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Using low-frequency (0.08–0.18 Hz) sinusoidal galvanic vestibular stimulation (sGVS), we recently showed that two peaks of modulation of muscle sympathetic nerve activity (MSNA) and skin sympathetic nerve activity (SSNA) occurred for each cycle of stimulation: a large peak associated with the positive peak of the sinusoid (defined as the primary peak) and a smaller peak (defined as the secondary peak) related to the negative peak of the sinusoid. However, these recordings were only made from the left common peroneal nerve, so to investigate lateralisation of vestibulosympathetic reflexes, concurrent recordings were made from both sides of the body. Tungsten microelectrodes were inserted into muscle or cutaneous fascicles of the left and right common peroneal nerves in 17 healthy individuals. Bipolar binaural sinusoidal GVS (±2 mA, 100 cycles) was applied to the mastoid processes at 0.08 Hz. Cross-correlation analysis revealed that vestibular modulation of MSNA (10 bilateral recordings) and SSNA (6 bilateral recordings) on the left side was expressed as a primary peak related to the positive phase of the sinusoid and a secondary peak related to the negative phase of the sinusoid. Conversely, on the right side, the primary and secondary peaks were reversed: the secondary peak on the right coincided with the primary peak on the left and vice versa. Moreover, differences in pattern of outflow were apparent across sides. We believe the results support the conclusion that the left and right vestibular nuclei send both an ipsilateral and contralateral projection to the left and right medullary output nuclei from which MSNA and SSNA originate. This causes a “flip-flop” patterning between the two sympathetic outflows: when vestibular modulation of a burst is high on the left, it is low on the right, and when modulation is low on the left, it is high on the right.

Studies previously performed in our laboratory have shown that sinusoidal galvanic vestibular stimulation (sGVS), a means of selectively modulating vestibular input without affecting other inputs, can cause partial entrainment of muscle sympathetic nerve activity (MSNA) at frequencies ranging from 0.2 to 2.0 Hz. Here we test the effect of sGVS on sympathetic outflow when stimulating the vestibular system at lower frequencies. MSNA was recorded via tungsten microelectrodes inserted into the left common peroneal nerve in 12 awake, seated subjects. Bipolar binaural sinusoidal GVS (±2 mA, 100 cycles) was applied to the mastoid processes at 0.08, 0.13 and 0.18 Hz. Cross-correlation analysis revealed two bursts of modulation of MSNA for each cycle of stimulation. We believe the primary peak is related to the positive phase of the sinusoid, in which the right vestibular nerve is hyperpolarised and the left vestibular nerve depolarised. Furthermore, we believe the secondary peak is related to the negative phase of the sinusoid (depolarisation of the right vestibular nerve and hyperpolarisation of the left vestibular nerve). This was never observed at higher frequencies of stimulation, presumably because at such frequencies there is insufficient time for a second peak to be expressed. The incidence of double peaks of MSNA was highest at 0.08 Hz and lowest at 0.18 Hz. These observations emphasise the role of the vestibular apparatus in the control of blood pressure, and further suggest convergence of bilateral inputs from vestibular nuclei onto the output nuclei from which MSNA originates, the rostral ventrolateral medulla (RVLM).

Skin on the fingertips of humans and monkeys was stimulated by a probe vibrating with a sinusoidal displacement. The probe and the skin were illuminated stroboscopically and were viewed through a dissecting microscope. The stroboscope was triggered by the sinusoidal generator via a digital delay, so that the position of both the probe and the skin could be measured at regular intervals during the cycle. Six frequencies and 3 amplitudes of vibration were used. During a portion of the cycle the probe and the skin separated, so that the skin waveform was a clipped sinusoid. An increase in stimulus frequency increased the fraction of the cycle during which the probe and the skin were separated. Adding a static pre-indentation to the vibration reduced this fraction, and for this condition a decrease in vibratory amplitude also decreased the fraction. Thus the skin motion contained harmonics that were not present in the probe motion, and the harmonic content differed for different stimulus conditions.

Fluoride resistant acid phosphatase (FRAP) activity of the rat substantia gelatinosa Rolandi is confined to electron dense sinusoid terminals under normal conditions. Transection of dorsal roots or removal of dorsal root ganglia results in a rapid degeneration of more than half of the electron dense sinusoid axon terminals. First signs of degeneration ensue 20 hours after surgery; at the 24 hours state osmiophilic degeneration bodies develop that are translocated into glial elements in the course of the second postoperative day. At the same time, light microscopically visible FRAP-activity of the Rolando substance disappears. Electron histochemical investigations reveal that decreased enzyme activity is due to degeneration of FRAP-positive terminals. It is concluded that FRAP-positive terminals, representing the majority of electron dense sinusoids in the Rolando substance, are dorsal root collaterals; the origin of non-degenerating FRAP-negative electron dense terminals remains unknown for the time being.

A Golgi and electron microscope study, using also secondary degeneration after dorsal root transection and chronically isolated dorsal horn preparations, were undertaken with the objective to clarify the large (glomerulus-like) synaptic complexes in lamina II of the dorsal horn. The large sinusoid axon terminals forming the centers of these synaptic complexes are of intraspinal origin and are thought to arise from the hitherto unknown type of pyramid-shape nerve cells, situated at the border between laminae III and IV. The sinusoid axon terminals establish axo-dendritic synapses with substantia gelatinosa neurons and abundant axo-axonic synapses with smaller terminals that could be identified (at least partly) as endings of primary sensory afferents. The central sinuous axon terminals of the synaptic complexes are always presynaptic to the smaller axons and thus might be considered as a device for 1. presynaptic inhibition of impulse transmission from primary afferents to substantia gelatinosa neurons, and 2. as the anatomical basis for primary afferent depolarization.