M. Chaimovitz

COMPULSIVE GNAWING IN RATS AFTER IMPLANTATION OF DRUGS INTO THE VENTRAL THALAMUS. A CONTRIBUTION TO THE MECHANISM OF MORPHINE ACTION

1 Implantation of morphine into various parts of the corpus striatum of rats evokes only weak gnawing responses. 2 Deposition of apomorphine, morphine or methadone in the region of the nucleus ventralis thalami produces a biphasic response, i.e. general excitation, followed by a period of intense gnawing. 3 The effect of both apomorphine and morphine is blocked by chlorpromazine, haloperidol and pimozide. However, pretreatment with α‐methyltyrosine methyl ester or α‐methyldopa prevents only the gnawing response to morphine, but not to apomorphine. 4 Systemic nalorphine, morphine or pethidine suppress the gnawing response, evoked by thalamic implants of apomorphine or morphine. 5 Systemic amphetamine potentiates the effect of thalamic deposits of morphine. 6 Compulsive gnawing, following implantation of morphine into the ventral region of the thalamus, probably results from enhanced production and release of catecholamines.

Nystagmus evoked by stimulation of the optic pathways in the rabbit

Abstract Horizontal nystagmus can be regularly evoked in the rabbit by electrical stimulation applied to the optic pathways or directly to the cornea. The rapid phase of the nystagmus is directed toward the eye in which the stimulated fibers take origin. The response varies with the frequency of stimulation, with an optimum at about 40 cycle/sec. The nystagmus response is enhanced by optokinetic stimulation and by side position of the head. Continuous illumination of the eyes inhibits the eye movements, while sectioning of the optic chiasm enhances them. The relation of electrical stimulation of the optic nerve to various modes of excitation of the retina is discussed.

Nystagmus evoked by intermittent photic stimulation of the rabbit's eye

Monokuläre Reizung des Kaninchens durch Lichtblitze ruft einen Nystagmus hervor, dessen Richtung identisch ist mit der Richtung der Augenbewegungen, die durch elektrische Stimulierung des ipsilateralen Nervus opticus verursacht werden. Die anhaltende Beleuchtung des kontralateralen Auges hemmt die Nystagmusreaktion.

Blood Pressure Responses to Electrical Stimulation of Peripheral Nerves and their Modification by Nembutal

Abstract1. Blood pressure changes, evoked by stimulation of peripheral nerves, decline if the frequency of stimulation passes beyond the optimal range. Instability of a response develops progressively and is ascribed to the increasing influence of inhibitory components in a given circuit.2. Unstable reactions can be converted into sustained responses by two methods: a by intermittent stimulation, which prevents the inhibitory effects to summate to their threshold value; and b by application of barbiturate, which produces selective block of inhibitory transmission.3. With graded doses of nembutal, a double reversal of the blood pressure response to sciatic stimulation can be produced. This phenomenon is interpreted on the basis of the complex composition of the nerve, which sends fibres to autonomic centres in the hypothalamus and the medulla.

Seizure activity evoked by implantation of ouabain and related drugs into cortical and subcortical regions of the rabbit brain

Abstract Ouabain, digitoxin, ethacrynic acid and mercuric acetate, all of which block active sodium transport by inhibition of membrane ATPases, were implanted into various regions of the rabbit brain. The epileptogenic effect of these compounds was measured by electroence-phalographic recordings from various subcortical and cortical structures. Application of the drugs to the hypothalamus evoked seizure activity first in the hippo-campus and later in other subcortical regions and in the cortex. Conversely, implantation into the hippocampus elicited epileptic discharges first in the hypothalamus and later in other parts of the brain. The sensitivity to ouabain varied greatly from one region to another. The dorsal hippocampus responded to doses of 1 μg or less with spiking activity; in the thalamus, lateral geniculate body and caudate nucleus, 1–2 μg of the glycoside were necessary to evoke hippocampal and cortical seizures; however, in the mesencephalic reticular formation and in the frontal lobe, only doses of 50 μg were able to cause hippocampal and cortical discharges. On the other hand, the lethal effect of ouabain was about the same when applied to various subcortical structures ( ld 50 , about 50 μg), but in the frontal lobe only much larger doses proved fatal. Deposition of ouabain in solid form represents a useful method for the study of intracerebral connections. The present results suggest that in the rabbit brain, both the lateral geniculate body and the caudate nucleus are linked to the contralateral hippocampus.

NYSTAGMUS EVOKED FROM THE SUPERIOR COLLICULUS OF THE RABBIT.

Abstract From the superior colliculus of the rabbit, contraversive horizontal nystagmus can be evoked only under the influence of enhancing factors, such as exclusion of light, simultaneous optokinetic stimulation or application of subnarcotic doses of pentobarbitone. It is concluded that the superior colliculus forms part of the pathway of central as well as optokinetic nystagmus. Stimulation of the mesencephalic reticular formation enhances both central and optokinetic nystagmus. This effect is unspecific, i.e., direction-independent.

Central nystagmus under continuous and intermittent stimulation

Abstract Central nystagmus is produced by stimulation in the nystagmogenic area, situated in the mesodiencephalon of the rabbit. The response depends on the frequency of stimulation: Beyond the optimal frequency range the reaction is not sustained, but declines. Intermittent stimulation with appropriate spacing prevents this decay. Afternystagmus varies not only with the frequency of stimulation, but also with the length of the stimulation period: The after-reaction decreases if stimulation is extended beyond its optimal span. These observations can be explained by the assumption that stimulation in the nystagmogenic area activates both excitatory and inhibitory components of the nystagmus circuit, temporal summation of the inhibitory part displaying a lag relative to the excitatory component. The divergence in the time course of the two contributions to the nystagmus response may be accounted for by anatomical or functional differences.

Cerebral application of enkephalins.

Implantation of enkephalins A or B into the ventral thalamus or injection into the lateral ventricle of rats evoked only weak signs of stereotyped behavior, but did not cause gnawing.

Interaction of central and flash nystagmus

Abstract Central nystagmus is evoked in the rabbit by electrical stimulation of one optic pathway. The response is strongest in the dark and is depressed by illumination of the heterologous retina. Flash nystagmus results from intermittent photic stimulation of one eye. Combination of central nystagmus with synergistic flashing potentiates the response markedly. Combination with antagonistic flashing at a rate of 25–30/sec depresses central nystagmus strongly, but at 5–10/sec it breaks the inhibitory effect of illumination on central nystagmus and may raise the response to the level of the dark control.

Comparison of the influence of graded doses of phenothiazines and pentobarbitone on central nystagmus.

Abstract The effect of phenothiazines on central nystagmus depends on dosage. Small amounts (10–25 μg/kg) depress the response, while doses above 100 μg per kilogram produce a biphasic reaction, i.e., enhancement for 1 or 2 hours followed by prolonged depression. Similar gradation is found with pentobarbitone; its effects are however restricted to shorter periods. Different mechanisms are involved with these two types of drugs, as phenothiazines restore the nystagmus, suppressed by large doses of barbiturate, and vice versa. Interpretation of the results is based on the heterogeneity of the nervous elements in the nystagmus circuit.