1 148 



HANDBOOK OF PHYSIOLOGY 



NEUROPHYSIOLOGY II 



FIG. 9. Inhibition of 'tonic" sympathetic discharge in the 

 inferior cardiac ner\'e following a short burst of increased ac- 

 tivity induced by a brief period of hypothalamic stimulation. 

 White signal above lime marker gi\es duration of stimulus. No 

 rise of arterial pressure {upper record) to account for after-inhibi- 

 tion. Time: 0.2 sec. [From Bronk el al. (40}.] 



The region in which stimuhition produced activity in 

 one and the same peripheral neuron was surprisingly- 

 large. An approximately constant frequency of dis- 

 charge was found in the preganglionic neuron, even 

 when the electrode was shifted 3 mm dorsoventrally. 

 In other words, many hypothalamic neurons must 

 converge towards one and the same spinal neuron. 



The interference between the hypothalamic im- 

 pulses, on the one hand, and afferent inhibitory ex- 

 citatory impulses, on the other, was beautifully 

 demonstrated. On simultaneous hypothalamic stimu- 

 lation and activation of the baroceptors in the sinus 

 region, the cardiovascular discharge induced \'ia the 

 hypothalamus decreased. Simultaneous stimulation 

 of the hypothalamus and of an afferent nerve with a 

 pressor effect led to a summation of the effects, result- 

 ing in an increased cardiovascular discharge. Accord- 

 ing to Bronk et al., the hypothalamus may play the 

 role of a modifier in the various mechanisms that 

 regulate arterial pressure and heart rate. 



A frequency reversal — i.e. conversion of a pressor 

 to a depressor response — on changing from higher 

 to lower frequencies of stimulation was observed by 

 Hare & Geohegan (112) and by Berry et al. (36). 

 Bronk et al. gave a plausible explanation of such a re- 

 versal effect. They observed that with a change-over 

 from high-frequency (20 impulses per sec.) to low- 

 frequency (2 impulses per sec.) stimulation, there was 

 a temporary cessation of the tonic cardiovascular 

 discharge. The result of such interruption of the vaso- 

 constrictor firing will naturally be a fall of arterial 

 pressure. 



Characteristic of pressor effects elicited by hypo- 

 thalamic stimulation is a persisting poststimulatory 

 pressor effect. This has been attributed to a nervous 

 after-discharge [Grinker & Serota (i!i)j, though 

 Bronk et al. in no case observed such a discharge; on 

 the contrary, they often found, as mentioned above, 

 a poststimulatory inhibition (fig. 9). The poststimu- 



latory pressor effect is probably attributable to the 

 sluggishness of the peripheral effector organ or, pos- 

 sibly, to catechols secreted from the adrenals. Catechol 

 secretion is often activated by hypothalamic stimula- 

 tion — a fact that has long been recognized. 



Only a few investigators have made any detailed 

 study of the hypothalamically induced peripheral 

 vasomotor reaction patterns. Strom (258) found in 

 the hypothalamus of cats areas which when stimulated 

 electrically produced selectiv-e vascular responses in 

 the skin, either constriction or dilatation. Eliasson and 

 his associates (75, 76) were able to localize areas which 

 when stimulated activated the sympathetic vaso- 

 dilator outflow to the skeletal muscles and, simul- 

 taneously, produced cutaneous and intestinal vaso- 

 constriction. Local heating of temperature-regulating 

 areas in the anterior hypothalamus elicits cutaneous 

 vasodilatation [Folkow et al. (87, 88)]. 



HYPOTH.AL.AMicosPiN.'KL p.^TH\v.\YS. The va.sodilator 

 effects observed to occur in the skin and intestines 

 on hypothalamic stimulation must be due to inhibi- 

 tion of vasoconstrictor tone since no vasodilator in- 

 nervation is known to supply these vascular areas. 

 The occurrence of vasoconstrictor inhibition probably 

 means that inhibitory fibers pass from the hypothala- 

 mus down to the medullary or spinal vasomotor 

 neurons. The pathways for such inhibitory fibers 

 from the hypothalamus are unknown, although the 

 scattered depressor points found throughout the hy- 

 pothalamus and mesencephalon indicate the passage 

 of such inhibitory neurons. However, Alexander (7) 

 has suggested that a medial longitudinal depressor 

 band in the rostral part of the medulla oblongata 

 might be a descending inhibitory pathway from the 

 hypothalamus. 



Vasoconstrictor neurons pass from the lateral region 

 of the hypothalamus, probably around the aqueduct 

 in the central gray and in the tegmentum mesen- 

 cephali [Ranson & Magoun (181)]. 



An interesting question is whether, and if so to 

 what extent, vasomotor neurons emanating from the 

 hypothalamus and other supramedullary regions 

 converge towards the spinal vasomotor neurons and 

 pass the medullary pressor and depressor regions 

 without having any synapses there. It seems prob- 

 able — not least from the analysis presented by Bronk 

 et al. — that some vasomotor neurons, and perhaps the 

 majority, have synapses in the vasomotor centers of 

 the medulla oblongata. Some vasomotor neurons, 

 however, undoubtedly pass outside the medullary 

 vasomotor regions. This applies, for instance, to the 



