In the present experiments an attempt was made to locate the site where tubocurarine acts to produce the convulsive effects and the accompanying changes in electrical activity of the brain on injection into the lateral cerebral ventricle. Two different approaches were made. By recording the electrical activity from two points on either side of the mid line, it could be demonstrated that the activity produced by the unilateral injection occurred with similar latencies on both sides. This excludes structures lining the lateral ventricles as the sites at which the activity originated. In the course of these experiments it was found that records obtained from the cellular layer of Ammon's horn during the action of tubocurarine showed a characteristic pattern different from the patterns found in any other region so far examined.In the second approach the tubocurarine was perfused through a cannula ending in the lateral ventricle and the effluent was collected from various points between the third ventricle and the cisterna. In these experiments the muscular effects were recorded on a myograph and changes in excitability tested by the response of the quadriceps muscle to tapping its tendon.
METHODSThe experiments were performed on cats under chloralose anaesthesia (60 mg/kg intravenously).In experiments in which records were taken of the electrical activity of the brain and in which evoked responses to peripheral nerve stimulation (peroneal nerve) were recorded before and after an intraventricular injection of tubocurarine, the methods used were those previously described (Feldberg, Malcolm & Smith, 1957), and tubocurarine was injected intravenously. In those experiments in which tubocurarine was perfused through a cannula in the lateral ventricle and the effluent was collected from the cisterna or the aqueduct, the methods were essentially those described by Feldberg & Bhattacharya (1958), but the perfusion fluid used was not always Locke's solution but often an 'artificial cerebrospinal fluid' introduced by Merlis (1940) and later used by Leusen (1949). Its composition was as follows (g/l.): NaCl 8-10, KCI 0-25, CaCI2 014, MgCl2 0-11, NaHCO3 1-76, NaH2PO4 0 07, (NH2)2CO 0-13, glucose 0*61. No difference was observed in the effects of tubocurarine when Locke's solution or artificial c.s.f. was used for perfusion. The rate of * Present address: Department of Physiology, Marischal College, Aberdeen.