting results. That is to say, 
shivering can be evoked by dorsomedial posterior hypothalamic 
stimulation and suppressed by ventrolateral posterior hypothalamic 
stimulation. It can also be suppressed by ventrolateral posterior 
hypothalamic destruction in an acutely observed anesthetized prep- 
aration. Following such destruction shivering does return in the 
unanesthetized, chronically maintained preparation. 
This does not mean that all Birzis and Hemingway's acute 
lesion experiments are subject to question. They have hitherto 
unreported confirmation of the validity of this shivering pathway 
in the midbrain, pons, and bulb in that they have demonstrated the 
lack of shivering in chronic animals with bilateral lesions in the 
region in which the tissue destroyed is similar to that destroyed in 
the acute experiments. Perhaps the reason for their diverse hypo- 
thalamic result is that the majority of their efforts were directed 
to the descending paths, rather than the central origin of impulses 
related to the production of shivering. 
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