Direct Cortical Response Research Articles

Spread of transcallosally evoked responses in immature association cortex

Stimulation of the anterior middle suprasylvian gyrus (AMSG) in kittens (newborn to 6 weeks of age) elicits maximal transcallosally evoked responses (TCR) from homotopic sites in contralateral AMSG and smaller responses at variable distances from the site of homotopic registration. Distant (nonhomotopic) TCRs survive incisions of cortex around the site of stimulation which preserve callosal projections but interrupt lateral connections of the site of stimulation with other regions of AMSG. Nonhomotopic responses may be differentially enhanced or suppressed by changes in stimulus parameters or when conditioned by direct cortical responses. These observations indicate that nonhomotopic TCRs are generated by spread of synaptic activity linearly along the AMSG from homotopic projection sites. In kittens less than 3 weeks old spread of TCRs along the AMSG occurs with greater facility when stimulation is applied to contralateral rostral portions of AMSG than when caudal regions are stimulated. Thus in very young kittens activity generated by TCRs spreads preferentially in a rostral-to-caudal direction. This situation is reversed in kittens older than 3–4 weeks. This reversal of the polarity of preferred spread of TCRs occurs in the late postanatal period and constitutes a maturational event that may be related to the functional development of interhemispheric transactions in association cortex.

The effect of morphine on primary somatosensory evoked responses in the rat cerebral cortex

Primary somatosensory potentials were evoked in the cerebral cortex of awake rats by stimulation of the superficial radial nerve. Morphine injected intravenously in a dose of 2 mg kg produced enhancement of the positive and the negative wave of the evoked potential, the effect on the negative wave being much more pronounced than the effect on the positive wave. The maximal effect of morphine developed more rapidly when halothane anesthesia was employed for the surgical procedure instead of pentobarbital anesthesia. Direct cortical responses elicited by stimulation of the cortical surface were also enhanced by morphine. The time course and the extent of the effect of morphine on the direct cortical and on the primary evoked response, however, did not run parallel. Levallorphan injected intravenously in a dose of 0.2 mg kg inhibited considerably more the effect of morphine on the evoked potential than on the direct cortical response. It is suggested that morphine enhances the primary somatosensory evoked potential by increasing the excitability of cortical neurones, an effect in which facilitatory processes in the thalamocortical system may be involved.

Effect of neurotropic drugs on cortical evoked potentials

In acute experiments on unanesthetized, curarized cats and rabbits and also on animals anesthetized with chloralose, recordings were made of direct cortical and transcallosal responses, responses in the pyramids of the medulla to peripheral stimulation and stimulation of the motor cortex, primary responses in area S-I, and interzonal somatomotor responses. The effect of narcotics on these cortical responses was shown to persist under conditions partially or completely excluding effects mediated through the reticular formation and other subcortical structures (intracarotid injection of the drugs or their local application to the cortex, experiments after premesencephalic section or on the isolated cortex). Neuroleptics have only a slight effect on these cortical evoked responses, mainly due to their blocking action on the reticular formation. Tranquilizers of the benzodiazepine series are active against the cortical responses studied, and this effect is due to their direct action on the cortex.

Direct cortical response and PGO spike during paradoxical sleep of the cat

Direct cortical response and PGO spike during paradoxical sleep of the cat

Occlusive behavior of negative-wave direct cortical response (DCR) and single cells in the cortex.

Occlusive behavior of negative-wave direct cortical response (DCR) and single cells in the cortex.J W Phillis, and S OchsJ W Phillis, and S OchsPublished Online:01 May 1971https://doi.org/10.1152/jn.1971.34.3.374MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByBrain stimulation and conscious experienceConsciousness and Cognition, Vol. 13, No. 3The effect of experimental ischaemia on the direct cortical response of the motor cortex in primatesElectroencephalography and Clinical Neurophysiology/Evoked Potentials Section, Vol. 71, No. 4Effects of methylprednisolone on cortical neural activity, blood flow, and water content in air exposure-induced cerebral edemaExperimental Neurology, Vol. 92, No. 3Long-term effects of early undernutrition on reactivity of the rat parietal association cortexNeuroscience Letters, Vol. 48, No. 2Effect of Early Iron Deficiency on Reactivity of the Rat Parietal Association Cortex7 July 2009 | International Journal of Neuroscience, Vol. 23, No. 3Temporal summation in rat prefrontal pyramidal cells. Differential effects of pre- and postsynaptic neurochemical manipulationsBrain Research, Vol. 276, No. 1Effect of early undernutrition on reactivity of the rat parietal association areaExperimental Neurology, Vol. 82, No. 1The action of noradrenaline on cortical neurons: effects of pHBrain Research, Vol. 35, No. 2 More from this issue > Volume 34Issue 3May 1971Pages 374-88 https://doi.org/10.1152/jn.1971.34.3.374PubMed5560039History Published online 1 May 1971 Published in print 1 May 1971 Metrics

Laminar DC studies of acetylcholine-activated epileptiform discharge in cerebral cortex

Epileptiform paroxysms induced by local application of neostigmine and acetylcholine (ACh) to intact and undercut cerebral cortex of the cat have been studied by simultaneous DC recording of electrical activity from the cortical surface together with a penetrating micro-electrode used to plot the field potentials in depth as well as to obtain extracellular records of associated unit discharge. Each spontaneous paroxysm was initiated by a sudden surface negative DC shift upon which was superimposed regular rhythmic oscillating waves at 8–20/sec. The surface negative DC field potential did not show a phase reversal except deep to the Vth layer in the cortical depth, increased in negativity with a maximum in layer V in vicinity of large pyramidal cells. The rhythmic oscillating waves showed a phase reversal in most superficial cortical layers only approximately 200 μ beneath the surface. Rapid unit discharge of deep pyramidal cells accompanied the negative DC shift in intact cortex and was interrupted by gating or inhibitory action of rhythmic waves. ACh paroxysms induced in acutely undercut cortex were not accompanied by detectable unit discharge, raising a puzzling problem about their mode of generation. It is suggested that neuronal depolarization and possibly glial cells may play a role in the generation of the DC shifts of the ACh paroxysm as shown for direct cortical responses and evoked potentials by Castellucci and Goldring (1970).

Facilitation of the direct cortical response of the visual cortex in association with rapid eye movement during paradoxical sleep in the cat

Facilitation of the direct cortical response of the visual cortex in association with rapid eye movement during paradoxical sleep in the cat

Facilitation of the direct cortical response of the visual cortex in association with rapid eye movement during paradoxical sleep in the cat

Facilitation of the direct cortical response of the visual cortex in association with rapid eye movement during paradoxical sleep in the cat

The influence of hypnotics and tranquillizers on some evoked cortical potentials

The influence of hypnotics (sodium thiopentone and sodium γ-oxybutyrate) and tranquillizers (chlorpromazine and Stelazine) on the direct cortical, transcallosal responses in the cortex and on responses in the bulbar pyramids has been investigated in acute experiments on 150 non-anaesthetized curarized rabbits and on 20 cats anaesthetized with chloralose. It was found that both the narcotics under investigation changed the positive components of the direct cortical response more than the negative ones. The transcallosal response was generally affected more by the drugs than the direct cortical response. These changes may have been caused by the direct cortical effect of the substances, not merely by the blockade of the afferent subcortical flow. Oxybutyrate and thiopentone induced similar changes, but oxybutyrate did not elicit a phase of deep depression of the potentials. The pyramidal response to peripheral stimulation showed high sensitivity to both the narcotics. After comparing the changes in this response with those in the primary cortical and antidromic pyramidal one, and in the intercortical response arising in the motor cortex after stimulation of the I somatosensory area, it was suggested that the narcotic drugs under investigation exerted a pronounced influence on the intercortical associative connections. Chlorpromazine and Stelazine, in doses not causing a hypotensive effect, did not greatly affect the direct cortical, transcallosal and associative pyramidal responses.

Regional features of background electrical activity and of direct cortical response by the intact or neuronally isolated cortex

Background electrical activity and thresholds for the appearance of direct cortical responses (DCR) were studied in acute and chronic experiments on cats in some gyri of the intact and neuronally isolated cortex (the whole cortex was subjected to neuronal isolation [10]). It was determined that in intact animals the suprasylvian gyrus, particularly its central part, differs by its higher electrical activity and lower DCR thresholds from the ectosylvian gyrus. These differences are retained after neuronal isolation of the cortex from the subcortical structures. Hence the differences found in the neurophysiologic characteristics of the gyri under study reflect specific properties and are not mediated by subcortical neural effects.

Neuroleptanalgesic “Thalamonal”の薬理学的研究(1)

Neuropharmacological properties of Thalamonal were investigated and compared with those of Fentanyl, Droperidol and Morphine. The following results were obtained. 1. Muscle relaxation and the impairment of the posture maintenance, muscle coordination and placing, hopping and righting reflexes were observed following i. v. administration of 0.1ml/kg of Thalamonal in dogs and cats. In addition, threshold for eliciting the nociceptive reactions by natural stimulation was elevated without any noticeable central excitatory symptom. 2. No anti-cardiazol and strychnine convalsive effects or anti-electroshock activity were shown. Thiobarbital anesthesia was potentiated by Thalamonal in mice. Thalamonal was suppressive of apomorphine induced vomiting in dog and also had a slight hypothermic activity at 0.37ml/kg in rabbit. 3. The ED50s of analgesic activity in mice measured by Haffner's method were 0.32ml/kg, 0.087mg/kg for Thalamonal and Fentanyl, respectively, Fentanyl possessed an analgesic potency about 100 times as strong as that of Morphine. 4. In rabbit with chronically implanted electrodes “pain reactions” were induced by tooth pulp stimulation. Doses at which the threshold values were doubled were 0.6ml/kg, 0.03mg/kg, and 10mg/kg for Thalamonal, Fentanyl and Morphine, respectively. Droperidol was not effective at 1.5mg/kg. This threshold elevating effect was shortlasting. 5. By small doses of Thalamonal the EEG activity of both acute and chronic rabbits showed the tendency that the spindle burst waves became frequent, slow waves of high amplitude dominant in the cortex and the theta wave activity was abolished and slow wave became dominant in the hippocampus. Threshold for the EEG arousal response by brain stimulation became higher. 6. In the cat slowly developing potentials of the CM nucleus of the Thalamus evoked by the stimulation of the splanchnic nerve and the canine tooth pulp were abolished by 1.0ml/kg Thalamonal and 0.1mg/kg Fentanyl but rapidly developing evoked potentials of the cortical first and second somatosensory areas from the tooth pulp were not influenced. 7. The direct cortical response at the neocortex was almost uninfluenced even by 2.0ml/kg of Thalamonal.

Effects of asphyxia on the electrocorticogram of newborn rabbits

The asphyxia resistance of the electrocorticogram (EEG) was studied in developing postnatal rabbits. Asphyxia was found to block the EEG completely within 100 sec at all ages studied. The longest period of asphyxia which the EEG of the rabbits could survive decreased from about 40 min at birth to about 6 min at 18 days of age. After a fixed period of asphyxia the reappearance of the EEG was faster in the younger than in the older animals. After long periods of asphyxia this difference was more pronounced. In one series of experiments the animals were subjected to asphyxia after the administration of noradrenaline, a treatment which increases the asphyxia tolerance of the direct cortical response. The asphyxia tolerance of the EEG was not changed by this treatment.

Direct cortical responses during formation and extinction of a conditioned defensive reflex in dogs

Direct cortical responses during formation and extinction of a conditioned defensive reflex in dogs

Short latency reticulocortical potentials: Effect of muscarinic anticholinergic drugs

The effects of muscarinic anticholinergic drugs on evoked cortical potentials were studied in unanaesthetized, curarized cats. Potentials were evoked by electrical stimulation of different sites: the cortical surface evoking the direct cortical response (DCR); the midline and medial regions of the midbrain tegmentum evoking the reticulocortical potentials (RCP-1 and-2); and peripheral (radial) nerve stimulation evoking the primary responses (PR). Using a method of paired stimulation a facilitatory action of the RCP on the DCR and PR was demonstrated. When the PR preceded the RCP, the negative component of the RCP remained, even after the positive component had vanished. Thus, it seems probable that the negativities of the RCP and of the PR have different generating mechanisms. The cortical application of the muscarinic anticholinergic drugs, benactyzine and atropine, inhibited the negative deflections of the RCP and the DCR, but increased the PR amplitude. The intravenous administration of these drugs produced a total inhibition of the RCP and to a considerable extent suppressed the DCR, but the PR was somewhat augmented. The application of the anticholinesterase, galanthamine, markedly potentiated the RCP-1, RCP-2 and the DCR. Intravenous galanthamine increased the RCP amplitudes, but somewhat reduced and stabilized those of PR. The inhibition of the negative components of the RCP and of the DCR observed with anticholinergic drugs appears to be produced by blockage of certain muscarinic cholinergic synapses in the cortex, through which the depolarization of apical dendrites under the influence of impulses propagating from the reticular formation is effected.

Evoked cortical potentials in prenatally irradiated rats

The direct cortical, callosal, specific-sensory and interhemispheric responses have been evoked in mature cortex of rats x-irradiated on the nineteenth and twenty-first days of gestation (a procedure which prevents the development of layers II, III, and IV). In general, responses recorded from the cortex of animals irradiated on the twenty-first day of gestation exhibit increased conduction velocities lowered thresholds, and raised amplitude. Threshold is also lowered in rats irradiated on the nineteenth day of gestation although the recorded responses tend to be very variable and to demonstrate normal or lowered amplitude and slowed or normal conduction velocities. The afterdischarge of responses in both groups of animals remains normal and appears to be conducted without decrement over the distances studied. Attenuation of the direct response with distance from the point of stimulation is increased as a result of irradiation on the nineteenth day of gestation but is normal in the group irradiated later in life.

Spreading depression of negative wave of direct cortical response and pyramidal tract responses

(1) The effect of spreading of depression (SD) in cats and rabbits on elements subserving the negative wave type of direct cortical response (N wave DCR) was studied by confining SD to either the stimulated site or the responding site. When SD occupied the N wave DCR stimulated site, a 2 min block of excitation occurred. Axons at the stimulated site are directly excited by the applied currents to give rise to the N wave DCR and a block at the stimulated site is evidence for the action of a depressive cut preparations and GABA to the N wave DCR recording site, the duration of the block varied but was generally longer; recovery time took approximately 3–13 min. The longer lasting effect was related to an action SD on dendrites of pyramidal cells. (2) A radial descent of SD into the lower layers of the cat cortex was shown by a depression first of the N wave DCR followed later by a depression of the antidromically activated pyramidal tract (PT) cells recorded extracellularly with microelectrodes. The latency-depth relation gave a rate for the downward propagation of SD of 0.75 mm/min measured between cortical depths of 1–2 mm. Depression of the antidromic PT response was brief, lasting approximately 1.4 min, consistent with a depressive agent acting directly on the membrane of the PT cell. (3) Just preceding PT cell invasion there was often a short period of increased activity as evidenced by a repetitive discharge. A similar brief period of repetitive discharge was also seen for a short time after recovery of PT responses. This was interpreted as a ‘release’ phenomenon with neurons in the upper layers of the cortex having an inhibitory effect on the lower layer PT neurons. (4) In some cases SD did not fully penetrate into the deeper layers as shown by depression of the surface N wave DCRs with PT cell responses remaining undepressed. This phenomenon suggests a variation in the safety factor for downward propagation in the cortex.

The effect of local cooling upon spontaneous and evoked electrical activity of cerebral cortex.

The effect of local cooling of the surface of the cerebral cortex by means of a metal chamber implanted in the skull was studied while recording evoked and spontaneous electrical activity from the center of a cooled area of 1 cm2. Direct cortical responses to local stimulation of the cortical surface decreased rapidly and progressively to disappear at surface temperatures of 20–22 °C. Onset and peak latencies were prolonged with a Q10 of 1.4 and 1.7 respectively. Response duration was prolonged with decreasing amplitude, having a Q10 of about 2.6. Surface cooling to 8–12 °C was necessary to abolish all postsynaptic components of somatic and auditory evoked potentials, recruiting responses, and spontaneous barbiturate spindles. Latencies of these responses were also increased with a Q10 of 1.3–1.4 while the Q10 for amplitude was consistently higher (2.0–2.6). Allowing for a gradient of increasing temperature from surface to depth it is concluded that all synaptic processes are blocked at temperatures of 20–22 °C. Synaptic mechanisms determining latency were consistently different from those determining amplitude as judged by consistent differences in the Q10 of latency and amplitude for all postsynaptic responses studied in these experiments.

Role of cholinergic mechanisms in the genesis of some cortical responses

The dynamics of evoked potentials during blocking of cholinergic cortical structures was investigated in unanesthetized cats. Application of the anticholinergic drug benactyzine inhibits the negative phases of cortical responses to stimulation of the reticular formation and non-specific thalamic nuclei and also of responses to direct cortical stimulation. Direct cortical responses (DCRs), inverted by γ-aminobutyric acid, are also depressed, indicating the role of cholinergic mechanisms in the genesis of these responses. During blocking of cholinergic synapses, negative phases of the primary response (PR) and response to stimulation of the specific thalamic nucleus are facilitated. A tendency is then observed toward grouping of spontaneous unit discharges and abolition of inhibition of cortical neurons produced by high-frequency stimulation of the reticular formation. One cause of the increase in amplitude of the primary response (PR) to the action of anticholinergic drugs may be widening of the zone of cortical neurons involved in the response because of abolition of the localizing effect of inhibitory neurons.

Negative components of the direct cortical response

Dendritic (DPs) and slow negative potentials (SNPs) arising in response to direct electrical stimulation of the cortex in cats under deep Nembutal anesthesia were studied. Monosynaptic DPs reflect EPSPs of apical dendrites; they develop in response to impulses arriving from fibers in layer I. DPs are strengthened by application of eserine and by Ca++, and weakened by the action of Mg++, Br−, and caffeine. Analysis of changes in DPs evoked by paired stimuli indicates that Ca++, Mg++, and Br− influence the presynaptic elements of axo-dendritic synapses, while caffeine acts on their postsynaptic elements. DPs are abolished by application of GABA; strychnine does not affect them. From these and other facts it can be concluded that there are no inhibitory synapses on apical dendrites. Evidence of the participation of the neuroglia in SNP genesis is analyzed. SNPs are selectively depressed by x-rays, strengthened by Ca++, and weakened by Mg++. Against the background of SNPs, DPs are inhibited and the ratio between amplitudes of DPs evoked by paired stimuli is changed. It is concluded that during SNPs the dendrites and presynaptic terminals of axo-dendritic synapses are deploarized.

Effects of noradrenaline upon cerebrocortical activity in asphyxiated newborn rabbits.

AbstractThe asphyxia resistance of the direct cortical response (DCR) and the electrocorticogram (ECG) was determined in noradrenaline treated and untreated newborn rabbits. The resistance of the untreated animals was similar to what has previously been found for the adult, the DCR being blocked within 3 1/2 min and the ECG within 2 min of asphyxia. After the ad ministration of noradrenaline the DCR became more resistant to asphyxia and could be evoked for 8–17 min. The ECG was not sustained by noradrenaline, and was blocked within 2 min of asphyxia as it was in the untreated animals.An increased ability of the DCR to withstand asphyxia has been described for the fetus. In view of the above mentioned effect of noradrenaline, it was proposed that this resistance of the fetal DCR to asphyxia is due to the fact that in the fetus asphyxia stimulates the release of noradrenaline from the preaortal paraganglia and the adrenal medulla. Possible mechanisms whereby the increased resistance of the DCR could be effected by noradrenaline were discussed.