Subcortical Electrical Activity Research Articles

Isoflurane blunts electroencephalographic and thalamic-reticular formation responses to noxious stimulation in goats.

Anesthetics, including isoflurane, depress the electroencephalogram (EEG). Little is known about the quantitative effects of isoflurane on EEG and subcortical electrical activity responses to noxious stimulation. The authors hypothesized that isoflurane would depress the results of EEG and subcortical response to noxious stimulation at concentrations less than those needed to suppress movement. Furthermore, determination of regional differences might aid in elucidation of sites of anesthetic action. Ten goats were anesthetized with isoflurane, and minimum alveolar concentration (MAC) was determined using a noxious mechanical stimulus. Depth electrodes were inserted into the midbrain reticular formation and thalamus. Needle electrodes placed in the skull periosteum measured bifrontal and bihemispheric EEG. The noxious stimulus was applied at each of four anesthetic concentrations: 0.6, 0.9, 1.1, and 1.4 MAC. At an isoflurane concentration of 0.6 MAC, the noxious stimulus activated the midbrain reticular formation, thalamic, and bifrontal-hemispheric regions, as shown by decreased high-amplitude, low-frequency power. For all channels combined (mean +/- SD), total (-33+/-7%), delta (-47+/-12%), theta (-23+/-12%), and alpha (-21+/-6%) power decreased after the noxious stimulus (P < 0.001); beta power was unchanged. At 0.9 MAC, total (-35+/-5%), delta (-42+/-7%), theta (-35+/-8%), and alpha (-23+/-11%) power decreased after the noxious stimulus (P < 0.001); beta power was unchanged. At 1.1 MAC only one site, and at 1.4 MAC, no site, had decreased power after the noxious stimulus. Isoflurane blunted EEG and midbrain reticular formation-thalamus activation response to noxious stimulation at concentrations (1.1 MAC or greater) necessary to prevent movement that occurred after noxious stimulation. It is unknown whether this is a direct effect or an indirect effect via action in the spinal cord.

Correlations between the functional state of the CNS and thyroid activity in chronic emotional stress

Cortical and subcortical electrical activity was recorded during chronic emotional stress in cats and the state of thyroid function determined. Correlation was found between the functional state of the CNS and the level of thyroxine secretion. The trigger role of the posterior hypothalamic nucleus in the genesis of hypersynchronized activity in stress was demonstrated.

Effect of lithium hydroxybutyrate on cortical and subcortical excitability in rabbits

Microinjections of lithium hydroxybutyrate (10 μg/μl) had a depriming action on spontaneous cortical and subcortical electrical activity. The compound reduced the excitability of the motor cortex, hippocampus, caudate nucleus, thalamus, posterior hypothalamus, and mesencephalic reticular formation; the excitability of the amygdala was increased. In its depriming effect, lithium hydroxybutyrate surpassed lithium chloride.

Cortical and subcortical electrical activity during the development of hypoxia from blood loss

Compatibility of depressed F-like plasmid FB1drd integrated into E. coli K12 cell chromosome with standard plasmids of FI-FVI compatibility groups was studied. The results obtained show that such plasmids can stably coexist in the same cell with plasmid FB1drd. On these grounds it is supposed that the latter belongs to the new compatibility group (FVII).

Electroencephalographic changes in hypo- and hypertensive responses to hypothalamic stimulation

Changes in cortical and subcortical electrical activity during hypo- and hypertensive vascular responses to electrical stimulation of the hypothalamus were investigated before and after injection of the monoamine oxidase inhibitor vetrazin, in experiments on rabbits anesthetized with urethane. Vetrazin completely blocked the hypertensive response and its electroencephalographic manifestation but had no effect on hypotensive hypothalamic responses. The results are interpreted from the standpoint of differences in the neurochemical mechanisms of hypothalamic pressor and depressor responses.

Magnesium: electroencephalographic and behavioral effects in cats.

Magnesium sulfate was given intravenously to eight cats with recording electrodes permanently implanted in the brain. The MgSO4 caused marked behavioral changes; yet, brief amplitude depression aside, cortical and subcortical electrical activity remained unchanged. Small doses of MgSO4 (25 mg/kg) caused retching only; larger doses (50 and 75 mg/kg) produced muscle paralysis and respiratory depression. Even so, there were no electroencephalographic signs of sedation or narcosis. Any anesthetic or analgesic action of magnesium is overshadowed by its neuromuscular blocking effect.

Changes in correlation functions of cortical and subcortical electrical activity in various stages of anesthesia

Changes in correlation functions of cortical and subcortical electrical activity in various stages of anesthesia

Effects of lidocaine on spontaneous cortical and subcortical electrical activity. Production of seizure discharges.

ALTHOUGH the actions of local anesthetics on the peripheral nervous system have been studied in detail for a number of years, 1-6 only relatively recently has attention been focused on the central effects produced when these agents are given intravenously. This recent interest is due in great measure to the current use of lidocaine (Xylocaine) as an anticonvulsant 7-9 and as an adjunct in general anesthesia. 10-12 An action of the local anesthetics which is difficult to relate to these effects is the production of convulsions in animals 9,13-16 and man 17,18 when higher doses are administered. The effects of intravenously administered lidocaine and other local anesthetics on the electroencephalogram recorded from the surface have been described in cat, 13 rabbit, 16 monkey, 9 and man. 18,19 The effects of the drug upon subcortical activities have not been thoroughly studied. Lesse and Gault 20 described an alteration in amygdaloid

Note on the ganglionic and central actions of galantamine.

Abstract The actions of galantamine on ganglionic transmission in the superior cervical ganglion of the cat and the spontaneous bioelectrical activity of the brain were investigated and compared with those of physostigmine. Galantamine prevented ganglionic blockade due to C 6 more strongly than physostigmine and increased ganglionic depolarization induced by acetylcholine. This compound caused periodic asynchronous postganglionic firing in the cat superior cervical ganglion. It is suggested that the mechanism of action of galantamine resembles that of neostigmine rather than that of physostigmine and is not limited to the excitation of “muscarinic cholinoceptive sites” alone. Galantamine administered intravenously in unanaesthetized cats caused a marked desynchronization of cortical and subcortical electrical activity, which was completely abolished by atropine or benactyzine.

Effect of imipramine, physostigmine and amphetamine on the electrical activity of the brain in the cat.

The results of the interaction of imipramine, physostigmine and d/l amphetamine in various intravenously administered dosages were studied on the cortical and subcortical electrical activity of cats.

Effect of hydrocortisone on electrical activity, arousal thresholds and evoked potentials in the brains of chronically implanted rabbits

The effects of intravenously administered hydrocortisone succinate on cortical and subcortical electrical activity, arousal thresholds, evoked potentials and their neuronal recovery were studied in the brains of unrestrained rabbits with chronically implanted electrodes in the cortex, hippocampus, amygdala, septum, hypothalamus and midbrain reticular formation. Hydrocortisone caused in various animals the appearance of prolonged electrical arousal, generalized slowing, spikes, fast activity in the amygdala and localized epileptic discharges in the ventromedian hypothalamus and septum. These were followed by spread of seizure activity to other structures and generalized bursts of epileptic activity. No behavioural seizures were observed in these animals. The hormone caused an increase in the amplitude of potentials evoked by central and photic stimulation in these forebrain regions. Hormone administration also enhanced neuronal excitability and shortened the recovery cycle of these responses. Hydrocortisone had no effect on electrical arousal thresholds following high frequency stimulation of the reticular formation. The clinical and experimental literature on central nervous system effects of adrenocortical hormones and their mode of action is briefly reviewed. The present results would suggest that the adrenocortical hormones affect the central nervous system through their direct action on forebrain and related limbic structures.

Circadian sleep and waking patterns in the laboratory cat

Eight adult cats were observed for repeated 23 h periods spent in an experimental chamber under stable environmental conditions. Behavior, EEG, subcortical electrical activity and somatic muscle discharge were continuously monitored during these observations. On the basis of the total information obtained from the collection of these data, four basic behavioral-electrophysiological patterns were defined: (a) awake, activated; (b) drowsy, slow wave; (c) asleep, spindle burst; and (d) asleep, activated, and each minute of recording was classified according to its dominant pattern. Analysis of these data disclosed several quantitative measures which were highly consistent both for a given animal and among the animals observed. These were: (1) The percentage occurrence of each of the patterns during a 23 h period. The group means and standard deviations were: awake, 28 ± 4.2%; drowsy, 14.3 ± 1.2%; spindle burst sleep, 42.2 ± 4.1%; and activated sleep, 15.5 ± 2.2%. The percent of total sleep time for activated sleep was 27.5%. (2) Pattern percentage in relation to time: a general periodicity in the occurrence of sleeping and waking patterns indicated reciprocal peaks related to specific time periods. During the peak occurrence of the sleep patterns, a sleep EEG cycle of 25.8 ± 7.1 min was determined. Other interesting electrophysiological characteristics of the observed patterns were noted, including transitional phenomena associated with their respective interactions. It is suggested that the stable percentage data provide the basis for a statistical approach to the experimental study of sleep mechanisms.

Pharmacological properties of 1-(4-methoxybutylamino)-2-(1-4-benzodioxan-2-yl)-ethane (2802 IS).

The pharmacological properties of 1-(4-methoxybutylamino)-2-hydroxy-2-(1,4-benzodioxan-2-yl) ethane (2802 IS) are described. 2802 IS when administered by vein to anesthetized dogs and cats in doses of 0.025-0.05 mg/kg lowered the blood pressure. In an instrumental reward discrimination exercise in rabbits the depressant effects of the compound were demonstrated at 0.25-0.5 mg/kg i.v. 2802 IS provokes significant changes of the cortical and subcortical electrical activity of the unanaesthesized rabbit and a dampening of the arterial pressure response to the electrical stimulation of the hypothalamus. The site of action of the central effect of the compound is discussed.

Action de la chlorpromazine, de la prochlorpémazine et de la lévomépromazine sur l'électroencéphalogramme et sur le comportement du lapin

The cortical and subcortical electrical activity of the rabbit has been recorded with implanted electrodes. The records were studied in normal unrestrained animals under the influence of various sensory stimuli, during spontaneous movements and mastication. The influence of three derivatives of phenothiazine, i.e. chlorpromazine, levomepromazine and prochlorpemazine was investigated. Levomepromazine was most active as judged by the influence on the EEG; already in feeble doses it caused synchronisation of the EEG and there was no response to wakening stimuli; prochlorpemazine on the other hand appeared to be the least active of the 3 products. These findings are discussed and compared with data obtained with other experimental methods and by clinical observation.

Cortical and rhinencephalic electrical potentials during hypoglycemia.

Observations on EEG changes during insulin hypoglycemia were initiated by Hoagland et al., 1 who noted the disappearance of alpha waves in schizophrenics subjected to insulin hypoglycemic treatment. Himwich and associates 2 found that the disappearance of the alpha waves occurred at the time the patient loses environmental contact. In a series of observations on dogs, Hoagland and co-workers 3 reported that subcortical waves continued after the cortical undulations had disappeared. Differences between cortical and subcortical electrical activity in hypoglycemic rabbits have also been disclosed in the work of Tokizane and Sawyer, 4 who observed seizure patterns in subcortical areas, i. e., amygdala and hippocampus, when the cortical recordings were devoid of such hyperactivity. Further analysis of the differential cortical and subcortical electrical potentials of cats made by Fernandez and Brenman 5 revealed that the auditory cortex retained the evoked response to the click stimulus even in very pronounced hypoglycemia,

Contribution à l'étude des rapports entre le potentiel réticulaire évoqué, l'état d'anesthésie et l'activitéélectrique cérébrale

The present paper reports the results obtained in studying the influence of some drugs on the reticular responses and on the EEG pattern, in order to obtain data on the correlations between peripherally evoked reticular potentials, the mediation of the electrocortical arousal response and the anesthetic state. The experiments were undertaken in unanesthetized non-curarized rabbits. The response to single sciatic stimulations were recorded at various reticular levels, together with cortical and subcortical electrical activity. With pentobarbital (Nembutal) an inhibition of the reticular potential together with EEG synchronization was found, but blocking of the EEG arousal reaction to external stimulation appears before the disappearance of the reticular potential. With ether the inhibitory action of the evoked reticular response is connected to the anesthetic state, but is independent from cortical synchronization. On the other hand with scopolamine, it is possible to obtain an EEG synchronization with blocking of arousal to external stimuli without impairment of the reticular response to single sciatic shock. It seems reasonable to assume that the anesthetic state is not necessarily related to the slowing of EEG activity, blocking of the EEG “arousal response” or alteration of the reticular response to single sensory stimulation.

Pharmacology of the psychotherapeutic drug benactyzine (beta-diethylaminoethyl benzilate hydrochloride).

SummaryBenactyzine (β-diethylaminoethyl benzilate hydrochloride) an antispasmodic that has been used in the treatment of psychoneuroses causes hyperexcitability and clonic convulsions in animals. A taming effect was not observed. Hesobarbital anesthesia was markedly prolonged. the effects of acetylcholine on the isolated gut and blood pressure diminished and the action of epinephrine on blood pressure enhanced by this compound. Spinal reflexes were not affected and cortical and subcortical electrical activity was slowed. Mice receiving benactyzine often died during electroshock seizures which were tolerated by normal animals.

Subcortical electrical activity in the golden hamster during arousal from hibernation

1. 1. Results of a systematic electrical exploration of cerebral hemispheres and brain stem in golden hamsters ( Mesocricetus auratus) arousing from hibernation are presented. 2. 2. Three types of subcortical electrical activity were recorded during the process of arousal, namely ( a) transient, regular, initially 17/sec. activity, ( b) fairly continuous waves, and ( c) activity in bursts. 3. 3. The electrical activity recorded was confined to components of the limbic system and its presumed descending efferents. Olfactory bulbs, corpus striatum, thalamus, and anterior hypothalamus were conspicuously quiescent. 4. 4. These findings appear consistent with contemporary theories of the function of the limbic system and would serve to account for the apparent agitated state of the hamster immediately upon full arousal from hibernation. 5. 5. It is concluded that the process of arousal in the golden hamster is initiated when the limbic system is activated either directly or indirectly by afferent impulses from the periphery.

Cortical and subcortical electrical activity in experimental seizures induced by metrazol.

An electroencephalographic study has been made of both cortical and subcortical activity occurring in the brain of the cat during seizures produced by convulsive doses of metrazol and by auditory stimuli or direct stimulation of thalamic nuclei in the presence of subthreshold doses. The effect upon this activity of various lesions was also observed. The seizure induced by threshold doses of metrazol appeared, by every test, to be primary in the cerebral cortex and to radiate from it to deep structures. Prominent activity in the internal capsule, basis pedunculi, subthalamus and midbrain tegmentum appeared to represent discharge descending to motor outflows. The basal ganglin did not display conspicuous seizure activity. The thalamus was prominently involved, its sensory relay nuclei exhibiting the most marked seizure discharge, paralleling that in related cortical areas. Associational thalamic nuclei were next most affected. The nuclei of the diffuse thalamic projection system were implicated later than their neighbors and manifested a markedly different type of activity, resembling giant spindle bursts. The possibility is suggested that this may be associated with loss of consciousness in seizures. With subconvulsive doses of metrazol, repetitive afferent stimulation led to development of a complex evoked potential in the receiving cortex, to its irradiation to other cortical area and, finally, to seizure induction. This series of events could still be provoked after destruction of the thalamus, except for the relay nucleus of the sensory pathway involved. It could be reproduced by direct stimulation of the thalamic sensory relay nuclei, but not the nuclei of the diffuse thalamic projection system. It was abolished by ablating the sensory receiving area of the cortex. The ascending sensory pathway and the cerebral cortex itself seem to be the only structures essentially involved in such seizure induction.