Electrical Activity In Rats Research Articles

In vivo multi-channel measurement of electrical activity of the non-pregnant rat uterus.

In the uterus, the characteristics of smooth muscle contraction and the electrical activity that drives this contraction depends on hormonal cycles, and pregnancy status. Smooth muscle contraction is initiated by a change in membrane electrical potential, due to the flux of ions in and out of the intracellular space. Chains of action potentials throughout a section of muscle can result in coordinated contraction events. In this study, flexible printed circuit electrode arrays were applied to measure the bioelectric signals on the surface of a rat uterus in vivo. Variations in the electrical activity were quantified, including intermittent periods of activity and inactivity, which contain both slow-wave type activity (0.039 Hz ±0.017 Hz) and faster, spike-like activity (3.26 Hz ±0.27 Hz). The spike activity initiated at the ovarian end of the uterine horn, spreading towards the cervical end with a propagation velocity of 5.34 ± 2.32 mm [Formula: see text]. In conclusion, this pilot study outlines a new method of in vivo measurement of uterine electrical activity in rats. Clinical Relevance- Measurement of bioelectrical data using in vivo techniques provides insight into the electromechanical function of uterine smooth muscle, which could provide insights into what drives coordinated contraction in the uterus.

A Method for Chronic Registration of Brain Cortical Electrical Activity in Rats

A Method for Chronic Registration of Brain Cortical Electrical Activity in Rats

Effects of Alpha-2 Adrenergic Agonist Mafedine on Brain Electrical Activity in Rats after Traumatic Brain Injury.

The search for and development of new neuroprotective (or cerebroprotective) drugs, as well as suitable methods for their preclinical efficacy evaluation, are priorities for current biomedical research. Alpha-2 adrenergic agonists, such as mafedine and dexmedetomidine, are a highly appealing group of drugs capable of reducing neurological deficits which result from brain trauma and vascular events in both experimental animals and human patients. Thus, our aim was to assess the effects of mafedine and dexmedetomidine on the brain’s electrical activity in a controlled cortical-impact model of traumatic brain injury (TBI) in rats. The functional status of the animals was assessed by electrocorticography (ECoG), using ECoG electrodes which were chronically implanted in different cortical regions. The administration of intraperitoneal mafedine sodium at 2.5 mg∙kg−1 at 1 h after TBI induction, and daily for the following 6 days, restored interhemispheric connectivity in remote brain regions and intrahemispheric connections within the unaffected hemisphere at post-TBI day 7. Animals that had received mafedine sodium also demonstrated an improvement in cortical responses to photic and somatosensory stimulation. Dexmedetomidine at 25 μg∙kg−1 did not affect the brain’s electrical activity in brain-injured rats. Our results confirm the previously described neuroprotective effects of mafedine sodium and suggest that ECoG registration and analysis are a viable method evaluating drug efficacy in experimental animal models of TBI.

Omega-3 effects on electrocorticographic patterns of adult Wistar rats exposed to ionizing radiation

This study aimed to assess the effect of supplementation with omega-3 in Wistar rats exposed to ionizing radiation in a dose of 18 Gy on the cortical electrical activity, using mathematical methods such as the power spectrum (PS) and the detrended fluctuation analysis (DFA) in the evaluation of the electrocorticogram (ECoG) record. The PS analysis showed that in non-irradiated animals but supplemented with omega-3 there was a decrease in the power of the beta rhythm, while the DFA applied to different frequency ranges of the ECoG showed a significant increase in the long-range correlation only for the theta wave when compared with non-supplemented animals. In the evaluation of the radiation effect through the PS, an increase in the power of the theta rhythm was observed in both groups (non-supplemented and supplemented animals) only when they were evaluated one week after irradiation. The DFA method also showed difference in this wave. The PS and DFA methods applied to the ECoG record allowed a quantitative analysis of the cortical electrical activity in rats in response to the omega-3 effects, ionizing radiation, or both.

A Simple and Efficient Methodology for the Study of Cardioprotective Drugs in Animal Model of Cardiac Ischemia-Reperfusion

To study cardioprotective drugs, we developed a simple and efficient methodology to evaluate effects of drugs on cardiac electrical activity using electrocardiogram (ECG) in rats submitted to cardiac ischemia-reperfusion (I/R). Using adult male Wistar rats (14 - 16-week-old) anesthetized (urethane 1.25 g/kg, i.p.) and kept under mechanical ventilation, we used surgical procedures to induce cardiac I/R by means mechanical occlusion of left anterior descendent coronary artery for 10 min (ischemia) with silk suture (tourniquet) followed by its removal to allow coronary recirculation (reperfusion). To evaluate the effects of surgical process, a group of rats (SHAM-operated) was submitted to surgical procedures previously described, but without coronary occlusion. To evaluate cardiac electrical activity in rats submitted to cardiac I/R and SHAM-operated, the ECG system was coupled to animal body to determine the incidence of ventricular arrhythmia (VA), atrio-ventricular blockade (AVB) and lethality (LET). To evaluate injury biomarkers production in rats submitted to cardiac I/R and SHAM-operated, serum concentrations of creatine kinase fraction (MB/CK-MB) and troponin I were determined by biochemical techniques. Using the methodology proposed in this work, we observed that VA, AVB and LET incidence was significantly higher in cardiac I/R group (85%, 79% and 70%, respectively) than in SHAM-operated group (0%, 0% and 0%, respectively). Serum levels of CK-MB and troponin I were also significantly higher in cardiac I/R (1,850 ± 222 U/L and 0.031 ± 0.009 ng/mL, respectively) compared to SHAM-operated group (808 ± 72 U/L and 0.200 ± 0.027 ng/mL). To evaluate efficiency of methodology proposed in this work to study the effect of cardioprotective drugs, the effects of the L-type Ca2+ channel blocker (CCB) nifedipine (30 mg/kg, intravenously - IV) in rats submitted to cardiac I/R were studied. The treatment with nifedipine (before ischemia) significantly reduced the incidence of VA (from 85% to 28%), AVB (from 79% to 14%), and LET (from 70% to 14%). These results indicate that the methodology described in the present work is simple, and efficient, to evaluate cardiac functional and biochemical alterations induced by cardiac I/R, and also the study of cardioprotective drugs in rats. This methodology could contribute to the development of new pharmacological cardioprotective strategies for to treatment of ischemic cardiac diseases in humans, such as myocardial infarction.

Direct detection of optogenetically evoked oscillatory neuronal electrical activity in rats using SLOE sequence

The direct detection of neuronal electrical activity is one of the most challenging goals in non-BOLD fMRI research. Previous work has demonstrated its feasibility in phantom and cell culture studies, but attempts in in vivo studies remain few and far between. Most recent in vivo studies used T2*-weighted sequences to directly detect neuronal electrical activity evoked by sensory stimulus. As neuronal electrical signal is usually comprised of a series of spectrally distributed oscillatory waveforms rather than being a direct current, it is most likely to be detected using oscillatory current sensitive sequences. In this study, we explored the potential of using the spin-lock oscillatory excitation (SLOE) sequence with spiral readout to directly detect optogenetically evoked oscillatory neuronal electrical activity, whose main spectral component can be manipulated artificially to match the resonance frequency of spin-lock RF field. In addition, experiments using the stimulus-induced rotary saturation (SIRS) sequence with spiral readout were also performed. Electrophysiological recording and MRI data acquisition were conducted on separate animals. Robust optogenetically evoked oscillatory LFP signals were observed and significant BOLD signals were acquired with the GE-EPI sequence before and after the whole SLOE and SIRS acquisitions, but no significant neuronal current MRI (ncMRI) signal changes were detected. These results indicate that the sensitivity of oscillatory current sensitive sequences needs to be further improved for direct detection of neuronal electrical activity.

Dynamics of the Indices of Electrohippocampogram Recorded from Rats under Conditions of Long-Lasting Stress: Effects of Modulators of Synaptic Transmission

We studied the effects of modulation of the activity of noradrenergic and GABA-ergic cerebral transmitter systems on the hippocampal electrical activity in rats during long-lasting (21 weeks) stress induced by a zooconflict situation. The background field electrical activity of the hippocampus (electrohippocampogram, EHcG) was recorded from control and stressed rats in the state of residual ketamine-barbiturate anesthesia. We used injections of the following modulators of central neurotransmission: amitriptyline, aminazine, and carbamazepine, which are extensively used in clinics for intensification of the activity of the antistress GABA system based on the influence of these agents on the monoaminergic cerebral systems. Under such conditions, we found the two-phase dynamics of spectral powers of EHcG components. In the first phase, where changes in the excitatory influences on central neurons prevailed, the total power of EHcG oscillations and spectral powers of its components were significantly lower with respect to the control, while in the second phase we observed rapid increases in the above indices, which probably resulted from parallel hyperactivation of both excitatory and inhibitory (GABA-ergic) elements of neuronal networks of the hippocampus. In rats forming the groups for comparison (control animals and stressed ones with no injections of synaptic modulators), changes in the powers of EHcG oscillations during the 21-week-long experiment waves were three-phase; in the latter animal group, the above characteristics differed from each other mostly quantitatively. Such changes in stressed rats with respect to the control ones could reflect modulation of the mediator/hormonal influences on hippocampal neurons during three phases of the stress reaction of the organism.

Changes in spectral measures of brain electrical activity in rats after transection of the sciatic nerve

Electrophysiological measures of brain electrical activity were studied in rats during the development of neurogenic pain syndrome induced by transection of the sciatic nerve. At the peak of development of pain syndrome, three weeks after deafferentation, rearrangements in the spectra of electrical activity were seen in the limbic structures of the brain (hippocampus, amygdala, nucleus accumbens), in the frontal areas of the neocortex, and in the caudate-putamen complex: changes consisted of increases in the relative power of the delta and alpha ranges as compared with controls, along with a decrease in relative power in the beta-2 range. Changes in spectral measures of electrical activity in the limbic structures of the brain occurred independently of the clinical manifestations of neurogenic pain syndrome (autotomy). The increase in relative power in the alpha range of the spectrum of electrical activity in all the structures studied suggests that the reticular nucleus of the thalamus is involved in the pathogenetic mechanisms of neurogenic pain syndrome.

Effects of L-Arginine on Electrical Activity in Rats Subjected to Cerebral Ischemia-Reperfusion

Event Abstract Back to Event Effects of L-Arginine on Electrical Activity in Rats Subjected to Cerebral Ischemia-Reperfusion D. Tekin1, Asli Zengin1*, R.B Yildiz1, C. Kayacilar1, A. Nurten1 and I. Kara1 1 Istanbul University, Turkey Nitric oxide (NO) is an important endogenous vasodilatator, which has a variety of physiological and pathological effects in biological system. NO acts as an arterial vasodilator, synthesized from L-arginine by the enzyme nitric oxide synthase, is a biological mediator that facilitates perfusion to affected areas during ischemia-reperfusion (I/R). In present study, we investigated the effects of L-arginine on electrical activity of the hippocampal CA1 areas in rats subjected to cerebral I/R. Male Wistar albino rats, anaesthetized with thiopental (50 mg/kg i.p.), were implanted with electrodes in CA1 areas in stereotaxic apparatus bilaterally. One week after operation, continuous EEG recordings were taken under anesthesia for five minutes. Animals were divided into two groups as saline treated control group (n=6) and L-arginine treated (30 mg/kg i.p.) L-arginine group (n=6). One day after injection, bilateral carotid arteries of all animals were clamped. Thirty minutes after occlusion, clamps were re-opened and EEG recordings were taken in following ten minutes. Continuous EEG recordings were divided into 2-second epochs and analyzed by averaged frequency spectra (0.5-50 Hz) then two tailed paired Student’s t-test was applied. In control group animals, I/R induced the increase in amplitude of low frequency bands and decrease in amplitudes of high frequency bands in CA1 regions significantly compared to basal values. In L-arginine group animals, the electrical activities of CA1 regions in I/R have similar effects to control group animals. This study showed that acute treatment of 30 mg/kg L-arginine, before to the rats subjected to I/R, has no protective effects on electrical activity on hippocampal CA1 regions. Conference: 10th International Conference on Cognitive Neuroscience, Bodrum, Turkey, 1 Sep - 5 Sep, 2008. Presentation Type: Poster Presentation Topic: Animal Models of Cognition Citation: Tekin D, Zengin A, Yildiz R, Kayacilar C, Nurten A and Kara I (2008). Effects of L-Arginine on Electrical Activity in Rats Subjected to Cerebral Ischemia-Reperfusion. Conference Abstract: 10th International Conference on Cognitive Neuroscience. doi: 10.3389/conf.neuro.09.2009.01.082 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 02 Dec 2008; Published Online: 02 Dec 2008. * Correspondence: Asli Zengin, Istanbul University, Istanbul, Turkey, aslizenginn@yahoo.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers D. Tekin Asli Zengin R.B Yildiz C. Kayacilar A. Nurten I. Kara Google D. Tekin Asli Zengin R.B Yildiz C. Kayacilar A. Nurten I. Kara Google Scholar D. Tekin Asli Zengin R.B Yildiz C. Kayacilar A. Nurten I. Kara PubMed D. Tekin Asli Zengin R.B Yildiz C. Kayacilar A. Nurten I. Kara Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Effect of artemether on pentobarbitone sleep and electrical activity in rats

Artemether (AM), a highly effective treatment for multidrug-resistant malaria and a component of artemisinin combination therapy, has been associated with some neurotoxicity following repeated high doses. This study was aimed at investigating the effect of AM on pentobarbitone sleep and electrical activities in rats. Wistar rats received AM i.p. at 3 dose levels: 1.5, 7.5, and 15 mg/kg, whereas control rats received 0.2 mL of the vehicle (3% v/v Tween 80). AM administered 20 min before pentobarbitone had no significant effect on the onset and duration of sleep. However, after a 7-day pretreatment, AM dose-dependently prolonged pentobarbitone sleep, as did chloramphenicol. Electroencephalogram and electromyogram recordings 20 min after pretreatment showed that AM (15 mg/kg) exhibited inhibitory activity similar to chlorpromazine as opposed to the excitatory effect of amphetamine. When pretreated for 7 days, rats receiving 1.5 mg/kg AM also showed inhibitory activity of the cortical centres, whereas desynchronization of the optic tectum and reticular formation was observed in rats pretreated with 7.5 and 15 mg/kg AM. The present data suggest that although the therapeutic equivalent dose of 1.5 mg/kg AM had no appreciable effects on pentobarbitone sleep but caused reduced electrical activity in rats, higher doses have more profound effects on both indices.

Actions of pulsed ultra-broadband electromagnetic irradiation on the EEG and sleep in laboratory animals

Irradiation of animals with ultrashort impulses of ultra-broadband magnetic irradiation with an impulse repetition frequency of 6 Hz for 1 h induced changes in the spectral composition of cerebral cortex electrical activity in rats, measured over the 5 min immediately after irradiation, as compared with controls. In particular, there was suppression of frequencies close to the impulse sequence frequency, along with a decrease in interhemisphere coherence. Continuous recording of polygrams for 22 h from rabbits after irradiation revealed a "delayed" effect--a significant increase in paradoxical sleep, starting 16 h after the end of irradiation and persisting to the end of the recording period. It is suggested that irradiation has a direct action both on the mechanisms of generation of the theta rhythm (septohippocampal) and on the system controlling circadian rhythms (the suprachiasmatic nucleus-epiphysis system).

Acute social stress and cardiac electrical activity in rats

This paper summarizes the results of experiments aimed at describing electrocardiographic responses to different acute social stressors in healthy male rats. Electrocardiograms were telemetrically recorded during maternal aggression, social defeat, and psychosocial stimulation, as obtained using the classical resident-intruder paradigm. Autonomic input to the heart was indirectly evaluated by means of heart rate variability measures and plasma catecholamine level determinations. Social stressors produced changes in cardiac electrical activity that were markedly higher than those observed in nonsocial challenging conditions such as novelty and restraint. Defeat, which produced the highest catecholaminergic responses, was the most potent as a social aversive experience in inducing heart rate accelerations and arrhythmias, particularly when applied to a wild-type strain of rats. The far most frequent arrhythmic events were ventricular and supraventricular premature beats, either as isolated events or grouped. Ventricular premature beats usually occurred immediately after attacks and in association with higher heart rate values and lower heart rate variability scores. The relationships between the type of stressor used (either social or nonsocial), the different contributions of the emotional and physical components of stress response, the resulting modulation of autonomic control over cardiac electrical activity, and the incidence of arrhythmic events are discussed. Aggr. Behav. 24:287–296, 1998. © 1998 Wiley-Liss, Inc.

The role of 5-HT 1A serotonin and D 2 dopamine receptors in buspirone effects on cortical electrical activity in rats

The effects of buspirone (5 and 10 mg/kg i.p.), 8-OH-DPAT (0.25 mg/kg) and raclopride (2.5 mg/kg) on the EEG power spectra of the sensorimotor cortex were studied in freely moving rats. Buspirone (5 mg/kg) and 8-OH-DPAT produced selective slowing of the theta-activity. Buspirone (10 mg/kg) produced slowing of the theta-activity and increased the power of the alpha-band (9–11 Hz). Raclopride alone did not influence EEG power spectra. Simultaneous injection of 8-OH-DPAT and raclopride produced marked slowing of the theta-activity and increased the power of the alpha-band. The role of 5 HT 1A and D 2 dopamine receptors in buspirone effects on cortical electrical activity in rats was discussed.

Changes in cerebral cortical electrical activity in rats with compression of the infraorbital nerve

Changes in cerebral cortical electrical activity in rats with compression of the infraorbital nerve

Effect of enantiomers of deprenyl (selegiline) and amphetamine on physical abuse liability and cortical electrical activity in rats

In the present study, whether the repeated administration of (−)deprenyl to rats resulted in physical dependency was investigated. In a second experiment, the effect of (−)-deprenyl was investigated on the cortical electrical activity of freely moving rats and last, the influence of (−)-deprenyl on the behaviour of the animals was studied. In all experiments, different stereospecific configurations of amphetamine and deprenyl were also employed in order to establish differences and similarities. During and after the chronic oral administration of (−)-deprenyl (4 mg/kg) over 6 weeks, no signs of physical dependency were observed in rats after withdrawal of the drug. By contrast, (+)-deprenyl (5 mg/kg, p.o.) and (+)-amphetamine (5 mg/kg, p.o.) induced typlcal symptoms of amphetamine-dependency: during withdrawal of drug, the body weight of the rats was increased. A similar phenomenon was observed after oral administration of (±)-amphetamine (6 mg/kg, p.o.). After a single oral administration of (−)-deprenyl (1 and 5 mg/kg) and (−)-amphetamine (10 mg/kg, p.o.), decreases in delta and increases in theta frequency bands in the EEG were observed. In contrast, (+)-amphetamine (1 mg/kg, p.o.), (±)-amphetamine (5 mg/kg, p.o.) and (+)-deprenyl (1 and 5 mg/kg, p.o.) evoked increases in the mean power values in delta and decreases in theta frequency bands. In agreement with the EEG studies, the (-) and (+)-isomers of amphetamine and deprenyl caused differences in the behaviour of the animals. Based on these findings, it can be concluded that (−)-deprenyl undergoes a stereospecific metabolism in the organism and the amounts of its metabolites with (+) configuration might be negligible, even at the larger doses which are necessary to inhibit monoamine oxidase-B (MAO B) in brain.

Effects of atropine upon the hippocampal electrical activity in rats with special reference to paradoxical sleep

In freely moving male rats with implanted electrodes, the influence of atropine sulphate (5–30 mg/kg, i.p.) on the hippocampal theta activity was studied with special emphasis on paradoxical sleep (PS). In accordance with previous work with cats and rabbits, atropine was found to inhibit PS, in delaying its first appearance as well as in decreasing the duration of the first PS episode. The hippocampal theta activity during PS was also changed after atropinization. In particular, when REM occurred often, theta activity was increased not only in frequency but also in amplitude; however, with no or little REM, theta frequency was not changed but the regularity of theta rhythms was markedly disturbed. These findings are in contrast with the theta activity associated with gross body movement, which was not affected by atropine as was previous reported by Vanderwolf (1975). Thus, in contrast to commonly held views, the hippocampal theta activity during gross body movement may be different in its underlying mechanisms from that during PS.

Desynchronization of electrical activity in rats induced by deprenyl--an inhibitor of monoamine oxidase B--and relationship with selective increase of dopamine and beta-phenylethylamine.

Electrophysiological and biochemical effects of deprenyl and beta-phenylethylamine were studied in rats. d,1-Deprenyl, 1-deprenyl (4-6 mg/kg) and beta-phenylethylamine (75 mg/kg) induced a desynchronization of ECOG after i.p. administration of drugs. The effects lasted several hours. The biochemical analysis indicate that d,1-deprenyl (4 mg/kg) nearly doubled the concentration of brain dopamine (DA) while the concentration of noradrenaline was not altered. The maximal increase was reached at 60 min and the enhanced concentration of DA stayed at this level up till 180 min after administration of drug. Treatment of rats with alpha-methyl-p-tyrosine (200 mg/kg) did not antagonize a deprenyl induced desynchronization of ECOG. However, even low dose of haloperidol (0.1 mg/kg) abolished the arousal effect of d,1-deprenyl and beta-phenylethylamine. It is suggested that desynchronization of EEG induced by deprenyl is more likely due to increased endogenous beta-phenylethylamine than to increased concentration of endogenous DA in the brain.

Analysis of preseizure electrocorticographic changes in rats during hyperbaric oxygenation

The most defined and reproducible electroencephalographic manifestation of oxygen poisoning in animals culminates in a generalized synchronous electrical discharge and very often in clinical convulsions. The amplitude and frequency of the electrocortical activity (EEG) in the preseizure phase was studied in unanesthetized rats during exposure to hyperbaric oxygen. The preseizure EEG (electrocorticogram) of rats breathing 6 ATA (atmospheres absolute) oxygen showed reduction in the mean frequency starting 7 min before the appearance of the first electrical discharge and a decrease of the mean amplitude starting about 3 min before the onset of the first electrical discharge. Our findings demonstrated that there is a progressive deterioration of the cortical electrical activity in rats exposed to high oxygen pressure. This suggests that the toxic effect of oxygen on the brain is cumulative and interferes with its normal metabolic and electrochemical processes.

Effects of dexamethasone and stressful stimuli on hypothalamic electrical activity in rats with diencephalic islands.

Electrical activity in the hypothalamus was recorded following dexamethasone administration to intact and diencephalic-island animals. In intact animals, dexamethasone produced an equal number of increases or decreases in unit resting firing frequencies. At least half of these rate changes were accompanied by alterations in EEG. Of the units tested in the basal hypothalamus of diencephalic-island animals, 50 % were inhibited by dexamethasone within a 10–15 minute period, 9% showed an increased firing rate, and the remainder were unresponsive. The results indicate a direct effect of the hormone on neurons in the isolated basal hypothalamus. Hypothalamic electrical activity was also recorded following the administration of vasopressin and histamine, two agents known to activate the adrenocortical system. The compounds uniformly produced rapid inhibition in unit firing in both intact and diencephalic-island animals. Thus, compounds with opposite actions on ACTH secretion, i.e., dexamethasone or vasopressin and histamine, produce the same inhibitory effect on the firing rate of hypothalamic neurons.

Efeitos do pentobarbital sódico sobre a atividade elétrica cerebral do rato com lesões da formação reticular mesencefálica

Para êste estudo foram empregados 35 ratos da raça Wistar em preparação aguda (24 com lesão bilateral e 11 com lesão unilateral) da formação reticular mesencefálica e 18 preparações crônicas. O método empregado na obtenção das preparações foi descrito em trabalho anterior12. O objetivo desta série de experiências foi o de verificar de que maneira o pentobarbital interfere sobre as características da atividade elétrica cortical após lesão da formação reticular mesencefálica. Para tal, em animais preparados agudamente, foram feitas lesões progressivamente mais extensas e o barbitúrico injetado por via intravenosa em doses crescentes. A fim de testar a integridade do sistema reticular ativador ascendente, além de estímulos dolorosos intensos, aplicávamos pulsos de 5 a 10 V, 100 Hz, e 0,1 ms à formação reticular mesencefálica situada abaixo da região lesada. A ausência de reação de alerta cortical (dessincronização) nos assegurava que tal sistema havia sido lesado completamente. Nas preparações crônicas o pentobarbital era injetado por via intraperitoneal. Dessas experiências concluimos o seguinte: 1. Aumento da sincronização do eletrocorticograma nos animais com lesões parciais ou totais da formação reticular mesencefálica. 2. Depressão acentuada e precoce da atividade elétrica cerebral nos ratos com lesão muito extensa (comprometendo também a porção ventrobasal do tálamo). 3. Isocronismo da atividade elétrica cortical nos dois hemisférios cerebrais. 4. O pentobarbital parece agir tanto sobre os sistemas ativadores como sobre o sincronizador do eletrocorticograma. As doses pequenas deprimem os primeiros, liberando o segundo, enquanto que as maiores bloqueiam também este último. Sòmente doses muito mais altas é que fazem desaparecer totalmente a atividade do córtex cerebral, que se mostra, portanto, mais resistente à ação da droga.