Effects of dopamine and norepinephrine on neuronal activity of the olfactory tubercle

The effects of iontophoretic administration of norepinephrine (NE) and dopamine (DA) on olfactory tubercle (OT) neurons that respond to lateral hypothalamus (LH) or locus coeruleus (LC) electrical stimulation were studied. NE and DA decreased the frequency of OT neurons which were increased or decreased by the LH stimulation. An increased firing of OT neurons following NE or DA administration was less frequently observed. NE administration decreased the firing of OT neurons that responded to LC stimulation. These results suggest that the LC fibers which reach the OT use NE as a neurotransmitter. DA administration also suppressed the unitary discharge of OT neurons responding to LC stimulation. The increase in frequency of OT neurons observed following LH stimulation cannot be attributed to DA. The possibility that other suspected neural transmitters are involved in this effect is discussed.     

Motor unit excitability changes mediating vestibulocollic reflexes in the sternocleidomastoid muscle.

OBJECTIVE: To investigate the patterns of motor unit firing in single motor units from the sternocleidomastoid (SCM) muscles in response to stimuli previously shown to be capable of evoking vestibulocollic reflexes (loud clicks and electrical stimulation) and to relate these to the previously described surface potentials (VEMPs, vestibular evoked myogenic potentials) evoked by the same stimuli. METHODS: Eleven male subjects (30-43-years-old) were studied. Local anaesthetic was used to block the SCM and confirm that the surface potentials (p13n23) arose from it. At another time, fine wire or needle electrodes were used to record single motor unit activity and peristimulus time histograms were constructed. RESULTS: Local anaesthetic block reduced or abolished the p13n23 response in 5 of 6 subjects. A total of 94 histograms of motor unit discharges were recorded. The excitability changes seen were always small. Loud click stimuli given ipsilaterally evoked short latency (mean 14.2 ms, uncorrected for triggering delays), and short duration (mean 3.6 ms) inhibition. Contralaterally, the effect was excitatory (latency 11.9 ms, uncorrected, mean duration 2.3 ms). For electrical stimulation, short latency inhibition occurred ipsilateral to the cathode (average latency 14.0 ms, uncorrected, mean duration 2.9 ms) and excitation occurred contralaterally. CONCLUSIONS: We confirmed that the SCM is the sole or dominant source of the VEMPs recorded from electrodes over it. Short latency, short duration motor unit firing changes are evoked in SCM by loud clicks and electrical stimulation, stimuli known to be capable of evoking vestibulocollic reflexes. VEMPs beginning with a positivity correspond to inhibition of the underlying motor unit firing and those starting with a negativity correspond to an underlying excitation, findings consistent with intracellular recordings of otolith effects. Qualitative explanations of how the surface potentials are generated by these excitability changes and relating to other properties of the surface responses are proposed. SIGNIFICANCE: This study has shown consistent patterns of single motor unit firing which underlie VEMPs evoked by both clicks and short duration galvanic stimulation.     

Brain stem auditory evoked potentials: significant latency differences between ipsilateral and contralateral stimulation

A number of electrical potentials can be recorded from the human scalp following acoustic stimulation. The potentials which occur within 10 msec of the stimulus onset have been termed the brain stem auditory evoked potentials (BAEPs). Latency appears to be the most stable measure and in consequence knowledge of the exact limits of normal latency of each wave is important. In this study the effects of ipsilateral and contralateral stimulation on BAEP latencies have been investigated in 23 normal subjects. The exact limits of normal latency of each wave have been established. It has been shown that significant latency differences exist between ipsilateral and contralateral stimulation. Possible hypotheses are put forward to explain the findings which demonstrate that different neural pathways are followed by ipsilateral and contralateral stimuli and that their respective responses can be investigated separately in man using BAEP recordings.     

Visual and somatosensory evoked potentials characteristics of patients undergoing hemodialysis and kidney transplantation.

The effects of prolonged hemodialysis and kidney transplantation on visual and somatosensory evoked potentials and EEG frequency were assessed. Significant changes were found in both amplitude and latency characteristics of evoked potentials recorded from eight hemodialysis patients. Their evoked potentials tended to be of longer latency and larger amplitude when compared to responses of an age-matched control group. This was true for visual and somatosensory responses recorded from several scalp locations. A correlational analysis revealed no consistent relationship between blood chemistries and evoked potential characteristics. EEG power spectral analysis showed that the dominant frequency of five of the eight dialysis patients was in the 8-10 c/sec range. Two other patients demonstrated EEG frequencies which were scattered across the 3-12 c/sec range while for another subject the dominant frequency was 7-8 c/sec. The evoked potential latencies and amplitudes of patients with successful kidney transplant tended to return to the normal range and their predominant EEG frequency increased to around 10 c/sec. A depression of function in those neural systems underlying the visual and somatosensory modalities, along with a reduction in the cortical suppression of afferent stimulation normally exerted by the thalamic reticular system and the basal ganglia were postulated to account for the reported findings.     

Cerebellar regulation of sensorimotor activity in brown trout

Evoked field potentials were recorded from the mesencephalic ('optic') tectum, cerebellar corpus, midline rhombencephalon, and spinal cord of decerebrated brown trout in response to single electrical shocks given to an optic nerve. Evoked responses were also recorded from the rhombencephalon and spinal cord following stimulation (singly and with trains) to the optic tectum and to the cerebellar corpus. The potentials recorded from the tectum in response to optic nerve stimulation were similar in form to those reported by other workers from other species of teleost. The rhombencephalic responses to optic nerve and tectal stimulation were complex and comprised presumed pre- and post-synaptic events. Cerebellar stimulation evoked no detectable responses in these brain regions, but when given prior to tectal stimulation (by up to 10 ms), tectally-evoked spinal cord responses were reduced in amplitude by as much as 85%. After cerebellar ablation, there was no difference from controls in the latency, form or amplitude of any response, even when tested with paired pulse stimulation. However, when the cerebellum was ablated, rhombencephalic and spinal responses to optic nerve and tectal stimulation were markedly enhanced (by 200-300%). These clear-cut complimentary consequences of cerebellar ablation or stimulation emphasize the gain-setting role of the cerebellum and indicate, at least in relation to optically evoked motor activity, that cerebellar regulation acts at the level of the supraspinal drive to spinal motor circuits and not within the sensory centers.     

Oestrogenic influences on the electrical activity of the olfactory pathway

CARTAS-HEREDIA, L., R. GUEVARA-AGUILAR AND H. U. AGUILAR-BATURONI. Oestrogenic influences on theelectrical activity of the olfactory pathway. BRAIN RES. BULL. 3(6) 623–630, 1978.—The influence of the Oestrogenic hormones over the spontaneous and induced activity of the olfactory pathway was studied in normal female cats. Electrodes were placed chronically or acutely in the olfactory bulb (OB), olfactory tubercle (OT) and in the prepyriform cortex (PPC). Oestrogenic hormones were applied locally in the posterior hypothalamic region. Recordings were made during the two different phases of the oestral cycle. In addition, another group of castrated animals was studied. The oestral phase was induced in these cats by the subcutaneous administration of 17-β-oestradiol. Results indicate that the pattern of the electroencephalographic spontaneous activity as well as the response induced by hypothalamic stimulation changed. The number of the bursts for each 10 sec trace was higher in oestrus than in anoestrus for all the structures studied. The duration of each burst also changed, being shorter in oestrus than in anoestrus cats. The threshold for significant bursting in the olfactory structures following hypothalamic stimulation was lower in oestrus than in anoestrus. The evoked potentials recorded in the same three olfactory structures by hypothalamic stimulation exhibited changes in correlation with the hormonal administration. In all the structures studied the amplitude of the different components of the evoked potentials increased immediately after the hormones were administered. However, the most dramatic increase was observed in the olfactory tubercle. In order to further investigate these changes in acute preparations, a study evaluating the excitability changes was conducted. Applied pulse pairs, with different interpulse intervals between 200 to 1000 msec, were delivered in the hypothalamus before and after 200 μg of the hormone were administered into the posterior hypothalamus. Results illustrate that a significant increase in the amplitude of evoked potentials occurred following the smaller interpulse intervals in the OB. In the OT, the administration of the hormone resulted in a decrease in the amplitude of the potentials for all interpulse intervals studied. A relatively smaller decrease in evoked potential amplitude was observed for longer interpulse intervals in the PPC.     

Electrophysiology of the frontal granular cortex. I. Patterns of focal field potentials evoked by stimulations of dorsomedial thalamus in conscious monkey

Focal field potentials and unit discharges of impulses evoked by low frequency (2–10/sec) stimulations of dorsomedial thalamus (DM) were simultaneously recorded with microelectrodes in the middle and inferior frontal gyri of the dorsal frontal granular cortex (FC) in the normal unanesthetized monkey.The depth profiles and sequences of responses of the FC evoked by the stimulations of DM were observed to be generally similar to the augmenting type of responses reported previously by others in the sensorimotor cortex of encéphale isoléor paralyzed cat.Stimulations of DM evoked short latency (3.2–4.0 msec) negative waves at a depth of 0.6–1.7 mm and correlated positive waves on the surface of the FC. Additional waves of alternating polarity succeeded the primary waves during augmenting sequences according to variations of stimulus strength and frequency. Unit discharges recorded with the same electrode simultaneously with field potentials revealed that a brief burst of 2–4 impulses occurred in association with each of the short latency deep negative waves evoked by repetitive stimuli. The latency of the earliest of the spikes of a burst was in the range of 6.5–9 msec. Following the burst of spikes, there was a long period of absence of spikes in each response.Surface corticograms of FC and nearby precentral cortex revealed that the evoked responses were highly pronounced and restricted to the frontal granular cortex and did not spread diffusely to the agranular cortex. Only a prolonged (40–60 sec) stimulation caused a synchronizing tendency in the corticogram of the agranular area. Furthermore, the evoked potentials in the corticogram of FC were presently only during quiet wakeful states, and became highly disorganized and almost indecipherable during states of synchronizing EEG and decreased consciousness as in natural slow-wave sleep or under Nembutal anesthesia.From these results, it is concluded that the dorsomedial thalamus is organized more like a specific thalamic nucleus to the frontal association cortex, and less like an integral part of the diffuse projection system.     

Sensorimotor and auditory central conduction time in locked-in syndrome

Motor evoked potentials (MEPs) following magnetic cortical stimulation, somatosensory evoked potentials from median nerve (SEP) and auditory brain-stem responses (ABR) were recorded in a patient with locked-in syndrome during the acute and chronic phases of the clinical course. During the acute phase both ABR and SEP were normal. The MEP from the right upper limb showed a delayed and low voltage potential, while that from the left upper limb was absent. The CT scan showed a ponto-mesencephalic hypodensity. In the chronic phase the MEP from the left upper limb had reappeared and showed a normal latency, while the one from the right upper limb worsened; at that time a new small left fronto-parietal hypodensity had appeared on CT scan. The combined use of MEP, SEP and ABR was able to confirm that the brain-stem damage involved the pyramidal but spared the lemniscal pathways, while MEP changes during the clinical course appeared to reflect both clinical and radiological findings.     

Magnetic sources of the M50 response are localized to frontal cortex.

OBJECTIVE: To determine the source localization(s) of the midlatency auditory magnetic response M50, the equivalent of the P50 potential, a sleep state-dependent waveform known to habituate to repetitive stimulation. METHODS: We used a paired stimulus paradigm at interstimulus intervals of 250, 500 and 1000 ms, and magnetoencephalographic (MEG) recordings were subjected to computational methods for current density reconstruction, blind source separation, time-frequency analysis, and data visualization to characterize evoked dynamics. RESULTS: Each subject showed localization of a source for primary auditory evoked responses in the region of the auditory cortex, usually at a 20-30 ms latency. However, responses at 40-70 ms latency that also decreased following the second stimulus of a pair were not localizable to the auditory cortex, rather showing multiple sources usually including the frontal lobes. CONCLUSIONS: The M50 response, which shows habituation to repetitive stimulation, was not localized to the auditory cortex, but showed multiple sources including frontal lobes. SIGNIFICANCE: These MEG results suggest that sources for the M50 response may represent non-auditory, perhaps arousal-related, diffuse projections to the cortex.     

Cognitive evoked potentials to anticipated oesophageal stimulus in humans: quantitative assessment of the cognitive aspects of visceral perception

Evoked potential studies provide an objective measure of the neural pathways involved with perception. The effects of cognitive factors, such as anticipation or awareness, on evoked potentials are not known. The aim was to compare the evoked potential response to oesophageal stimulation with the cortical activity associated with anticipation of the same stimulus. In 12 healthy men (23.5 +/- 4 years), oesophageal electrical stimulation (15 mA, 0.2 Hz, 0.2 msec) was applied, and the evoked potentials recorded using scalp electrodes. A computerized model of randomly skipped stimuli (4:1 ratio) was used to separately record the evoked potentials associated with stimulation and those associated with an anticipated stimulus. The electrical stimulus represented the nontarget stimulus and the skipped impulse the target (anticipatory) stimulus. This anticipatory evoked potential was also compared to auditory P300 evoked potentials. Reproducible evoked potentials and auditory P300 responses were elicited in all subjects. Anticipatory evoked potentials (peak latency 282.1 +/- 7.9 msec, amplitude 8.2 +/- 0.7 microV, P < 0.05 vs auditory P300 evoked potential) were obtained with the skipped stimulus. This anticipatory evoked potential was located frontocentrally, while the auditory P300 potential was located in the centro-parietal cortex. The anticipatory evoked potential associated with expectation of an oesophageal stimulus, although of similar latency to that of the auditory P300 evoked response, originates from a different cortical location. The recording of cognitive evoked potentials to an expected oesophageal stimulus depends on attention to, and awareness of, the actual stimulus. Anticipatory evoked potentials to GI stimuli may provide an objective electrophysiological tool for the assessment of the cognitive factors associated with visceral perception.     

Effects of isoflurane on auditory middle latency (MLRs) and steady-state (SSRs) responses recorded from the temporal cortex of the rat

Auditory steady-state responses (SSRs) are believed to result from superimposition of middle latency responses (MLRs) evoked by individual stimuli during repetitive stimulation. Our previous studies showed that besides linear addition of MLRs, other phenomena, mainly related to the adaptive properties of neural sources, interact in a complex way to generate the SSRs recorded from the temporal cortex of awake rats. The aim of this study was to evaluate the effects of the inhalational general anesthetic, isoflurane, on MLRs and SSRs at several repetition rates (30-60 Hz) recorded from the temporal cortex of rats. Auditory evoked potentials were obtained by means of epidural electrodes in the awake condition and during anesthesia at three isoflurane concentrations (0.38, 0.76 and 1.13 vol.% in oxygen). MLR latency significantly increased during anesthesia in a concentration-dependent manner, while MLR amplitude, even when significantly attenuated with respect to the mean awake baseline value, failed to correlate with isoflurane concentration. SSRs decreased in amplitude and increased in phase during anesthesia in a concentration-dependent manner and the anesthetic-induced decrease of SSR amplitude appeared to be higher than the corresponding MLR attenuation. SSR prediction curves synthesized by linear addition of MLRs failed to predict SSRs in both amplitude and phase. Moreover, phase discrepancies proved to be higher during anesthesia. Our results suggest that MLRs and SSRs recorded from the temporal cortex of the rat exhibit differential sensitivity to isoflurane and that isoflurane could enhance the role of rate-dependent effects in SSR generation.     

Evoked potential decrements in auditory cortex. I. Discrete-trial and continual stimulation.

In experiment 1 cats were exposed to sets of clicks (trials) with 1 min inter-trial-intervals to determine if the effects of repetitive stimulation on potentials evoked in the auditory cortex would be cumulative despite discrete-trial stimulation. Evoked potentials were averaged to give one average evoked potential (AEP) for each trial for each electrode; there were four cortical electrodes per subject. To test for dishabituation pawshocks were given between trials 60 and 61. Subjects were paralyzed to insure stimulus constancy. The latency and peak-to-peak amplitude of each component of each AEP was measured; significant amplitude decremented; and decrements were more frequent in components with latencies greater than 15 msec. A few amplitude increments and latency changes were also observed...     

Changes in subcortical visual and auditory evoked potentials following amygdaloid kindling in cats

In this study we dealt with the changes in visual and auditory evoked potentials following kindling, to reveal the distant effects of epileptic activity. The experiments were performed using cats. Visual and auditory evoked potentials were obtained initially. Daily stimulation of 60 Hz (rectangular wave, 1 ms in duration, 500 microA in peak current, 2-s train) was given to the right amygdala, for kindling. After the completion of kindling, evoked responses were recorded again. In the auditory system the changes of responses in the cortex, medial geniculate nucleus, and cochlear nucleus were distinguished. The changes of potentials in the subcortex were larger than those at the cortical level. For visual evoked potentials there was a discrepancy between stimulation with light and electrical stimulation of the optic chiasm. There was no significant change in amplitude of visual evoked potentials by flash. In the case of optic chiasm stimulation, an enlargement of evoked responses was obtained. These results indicate modality-specific change of the auditory system and widespread subcortical change. These results might be caused by some vulnerability of the auditory system in the case of amygdaloid kindling, as a result of the epileptogenic process.     

Oxytocin actions on afferent evoked spinal cord neuronal activities in neuropathic but not in normal rats

A hypothalamic oxytocinergic-descending pathway that reaches the dorsal horn of the spinal cord has been well documented and recently related to states of pain and analgesia. In order to study the action of the neuropeptide oxytocin (OT) on pain-related responses, we compared dorsal horn neuronal responses to electrical and mechanical stimulation of receptive fields in normal and neuropathic rats. Spinal nerve (L5 and L6) ligation (Chung rats) was used to produce experimental neuropathy. Single unit activity was recorded at the L4-L5 level from neurons identified as wide dynamic range presenting latency responses corresponding to A-beta, A-delta, C fibers and also exhibiting post-discharge, and wind-up. We tested intrathecally applied doses of 0.05, 0.1, 1, 2, 5, 10 I.U. of OT. Minor effects on responses to electrical stimulation were present in normal rats. Mechanical responses evoked by von Frey filaments were slightly reduced in normal animals. In neuropathic rats a dose of 1 I.U. produced a significant reduction in C-fibers and post-discharge activities, and doses of 2 I.U. caused a further, pronounced reduction in post-discharge, wind-up, and input values. However, the most marked change was the post-discharge reduction at 10 and 20 min after OT administration. Mechanical responses were significantly reduced in terms of their discharge rate response in neuropathic rats. The contrasting results obtained in normal and neuropathic rats revealed an important distinction between these animals and indicate that plastic changes occur as a consequence of nerve damage. In neuropathic rats, mechanisms involving ascending noxious information to the paraventricular nuclei and descending OT activities could be altered so sensitizing the OT receptors of the spinal dorsal horn cells and could explain our observations. Our results point out an anti-algesic OT effect in neuropathic rats.     

Effects of deep brain stimulation on the primary motor cortex: Insights from transcranial magnetic stimulation studies

Deep brain stimulation (DBS) implanted in different basal ganglia nuclei regulates the dysfunctional neuronal circuits and improves symptoms in movement disorders. However, the understanding of the neurophysiological mechanism of DBS is at an early stage. Transcranial magnetic stimulation (TMS) can be used safely in movement disorder patients with DBS, and can shed light on how DBS works. DBS at a therapeutic setting normalizes the abnormal motor cortical excitability measured with motor evoked potentials (MEP) produced by primary motor cortical TMS. Abnormal intracortical circuits in the motor cortex tested with paired-pulse TMS paradigm also show normalization with DBS. These changes are accompanied with improvements in symptoms after chronic DBS. Single-pulse DBS produces cortical evoked potentials recorded by electroencephalography at specific latencies and modulates motor cortical excitability at certain time intervals measured with MEP. Combination of basal ganglia DBS with motor cortical TMS at stimulus intervals consistent with the latency of cortical evoked potentials delivered in a repetitive mode produces plastic changes in the primary motor cortex. TMS can be used to examine the effects of open and closed loop DBS. Patterned DBS and TMS delivered in a repetitive mode may be developed as a new therapeutic method for movement disorder patients.     

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.     

Cell responses evoked by tooth pulp stimulation above the marginal layer of the cat's trigeminal nucleus caudalis

In cats anesthetized with urethane, all-or-nothing, synaptically evoked recordings were made from 80 separate units in the descending spinal tract of the trigeminal nerve above the left trigeminal nucleus caudalis, at depths not exceeding 50 μm from the surface of the medulla. The units were excited by the left upper (21), left lower (25), either (28), or only on simultaneous stimulation of both (six) canine tooth pulps. There was no somototopic distribution. The latency of responses ranged from 4 to 82 msec. For the group of 28 units excited by upper and lower tooth pulps, there was close matching of response latencies from the two teeth. An abrupt decrease in latency upon increasing stimulation strength (“jumping”), and a gradual increase in latency during repetitive stimulation at a frequency between 1 and 20 Hz (“drifting”) was characteristic of most, but not all, responses. Units evoked by stimulation of the inferior dental or infraorbital nerves had similar characteristics. Stimulation of a tooth pulp at threshold for a particular unit was used to test the excitability of that unit after suprathreshold stimulation of the same or a different canine tooth pulp. Stimulation of the upper left canine tooth pulp was generally only facilitatory, while stimulation of the lower left canine tooth pulp was initially facilitatory and later inhibitory. Stimulation of the upper or lower right canine tooth pulps did not excite but could inhibit units excited by the left canine tooth pulps. There was a significant correlation between the frequency at which a unit would follow repetitive stimulation and the duration of the inhibition generated by the first of a pair of stimuli. Long inhibition was associated with poor frequency following.     

Pallidal inputs to subthalamus: Intracellular analysis

Neuronal responses of the subthalamic nucleus (STH) to stimulation of the globus pallidus (GP) and the substantia nigra (SN) were studied by intracellular recording in the decorticated rat. (1) GP and SN stimulation evoked antidromic spikes in STH neurons with a mean latency of 1.2 ms and 1.1 ms, respectively. Based on the above latencies, the mean conduction velocity of the STH neurons projecting toward GP was estimated to be 2.5 m/s, and that toward SN was 1.4 m/s. Many STH neurons could be activated following stimulation of both GP and SN, indicating that single STH neurons project to two diversely distant areas. In spite of differences in conduction distance of GP and SN from STH, differences in the conduction velocities of bifurcating axons make it possible for a simultaneous arrival of impulses in the target areas to which these STH neurons project. (2) GP stimulation evoked short duration (5-24 ms) hyperpolarizing potentials which were usually followed by depolarizing potentials with durations of 10-20 ms. These potentials were tested by intracellular current applications and intracellular injections of chloride ions. The results indicated that the hyper- and depolarizing potentials were IPSPs and EPSPs respectively. These IPSPs were considered to be monosynaptic in nature since changes in the stimulus intensities of GP did not alter the latency of IPSPs. The mean latency of the IPSPs was 1.3 ms. Based on the above mean latency the mean conduction velocity of GP axons projecting to STH was estimated to be 3.8 m/s. (3) Analysis of electrical properties of STH neurons indicated that: (i) input resistance estimated by a current-voltage relationship ranged from 9 to 28 M omega; (ii) the membrane showed rectification in the hyperpolarizing direction; (iii) direct stimulation of neurons by depolarizing current pulses produced repetitive firings with frequencies up to 500 Hz. (4) Morphology of the recorded STH neurons was identified by intracellular labeling of neurons with horseradish peroxidase. Light microscopic analysis indicated that the recorded neurons were Golgi type I neurons with bifurcating axons projecting toward GP and SN.     

Neuronal substrates of sensory gating within the human brain.

BACKGROUND: For the human brain, habituation to irrelevant sensory input is an important function whose failure is associated with behavioral disturbances. Sensory gating can be studied by recording the brain's electrical responses to repeated clicks: the P50 potential is normally reduced to the second of two paired clicks but not in schizophrenia patients. To identify its neural correlates, we recorded electrical traces of sensory gating directly from the human hippocampus and neocortex. METHODS: Intracranial evoked potentials were recorded using hippocampal depth electrodes and subdural strip and grid electrodes in 32 epilepsy patients undergoing invasive presurgical evaluation. RESULTS: We found evidence of sensory gating only in the hippocampus, the temporo-parietal region (Brodmann's areas 22 and 2), and the prefrontal cortex (Brodmann's areas 6 and 24); however, whereas neocortical habituating responses to paired clicks were peaking around 50 msec, responses within the hippocampus proper had a latency of about 250 msec. CONCLUSIONS: Consistent with data from animal studies, our findings show that the hippocampus proper contributes to sensory gating, albeit during a time window following neocortical habituation processes. Thus, sensory gating may be a multistep process, with an early phase subserved by the temporo-parietal and prefrontal cortex and a later phase mediated by the hippocampus.     

The development of stimulus following in the cochlear nerve and inferior colliculus of the mouse

The decrement of evoked response amplitudes during the presentation of repetitive clicks was examined quantitatively at the level of the eighth nerve and inferior colliculus in mice aged 13-60 days postnatal. The amplitudes of both these potentials were found to decline during the course of stimulation, this being much more severe at the onset of hearing than in adults. Furthermore the following response at the level of the cochlear nerve was adult-like by day 18, while the response at the level of the inferior colliculus continued to improve through day 24. Recordings in the inferior colliculus were consistently obtained in two different regions along the frequency axis. The regions that responded best to a lower range of frequencies (e.g. 3-9 kHz) showed a more rapid and severe decrement in the evoked response to repetitive stimulation than those regions responding best to a higher range of frequencies (e.g. 8-17 kHz). This was found to be the case for repetitive click stimuli and repetitive tone bursts. Single unit responses in the inferior colliculus were consistent with this differential decline as a function of stimulus rate seen along the frequency axis.