Figure 7. Physiological properties of a type III non-C1 neurone.

A, lowering arterial blood pressure (AP, mmHg) with the vasodilator agent sodium nitroprusside (SNP) increased the discharge rate of this neurone. The opposite effect was produced by increasing AP with phenylephrine (PE). Administration of phenylbiguanide (PBG, 10 μg kg⁻¹, i.v.) inhibited the cell. B, antidromic activation produced by hypothalamic stimulation. Hypothalamic stimulation (arrow) triggered by the spontaneous spike (s) elicits constant latency (antidromic, a) spikes (traces 1-5). Stimulation within the critical interval after occurrence of the spontaneous spike results in collision (traces 6-9). C, toe pinch elicits a burst of action potentials that was markedly and reversibly reduced by simultaneous elevation of AP (aortic occlusion). The three insets at the top of C represent the response of the cell to the three first toe pinches at an expanded scale.