E.G. Szekely

Cortical responses to rotation. I. Responses recorded after cessation of rotation.

Averaged cortical responses to labyrinthine stimulation induced by sudden cessation of single rotations were studied using a Mnemotron Computer of Average Transients. Following rotation there appeared in cats with the eyelids closed diffuse, slow, sometimes multiphasic responses. They were probably due to excitation of the diffuse thalamic system. In human subjects similar responses could be obtained either diffusely or prevalent or exclusively from the preoccipital and/or parastriate area. The responses observed in posterior parts of the cerebral hemisphere following cessation of rotation appeared also, if the animals were flaxedilized, or the second somatic sensory area was ablated in both hemispheres. Bilateral labyrinthectomy abolished these responses. While the observation of the ocular reactions to labyrinthine stimulation permits one to ascertain the excitability of the vestibulo-ocular reflex arc only, the recording of the cortical responses to rotation may perhaps be developed into a clinical too...

Striatal bradykinesia alleviated by intracaudate injection of l -dopa

Die durch chemische Reizung des Nucleus caudatus herabgesetzte Laufgeschwindigkeit konnte durch Injektion vonl-Dopa in dieses Ganglion wieder den ursprünglichen Werten nahegebracht werden.

The influence of stimulation of the hypothalamus and of the dorsomedial nucleus upon experimental bradykinesia and akinesia.

Abstract In an attempt to analyze mechanisms able to counteract bradykinesia and akinesia, alumina cream was injected into the caudate nucleus of cats, a procedure able to produce initially a marked slowing and eventually nearly complete cessation of spontaneous movements. In various stages following the alumina cream injection, the hypothalamus or the dorsomedial nucleus were stimulated through previously implanted electrodes. Such stimulations were able to increase the speed of the locomotor activity or to initiate locomotion in catatonic animals. Electrocoagulation around the foci of stimulation prevented such effects. Lesions of the dorsomedial nuclei, however, prevented the effect of hypothalamic stimulation only if relatively low voltages were used.

Cortical Responses to Rotation II.: Responses Recorded at the Onset of Rotation from the Second Somatic Sensory and Posterior Areas

Using a Mnemotron computer a method has been developed permitting one to study in cats the cortical responses appearing when angular acceleration is started. According to this method the entrance of labyrinthine impulses is not restricted to the second somatic sensory area (S2) but extends posteriorly, chiefly into parts of the auditory cortex and into the so-called association cortex (gyrus suprasylvius medius). At least in some of the experiments the anterior part of the gyrus ectosylvius posterior and the posterior corner of the gyrus suprasylvius medius (part of the second visual area) showed responses of relatively short latency. General muscle paralysis or bilateral ablation of S2 did not prevent such responses in posterior parts of the hemisphere, while bilateral labyrinthectomy abolished them.

Influence of the corpus striatum upon electrical potentials of the liver

Abstract The effect of stimulation of the caudate nucleus, hypothalamus, midbrain tegmentum, splanchnic nerve, or vagus nerve upon the liver was studied in cats using d-c potentials of the liver surface (LP) as an indicator. Stimulation of these areas or of the splanchnic nerve induced a gradual increase of the positive LP. The maximum (1–2 mv) was reached about 30 sec after the beginning of the reaction. The gradually declining curve returned to or close to the resting value about 30 to 60 sec later. Vagal stimulation usually produced a fluctuation of LP to the negative side. In control experiments, stimulation of the pole and basal parts of the frontal lobe, of the sigmoid gyri and of the dura did not significantly change LP. The effect of caudate stimulation upon the liver did not depend on the corticofugal fibers originating in the sigmoid gyri and frontal lobe, in contrast to the effect upon smooth muscles. The effect of stimulation of the caudate nucleus persisted after extensive homolateral lesions of the pallidum or of the amygdala, but it was no longer demonstrable after extensive combined lesions of these ganglia. It was distinctly decreased by large hypothalamic lesions on the side of the caudate stimulation and practically abolished by extensive bilateral lesions in the caudal hypothalamus. Transection of the spinal cord above the origin of the splanchnic nerves prevented or abolished the effect of stimulation of the caudate nucleus or the hypothalamus upon LP, whereas this reaction persisted after bilateral vagotomy. In aggreement with the assumption that the influence of the caudate nucleus and of the hypothalamus upon the liver is part of the central temperature regulation, it was found that the rise in LP was accompanied by an elevation of the liver temperature.

Variations in Motility Associated with Striatal Acetylcholine Levels

In the course of investigations of interstriatal relationships, studied with electrical stimulation, small unilateral lesions were placed into the dorsomedial reticular formation of rats at the superior collicular level. Following the placement of these lesions, the amplitudes of the summed and averaged interstriatal responses were greatly increased. A clinical correlate was reduction of the speed of locomotion, at times advancing to complete akinesia, catatonia, and frequently generalized clonus. The acetylcholine (Ach) level (as determined in five control animals) rose from the mean striatal level of 6.5 µg/g (±1.02) by 100% to 13.3 µg/g (±1.16) 6–8 h after the reticular lesion was placed. The Ach level was determined according to the method of Crossland after the animals were killed in liquid nitrogen. We then placed in a series of other rats large lesions into the amygdaloid complex, including the origin of the stria terminalis. Catalepsy did not occur when this procedure was followed by injury to the midbrain tegmentum. These rats showed spontaneous locomotion, and clonic seizures appeared only infrequently. In these animals, the mean amount of Ach in the striata was only slightly elevated to 7.1 µg/g (±0.76). The elevation of Ach in the striate, produced in the previous set of experiments by lesions in the reticular formations, was prevented by the prior placement of amygdaloid lesions. In addition, the amygdaloid lesion prevented an increase of amplitude of the interstriatally evoked and recorded responses. Symmetrel (amantadine hydrochloride) is known to enhance dopamine turnover in the striata of untreated rats. It also increases spontaneous running speed during the initial dosages. Thereafter, repeated daily administration of large doses of Symmetrel was followed by decreased locomotion and eventually bradykinesia or akinesia with rigidity. In these rats, the striatal Ach level increased to 10.7 µg/g (± 0.92). Since the above mentioned experimental catatonia developed as a consequence of striatal excitation associated with Ach increase, we followed this line of experiments in another group of rats with subcutaneous injections of small amounts of bulbocapnine measuring 11.5 µg/g (±0.91). This finding raised the possibility that the catatonia produced by bulbocapnine is the consequence of an elevation in the striatal levels of Ach and accompanying physiological events in the striatal system. The catatonia produced by the various manipulations described could be reversed by the injection of 80–100 mg L-dopa in solution, i.p. and sometimes locomotor activity was even greater than that observed in the control period.