Responses of globus pallidus neurons to cortical stimulation: intracellular study in the rat.

The responses of globus pallidus (GP) neurons to stimulation of the sensorimotor cortex, the neostriatum, and the subthalamic nucleus were intracellularly recorded in anesthetized rats. Stimulation of the cortex evoked a sequence of postsynaptic responses including an initial short EPSP, a short IPSP, and a late EPSP with multiple spikes in most of the repetitively firing GP neurons. The response pattern was very similar to those evoked by striatal stimulation, except that the latencies were longer. An acute knife cut placed immediately caudal to the substantia nigra caused no significant change in the responses to cortical and striatal stimulation. Stimulation of the subthalamic nucleus evoked a short latency EPSP overlapped with an IPSP. The polarity of all the IPSPs was reversed by a Cl- injection. A systemic injection of picrotoxin abolished all the IPSPs and unmasked large depolarizations with multiple spikes. An ibotenic acid lesion of the subthalamic nucleus eliminated both the initial short latency and late EPSPs to cortical and striatal stimulation and disclosed a prominent IPSP. Stimulation of the lesioned subthalamic nucleus also evoked large, short latency IPSPs without noticeable EPSPs. These results indicate that (i) the IPSPs evoked by cortical, striatal, and subthalamic stimulation were mediated by a GABAA receptor, (ii) both the initial and late EPSPs to cortical and striatal stimulation involved activation of the subthalamic nucleus but not brainstem nuclei, and (iii) cortically derived signals mediated through the neostriatum (i.e. long latency IPSPs) and the subthalamic nucleus (i.e. short latency EPSPs) converged on most GP neurons.     

The effects of focal epileptic activity on the somatosensory evoked potentials in the rat

Summary The cortical somatosensory evoked potential (SEP) of the rat, evoked by contralateral forepaw stimulation, consisted of early (P 1 and N 1) and late components (P 2 and N 2). Microelectrode recording yielded evoked unitary responses of short latencies in the range of the early components and responses of longer latencies in the range of P 2. During the development of focal epilepsy after topical application of penicillin, the late components of SEP were enhanced and the enhanced late negativity corresponded to a surface negative cortical spike. The prominent enlargement of later components was associated with prolonged, often recurrent discharges of longer latency unitary responses and with enlarged local field potentials. Early components of SEP remained relatively unaffected and so did unitary responses with short latencies.Epileptic spike-conditioned SEPs in the cuneate nucleus, thalamic sensory relay nucleus and sensory cortex were depressed from 100 ms (cuneate nucleus) to about 300 ms (thalamus and cortex) subsequent to spike discharge. Transmission in the cuneate nucleus was least affected. Thalamic and cortical early components of SEP had similar time courses of recovery, which differed markedly from that of cortical late components. Our findings suggest that two different neuronal activities generate different components of SEP and are differentially involved in the epileptic activities, which results in the different amplitude recovery following spontaneous epileptic spike discharges.This work was supported by the Deutsche Forschungsgemeinschaft (German Research Council)     

Periglomerular cell action on mitral cells in olfactory bulb shown by current source density analysis

The sign of action of periglomerular (PG) cells on the apical dendrites of mitral cells in olfactory bulb glomeruli was investigated by constructing current source density (CSD) profiles from potentials evoked by primary olfactory nerve (PON) and lateral olfactory tract (LOT) stimulation. Evoked potentials were recorded and averaged from anesthetized rabbit simultaneously with a1 × 16 array of electrodes positioned perpendicular to the bulbar surface. A one-dimensional CSD analysis with depth was made in the center of PON- and LOT-evoked potential activity. CSD was plotted vs depth for specific times during the average evoked potential (AEP): at the surface peaks of the first surface-negative wave (N1), the first surface-positive wave (P1), and the second surface-negative wave (N2). N1, P1 and N2 corresponded to excitation, dis-excitation (equivalent to inhibition), and dis-inhibition (re-excitation) of the granule cell population through mitral cell basal dendrites. The granule cells generated both PON and LOT oscillatory AEPs. When N1 and P1 profiles or P1 and N2 profiles were combined, the source and sink due to granule cell activity were minimized and another source-sink pair was revealed on PON but not LOT stimulation. PON-evoked N1 + P1 or P1 + N2 profiles showed a secondary souce-sink pair not present with LOT stimulation. The sink was located in the glomerular layer (GL) and outer plexiform layer (EPL) and the source in the inner EPL. It was concluded that long-lasting excitation of the mitral cells was taking place at the GL and GL/EPL border. This excitation was ascribed to concomitant PG cell activity, possibly in combination with prolonged monosynaptic PON excitation of the apical dendrites. The results support the occurrence of direct excitatory action of PG cells onto mitral cells.     

Frontal cortex stimulation evoked neostriatal potentials in rats: intracellular and extracellular analysis

Evoked potentials, action potentials and intracellular events were recorded in the neostriatum of urethane anesthetized rats to electrical stimulation of frontal cortex white matter, motor cortex and pre-limbic cortex. Five major waves of the evoked potential were identified. Wave N1 (3.9 msec latency) was small, preceded cellular events and probably represents activation of corticostriate terminals. Wave P1 (10.8 msec latency to peak following white matter stimulation) coincided with an EPSP and neuronal firing. Both wave N2 (38.0 msec latency to peak) and P2 (approximately 110 msec duration) overlapped the intracellularly recorded hyperpolarization and inhibition of cell firing. Based upon this correspondence and upon the behavior of waves N2 and P2 with changing current and during conditioning-test paired pulse stimulation, it was concluded that the waves represent different processes contributing to the cellular hyperpolarization. A late wave, N3 (175 msec onset latency) corresponded to a late rebound firing and cellular depolarization. This late wave was eliminated from the neostriatum, but not from the overlying sensorimotor cortex, by kainic acid lesions that destroyed medial thalamus but left thalamic lateral nuclei and reticular nucleus intact.     

Properties of Cortical Somatosensory Evoked Potentials in the Awake Rabbit

By appropriate experimental procedures it was possible to distinguish the components of the contra- and ipsilateral cerebral somatosensory potentials evoked by electrical stimulation of an extremity in the unrestrained rabbit.

The components of the contralateral response occur in the following order: an early positive primary wave (PI), a positive associative wave (P2), and ultimately a late negative N wave.

The components of the ipsilateral response occur in the following order: a small positive wave P, the latency of which is intermediate between those of the contralateral P1 and P2 waves, and a large negative wave N, similar to the contralateral N wave.

The different topographical distributions of these waves were elucidated by the use of insulated, chronically implanted electrodes glued onto the cortical surface. The properties of the waveform components were studied by various methods such as varying the stimulation parameters, simultaneous application of somesthetic and acoustic stimuli, and administration of narcotic drugs. The properties of PI were similar to those of P28 in humans; the properties of P2 can be compared to those of P45; and, finally, the N wave resembles the late negative components observed in humans.

Inconstant small positive waves of shorter latencies, which will be discussed in a following paper, may also be seen.

Interestingly enough, no early negative wave such as that observed in humans (N20) was ever found. If, as is presently thought, this wave is, in fact, due to the folding of the cortical surface (Broughton, 1969), its absence is to be expected in the rabbit because the cortical surface of this species is lissencephalic and thus devoid of gyri.     

Monosynaptic facilitatory pathway from the hypothalamic ventromedial nucleus to the frontal cortex in the rat

Stimulation of the ventromedial nucleus (VMH) evoked a short latency negative wave with two peaks cN₁ and cN₂ followed by a small positive wave (cP) at the ipsilateral dorsal frontal cortex (area 10) in the rat. The maximum response was observed from the lateral edge of the frontal pole. From the depth profiles of recordings, cN₁ changed polarity at a depth of about 4 mm and the cN₁?cN₂ changed into a large compound action potential at the medioventral part of the frontal pole at a depth of about 6 mm. Since the surface evoked potential and the compound action potential followed high frequency stimulation, these respective potentials are concluded to be due to antidromic and monosynaptic activation of the cortical neurons. This was verified by unit recording experiments. The cP was concluded to be produced by the initial rise of the monosynaptic EPSP.     

Inhibitory pathway from the frontal cortex to the hypothalamic ventromedial nucleus in the rat

Stimulation of the ventromedial nucleus (VMH) evoked a short latency negative wave with two peaks cN₁ and cN₂ followed by a small positive wave (cP) at the ipsilateral dorsal frontal cortex (area 10) in the rat. The maximum response was observed from the lateral edge of the frontal pole. From the depth profiles of recordings, cN₁ changed polarity at a depth of about 4 mm and the cN₁−cN₂ changed into a large compound action potential at the medioventral part of the frontal pole at a depth of about 6 mm. Since the surface evoked potential and the compound action potential followed high frequency stimulation, these respective potentials are concluded to be due to antidromic and monosynaptic activation of the cortical neurons. This was verified by unit recording experiments. The cP was concluded to be produced by the initial rise of the monosynaptic EPSP.     

The early negative potential evoked by stimulation of the tibial nerve in man

The scalp response to stimulation of the tibial nerve at the level of the medial malleolus was systematically analysed. It was recorded 2 cm posterior to the vertex and at the sites corresponding to cortical representation of the hand. The existence of an early negative wave with a peak latency of 37.2 ± 2.29 ms and amplitude of ?0.69 ± 0.40 μV was established (being half the amplitude of the first positive wave (P40) over the vertex). This wave was named N37 in respect of the peak latency and polarity. N37 was the first event recorded after stimulation of the tibial nerve at this level as the onset latency was 32.2 ± 1.75 ms and that of P40 over the vertex 33.8 ± 2.28 ms. It was recorded with the highest amplitude over the hand primary somatosensory area after stimulation of the opposite foot.N37 evoked by stimulation of the tibial nerve at the ankle and N20 evoked by stimulation of the arm nerve are both the primary negativities of the evoked potential. However, N37 is not recorded with maximum amplitude over the leg primary somatosensory area and it is rounded and longer lasting than N20. In spite of these differences the two initial negative electrical phenomena are not necessarily generated by different functional structures. The possible generators of N37 are discussed.     

Wakefulness-sleep modulation of the surface and depth auditory evoked potentials in man

Amplitude and latency changes of early and late components of surface and depth auditory evoked potentials were determined during wakefulness-sleep steady state shifts in epileptic patients, with implanted electrodes used as an electrophysiological procedure for surgical treatment of temporal lobe seizures. Early surface (I and V) and depth (N8 and N15) components of the auditory brainstem potentials and late surface (P2 and N2) and depth (B and C) components of the auditory evoked potentials were produced by either 8/s or single clicks, delivered monoaurally and simultaneously recorded from the vertex and contralateral thalamic (lateral geniculate thalamic nucleus) and frontotemporal (amygdala, hippocampus and orbitofrontal cortex) regions, while patients spontaneously shifted from initial wakefulness (W1) to slow wave sleep (SWS I, II and IV), to paradoxical sleep (PS) and to final wakefulness (W2). Amplitude of late surface (P2 and N2) and depth (B and C) components significantly decreased when patients shifted from SWS IV to PS and increased from PS to W2. Latency of components P2 and B increased while that of components N2 and C decreased from SWS IV to PS. No latency changes in late components were found from PS to W2. In addition, amplitude and latency of P2 and B components significantly decreased while those of N2 and C increased from W1 to SWS IV. Polarity of all late components remained unchangeable during all wakefulness-sleep state shifts, with the exception of that of component C which reversed from W1 to SWS IV. In contrast, early surface (I and V) and depth (N8 and 15) components showed no systematic changes in amplitude and latency during all consecutive wakefulness-sleep shifts, with the exception of a significant increase amplitude but no latency of component V from PS to W1.     

Cortical evoked potential changes in a rat model of acute ischemic stroke Detection of somatosensory evoked potential and motor evoked potential

BACKGROUND:Studies have shown that latency changes of some elements in a somatosensory evoked potential (SEP) and motor evoked potential (MEP) can reflect electrical activity of cerebral cortical neurons and conduction of white matter nerve fibers. However, there is a paucity of information regarding the dynamic observation of SEP and MEP following cerebral ischemic injury. OBJECTIVE:To explore SEP and MEP changes following acute ischemic stroke, and investigate the role of evoked potentials in monitoring brain function in stroke. DESIGN, TIME AND SETTING:A randomized, controlled, animal experiment was performed at the Chongqing Key Laboratory of Neurology, Affiliated Hospital of Chongqing Medical University from September 2007 to August 2008.MATERIALS:Hydrogen blood flow detector was purchased from Soochow University Medical Instrument Co., China, and Power lab system was purchased from AD Instruments, Inc., USA. METHODS:A total of 36 healthy, adult, male, Sprague Dawley rats were randomly assigned to four groups (n = 9), including three ischemia groups (12, 24 and 72 hours of ischemia) and a sham-surgery group. The rat model of acute ischemic stroke was established by middle cerebral artery occlusion (MCAO) in the left hemisphere.MAIN OUTCOME MEASURES:SEP and MEP of the left limbs were detected, and cerebral blood flow was measured by the hydrogen cleaning method.RESULTS:The latency of positive wave 1 (P1), negative wave 1 (N1) and positive wave 2 (P2) waves in SEP, and latency of negative wave 1, 2 (N1, N2) waves in MEP were significantly prolonged with increasing ischemic duration following MCAO (P < 0.01), but cerebral blood flow was significantly decreased (P < 0.05, or P < 0.01).CONLUSION:Ischemic stroke prolongs the latency of SEP waves (P1, N1, P2) and MEP waves (N1, N2), and cerebral cortical evoked potential may correlate with cerebral blood flow changes. This indicates that SEP and MEP can be used to evaluate brain function following acute ischemic stroke.     

Somatosensory evoked potentials (SEPs) and cortical single unit responses elicited by mechanical tactile stimuli in awake monkeys

The origins of surface recorded evoked potentials have been investigated by combining recordings of single unit responses and somatosensory evoked potentials (SEPs) from the postcentral gyrus of 4 alert macaque monkeys. Responses were elicited by mechanical tactile stimuli (airpuffs) which selectively activate rapidly adapting cutaneous mechanoreceptors, and permit patterned stimulation of a restricted area of skin. Epidurally recorded SEPs consisted of an early positive complex, beginning 8-10 msec after airpuff onset, with two prominent positive peaks (P15 and P25), succeeded by a large negative potential (N43) lasting 30 msec, and a late slow positivity (P70). SEPs, while consistent in wave form, varied slightly between monkeys. The amplitude of the early positive complex was enhanced by increasing the number of stimulated points, or by placing the airpuffs in the receptive fields of cortical neurons located beneath the SEP recording electrode. SEP amplitude was depressed when preceded 20-40 msec earlier by a conditioning stimulus to the same skin area. Single unit responses in areas 3b and 1 of primary somatosensory (SI) cortex consisted of a burst of impulses, beginning 11-12 msec after the airpuff onset, and lasting another 15-20 msec. Peak unitary activity occurred at 12-15 msec, corresponding to the P15 wave in the SEP. No peak in SI unit responses occurred in conjunction with the P25 wave. Although SI neurons fired at lower rates during P25, the lack of any peak in SI unit responses suggests that activity in other cortical areas, such as SII cortex, contributes to this wave. Most unit activity in SI cortex ceased by the onset of N43, and was replaced by a period of profound response depression, in which unit responses to additional tactile stimuli were reduced. We propose that the N43 wave reflects IPSPs in cortical neurons previously depolarized and excited by the airpuff stimulus. Late positive potentials (P70) in the SEP had no apparent counterpart in SI unit activity, suggesting generation at other cortical loci.     

The thalamic reticular nucleus is activated by cortical spreading depression in freely moving rats: prevention by acute valproate administration

This study investigated the effect of repetitive cortical spreading depression (CSD) on behaviour and the anatomical and physiological patterns of cellular activation of cortical and subcortical areas in awake, moving rats. Rat behaviours in response to repetitive CSD events evoked by the application of KCl were quantified with electrophysiological recording. Immunohistochemistry was used to quantify anatomical regions of cellular activation. The effects of acute valproic acid administration on the behavioural parameters and cellular activation were evaluated. CSD significantly decreased locomotor activity and induced freezing in awake, moving rats, and stimulated c‐Fos expression in the cortex, trigeminal nucleus caudalis (TNC), and amygdala. CSD also resulted in a prominent increase in c‐Fos expression in the ipsilateral thalamic reticular nucleus (TRN) visual sector. Electrophysiological recordings revealed propagation of CSD into the TRN. Valproic acid pretreatment decreased the duration of CSD‐induced freezing episodes and reversed the CSD‐induced reduction in locomotor activity. Acute valproic acid administration also significantly blocked CSD‐induced c‐Fos expression in the TNC and TRN. These findings show that CSD events cause consistent behavioural responses and activate specific brain regions in awake, freely moving rats. Selective activation of TRN by CSD and the suppression of this activation by valproic acid suggest that this brain region may play an important role in migraine pathogenesis and may represent a novel target for migraine therapy.     

Midbrain evoked potentials and oculomotor activity produced by optic nerve stimulation

Evoked potentials, produced by electrical stimulation of the optic nerve, were recorded from the superior colliculus and the midbrain close to the oculomotor nucleus. The experiments were done on 23 adult cats immobilized by gallamine triethiodide after hemidecerebration by prethalamic transection. The evoked potentials consisted of three components, namely, an early wave, a series of recurrent waves with latency of about 6 msec, and a late slow wave with latency of about 16–23 msec. It was concluded that the early wave was due to the arrival of optic nerve impulses, the recurrent wave to repetitive firing of collicular neurons, and the late slow wave to the collicular outflow onto the oculomotor nucleus. In the majority of instances in which the late slow wave was observed, the preceding optic nerve volley revealed facilitation of the antidromic spike of oculomotor nucleus. In a few instances in which the late slow wave was not obtained, either facilitation or inhibition of spontaneous oculomotor discharge was observed, indicating the dual facilitatory and inhibitory components of colliculofugal outflow to the oculomotor nucleus.     

Effects of reaction time performance on single-unit activity in the central auditory pathway of the rhesus macaque

The activity of single units at various locations in the central auditory pathway of rhesus macaques was recorded during the monkeys' performance and nonperformance in an auditory reaction time task. Evoked unit responses during performance were compared with those observed during passive delivery of identical stimuli. Single units were recorded from the cochlear nucleus, superior olivary complex, lateral lemniscus, inferior colliculus, medial geniculate nucleus, and auditory cortex. Significant effects of task performance on unit discharge patterns were observed at all levels of the central auditory pathway: Spontaneous discharge rates in the more peripheral auditory nuclei tended to be higher during performance. Evoked discharge that occurred relatively late during a stimulus presentation (greater than 75 msec after stimulus onset) was increased during performance, compared with the nonperformance condition, in nuclei above the cochlear nucleus. The initial latency of evoked discharge was increased during performance for subcortical nuclei but was decreased for units in auditory cortex. These results suggest that the effects of performance may be mediated by a tonic increase in the excitability of auditory units which operates primarily at peripheral auditory stations, and a descending, stimulus-evoked increase in excitability which primarily influences the cells of higher auditory nuclei. At the cortical level, these changes lead to increased signal-to-noise ratio of the evoked response during performance in the auditory task.     

The development of physiological responses of the piriform cortex in rats to stimulation of the lateral olfactory tract

Extracellular recording techniques in rats were used to follow the postnatal development of the evoked response of the piriform cortex to electrical stimulation of the lateral olfactory tract (LOT) from birth to adulthood. As in other species, LOT shock in adult rats produces short-latency activation of units in piriform cortex and an extracellular field potential consisting of three components: a surface-negative component, the A1 wave (corresponding to the cortical monosynaptic EPSP evoked by the LOT fibers); a second surface-negative component, the B1 wave (corresponding to reactivation of layer I dendrites by intracortical fibers); and a late surface-positive component, the period 2 wave. A conditioning shock 20-150 msec before the test shock profoundly inhibits both evoked unit activity and the B1 wave, while it facilitates the A1. At birth, units can be orthodromically activated by LOT stimulation in association with the A1 wave. There is also a surface-positive spikelike wave, the S wave, which represents the summation of cortical unit activity. The B1 wave is apparent early in the first postnatal week. However, in contrast to the prominent inhibition in the adults, for the first few days after birth, single-unit responses, multiple-unit activity, and the S wave are all facilitated by a preceding conditioning shock with intervals of 200 msec or less, in association with the facilitation of the A1 wave. A shift to inhibition is apparent with longer intershock intervals of 300-700 msec, which exceed the period during which paired shocks facilitate the A1 wave. During the remainder of the first two postnatal weeks,, partial suppression of evoked activity with intervals of less than 200 msec appears and progressively increases in strength, but inhibition at very long intershock intervals remains greater in magnitude. During this time, the duration of the inhibitory period also decreases to near the adult value of 200-300 msec. In the third postnatal week the pattern was similar to that in the adult, but the inhibition was still clearly weaker than in adults. These results suggest a delayed maturation of the cortical inhibitory circuitry; this conclusion has also been suggested by previously published observations in the developing neocortex and hippocampus. In addition, the acceleration with age of the conduction velocity of axons in the LOT was analyzed. The adult value of 9.6 m/sec was not achieved until some time after postnatal day 15, which parallels the myelinization of the tract as observed with the light microscope.     

Electroencephalographic response to transcranial magnetic stimulation in children: Evidence for giant inhibitory potentials

The electroencephalographic response to transcranial magnetic stimulation (TMS) recently has been established as a direct parameter of motor cortex excitability. Its N100 component was suggested to reflect an inhibitory response. We investigated influences of cerebral maturation on TMS-evoked N100 in 6- to 10-year-old healthy children. We used a forewarned reaction time (contingent negative variation) task to test the effects of response preparation and sensory attention on N100 amplitude. Single-pulse TMS of motor cortex at 105% motor threshold intensity evoked N100 amplitudes of more than 100 microV in resting children (visible in single trials), which correlated negatively with age and positively with absolute stimulation intensity. During late contingent negative variation, which involves preactivation of the cortical structures necessary for a fast response, N100 amplitude was significantly reduced. We conclude that (1) N100 amplitude reduction during late contingent negative variation provides further evidence that TMS-evoked N100 reflects inhibitory processes, (2) response preparation and attention modulate N100, and (3) TMS-evoked N100 undergoes maturational changes and could serve to test cortical integrity and inhibitory function in children. Parallels between the inhibitory N100 after TMS (provoking massive synchronous excitation) and the inhibitory wave component of epileptic spike wave complexes are suggested.     

Neural generators of the somatosensory evoked potentials: recording from the cuneate nucleus in man and monkeys

The neural generators of the somatosensory evoked potentials (SEPs) elicited by electrical stimulation of the median nerve were studied in man and in rhesus monkeys. Recordings from the cuneate nucleus were compared to the far-field potentials recorded from electrodes placed on the scalp. It was found that the shape of the response from the surface of the human cuneate nucleus to stimulation of the median nerve is similar to that of the response recorded more caudally in the dorsal column, i.e., an initially small positivity followed by a negative wave that is in turn followed by a slow positive wave. The beginning of the negative wave coincides in time with the N14 peak in the SEP recorded from the scalp, and its latency is 13 msec. The response from the cuneate nucleus in the rhesus monkey has a similar shape and its negative peak appears with the same latency as the positive peak in the vertex response that has a latency of 4.5 msec; the peak negativity has a latency of about 6 msec and thus coincides with P6.2 in the vertex recording. Depth recordings from the cuneate nucleus and antidromic stimulation of the dorsal column fibers in the monkey provide evidence that the early components of the response from the surface of the cuneate nucleus are generated by the dorsal column fibers that terminate in the nucleus. The results support the hypothesis that the P14 peak in the human SEP is generated by the termination of the dorsal column fibers and that the cuneate nucleus itself contributes little to the far-field potentials.     

Parallel activation of field CA2 and dentate gyrus by synaptically elicited perforant path volleys

Previous studies showed that dorsal psalterium (PSD) volleys to the entorhinal cortex (ENT) activated in layer II perforant path neurons projecting to the dentate gyrus. The discharge of layer II neurons was followed by the sequential activation of the dentate gyrus (DG), field CA3, field CA1. The aim of the present study was to ascertain whether in this experimental model field, CA2, a largely ignored sector, is activated either directly by perforant path volleys and/or indirectly by recurrent hippocampal projections. Field potentials evoked by single-shock PSD stimulation were recorded in anesthetized guinea pigs from ENT, DG, fields CA2, CA1, and CA3. Current source-density (CSD) analysis was used to localize the input/s to field CA2. The results showed the presence in field CA2 of an early population spike superimposed on a slow wave (early response) and of a late and smaller population spike, superimposed on a slow wave (late response). CSD analysis during the early CA2 response showed a current sink in stratum lacunosum-moleculare, followed by a sink moving from stratum radiatum to stratum pyramidale, suggesting that this response represented the activation and discharge of CA2 pyramidal neurons, mediated by perforant path fibers to this field. CSD analysis during the late response showed a current sink in middle stratum radiatum of CA2 followed by a sink moving from inner stratum radiatum to stratum pyramidale, suggesting that this response was mediated by Schaffer collaterals from field CA3. No early population spike was evoked in CA3. However, an early current sink of small magnitude was evoked in stratum lacunosum-moleculare of CA3, suggesting the presence of synaptic currents mediated by perforant path fibers to this field. The results provide novel information about the perforant path system, by showing that dorsal psalterium volleys to the entorhinal cortex activate perforant path neurons that evoke the parallel discharge of granule cells and CA2 pyramidal neurons and depolarization, but no discharge of CA3 pyramidal neurons. Consequently, field CA2 may mediate the direct transfer of ENT signals to hippocampal and extrahippocampal structures in parallel with the DG-CA3-CA1 system and may provide a security factor in situations in which the latter is disrupted.     

Laminar field potentials and unit activity in the cortex during visual evoked potentials in feline generalized penicillin epilepsy

Modifications of the visual evoked potential during generalized epilepsy were investigated in feline generalized penicillin epilepsy. Visual evoked potentials and their intracortical profiles were averaged during intraburst periods and during the wave of the spike and wave complex to a fixed latency from the preceding spike. During interburst periods, the evoked potentials showed an increase in the amplitude of the early positive peak and the appearance after a variable latency period of a second consistent peak during the late phase of the evoked potential. Laminar profiles of visual evoked potentials and their current source density analysis compared with the activity of single cortical units suggested an early excitation of neuronal populations at layers II, III and IV, as seen before penicillin, followed by a variable inhibitory period and by a subsequent rebounded excitation at those same levels. In evoked potentials recorded during the wave of the spike and wave complex, the early phase was unchanged and the late positive peak and the corresponding deep sink were greatly reduced or nonexistent, although the rebounded activation of cortical units was still evident. These data support the conclusion that during feline generalized penicillin epilepsy a larger number of cortical neurons are activated and a sequence of excitation-inhibition-excitation, probably involving also subcortical structures, is brought about. Moreover, the inhibitory phase of the spike and wave complex is soon disrupted whenever a consistent sensory stimulus arrives at the cortex.     

Sensory evoked potentials in herpes simplex encephalitis.

Flash visual potentials (FEPs), somatosensory evoked potentials (SEPs) and auditory brainstem responses (ABR) were recorded in a 66-year-old patient presenting with clinical, EEG and CT brain scan features of herpes simplex encephalitis (HSE). At the time of evoked potential study (10 days after onset of the disease) the patient was treated with iv barbiturate on controlled respiration (lidocaine and phenytoin were not utilized); core temperature was 37 degrees C and pupils were dilated and nonreactive. Cortical FEPs were not recognizable on 02 lead, whereas they were clearly evident on 01 with normal latency of early N1, P1, N2 waves and delayed P2 component. SEPs showed normal peripheral and central conduction times, but N20 peak was bilaterally absent with unrecognizable (on P3) or delayed (on P4) N33 wave. No ABR (including wave I) were found on stimulation of the right ear, whereas delayed wave V with prolonged interpeak I-V latency was found on stimulation of the left ear. In conclusion, changes in sensory evoked potentials in HSE seem to be caused either by necrotic-hemorrhagic damage (with the disappearance of some cortical responses), by coma (with alterations in middle-latency cortical responses) and by increased intracranial pressure (with subsequent ABR abnormalities).