NF-kappaB2 is a putative target gene of activated Notch-1 via RBP-Jkappa

Cutaneous stimulation of the face and hand with a CO2 laser in three awake patients evoked potentials (LEPs) recorded from the dominant left parasylvian cortex. These were recorded by means of a subdural grid of electrodes implanted for evaluation of epilepsy. Stimulation of the contralateral face resulted in waveforms consisting of a negative potential (N2, 162 +/- 5 ms; mean +/- SE) followed by a positive potential (P2, 340 +/- 18 ms). Both waves occurred at longer latency after hand than after facial stimulation. N2 and P2 potentials recorded from the grid correspond well in morphology to those recorded from the scalp in four additional patients tested with the same stimulation paradigm. The N2 waves recorded from the subdural grid occurred at significantly shorter latencies than did those recorded from the scalp (184 +/- 6 ms), but the P2 waves at the grid occurred at significantly longer latencies than did those recorded at the scalp (281 +/- 13 ms). The amplitudes of the potentials recorded from the grid were maximal over the parietal operculum both for contralateral stimulation of the face or hand and for ipsilateral stimulation of the face. Potentials also were recorded in this area after stimulation of the ipsilateral hand. The cortical distributions of these potentials suggest that their generators are located in the parietal operculum or in the insula, or in both, consistent with previous PET, magnetoencephalographic, and scalp LEP source analyses. These previous analyses provide indirect evidence of nociceptive input to parasylvian cortex because the interpretation of each analysis incorporates multiple assumptions. The present results are the first direct evidence of nociceptive input to the human parasylvian cortex.     

Positive correlation of plasma transforming growth factor-beta 1 levels with tumor vascularity in hepatocellular carcinoma

The initial somatosensory evoked magnetic fields following painful heat stimulation by CO2 laser beam applied to the upper and lower limb were investigated in normal subjects. The main deflections, 'Pain MA' and 'Pain ML' following the arm and leg stimulation, respectively, were identified in the bilateral second sensory cortices (SII). The onset latencies of Pain MA and Pain ML were approximately 150 and 200 ms, respectively. No consistent equivalent current dipole was found in other areas including the primary sensory cortex in each hemisphere. Therefore, we consider that neurons in the bilateral SII are initially activated following painful heat stimulation.     

Impact of chromosome 14q loss on survival in primary head and neck squamous cell carcinoma

OBJECTIVE: To investigate somesthetic functions of the perisylvian cortex. METHODS: Somatosensory evoked magnetic fields (SEFs) and somatosensory evoked potentials (SEPs) of the perisylvian cortex were recorded directly from subdural electrodes in a patient with a left frontal brain tumour. RESULTS: The most prominent SEP components after electrical stimulation of the right and left hands and the right foot were double peaked negativity recorded just above the sylvian fissure (latency 80 to 150 ms), respectively (N1a and N1b). Generator sources for the magnetoencephalographic counterparts of those peaks (N1a(m) and N1b(m)) were both localised at the upper bank of the sylvian fissure, and those of N1a(m) were more anteromedially located than those of N1b(m). CONCLUSIONS: These findings suggest the existence of at least two separate somatosensory areas within the human perisylvian cortex.     

A new pressure ulcer risk assessment scale for individuals with spinal cord injury

The topography of somatosensory evoked magnetic fields (SEFs) following stimulation of the upper and lower lips was investigated in 6 normal subjects. When the lateral side of the upper lip was stimulated, P20m and its counterpart, N20m, were identified in the hemisphere contralateral to the stimulated side. The equivalent current dipoles (ECDs) of N20m-P20m were considered to be located in lip area of the primary sensory cortex (SI). Middle latency deflections (N40m-P40m, N60m-P60m, and N80m-P80m) were identified in bilateral hemispheres. Their ECDs were located in the SI in both hemispheres. Long latency deflections (P110m-N110m) were recognized in both hemispheres, and their ECDs were located inferior to the SI, in an area considered to be the secondary sensory cortex (SII). When the midline of the lip was stimulated, similar short and middle latency deflections was also identified, but SII deflections (P110m-N110m) were decreased in amplitude. When the lower lip was stimulated, the ECDs of short and middle latency deflections were located at a site in the SI inferior to or near those elicited by upper lip stimulation. The ECDs of P110m-N110m were located in an area of the SII similar to that upon stimulation of the upper lip, but their orientations were different.     

Responses of neurons of the first and second somatosensory zones of the cortex to peripheral, thalamic and cortical stimulation

Experiments were performed on cats immobilized with d-tubocurarine or myorelaxin. Neuronal responses were studied in the first somatosensory cortex (SI) to the second somatosensory cortex (SII), ventroposterior nucleus (VP) and contralateral forepaw stimulation. Besides, neuronal responses in SII to SI, VP and contralateral forepaw stimulation were also studied. It was shown that in SII the percentage of neurons excited by afferent volley with two or more synaptic change-overs in the cerebral cortex was larger than in SI. Neurons of SI and SII responded to cortical stimulation ortho- and antidromically, thus confirming the existence of bilateral cortico-cortical connections. Both in SI and SII, PSPs to cortical stimulation were similar in character to PSPs in the same neurons to VP stimulation. In 50.0% of SI neurons and 37.1 of SII neurons the difference in latencies of orthodromic spike potentials to VP and cortical stimulation was less than 1.0 ms. In 19.6% of SI neurons and 41.4% of SII neurons the latency of the response to cortical stimulation was 1.6-4.7 ms shorter than that of the response in the same neuron to VP stimulation. It is supposed that impulses from SI participate significantly in afferent activation of SII neurons.     

Attention modulates both primary and second somatosensory cortical activities in humans: a magnetoencephalographic study

To clarify the role of primary and second somatosensory cortex (SI and SII) in somatosensory discrimination, we recorded somatosensory evoked magnetic fields during a stimulus strength discrimination task. The temporal pattern of cortical activation was analyzed by dipole source model coregistered with magnetic resonance image. Stimulus intensity was represented in SI as early as 20 ms after the stimulus presentation. The later components of SI response (latency 37.7 and 67.9 ms) were enhanced by rarely presented stimuli (stimulus deviancy) during passive and active attention. This supports an early haptic memory mechanism in human primary sensory cortex. Contra- and ipsilateral SII responses followed the SI responses (latency 124.6 and 138.3 ms, respectively) and were enhanced by attention more prominently than the SI responses. Active attention increased SII but not SI activity. These results are consistent with the concept of ventral somatosensory pathway that SI and SII are hierarchically organized for passive and active detection of discrete stimuli.     

Task-dependent modulation of inhibitory actions within the primary motor cortex

In 11 healthy subjects motor-evoked potentials (MEPs) and silent periods (SPs) were measured in the right first dorsal interosseus (FDI) and abductor pollicis brevis muscles (APB): (1) when transcranial magnetic cortex stimulation (TMS) was applied at tonic isometric contraction of 20% of maximum force, (2) when TMS was applied during tactile exploration of a small object in the hand, (3) when TMS was applied during visually guided goal-directed isometric ramp and hold finger flexion movements, and (4) when at tonic isometric contraction peripheral electrical stimulation (PES) of the median nerve was delivered at various intervals between PES and TMS. Of the natural motor tasks, duration of SPs of small hand muscles was longest during tactile exploration (APB 205+/-42 ms; FDI 213+/-47 ms). SP duration at tonic isometric contraction amounted to 172+/-35 ms in APB and 178+/-31 ms in FDI, respectively. SP duration in FDI was shortest when elicited during visually guided isometric finger movements (159+/-15 ms). At tonic isometric contraction, SP was shortened when PES was applied at latencies -30 to +70 ms in conjunction with TMS. The latter effect was most pronounced when PES was applied 20 ms before TMS. PES-induced effects increased with increasing stimulation strength up to a saturation level which appeared at the transition to painful stimulation strengths. Both isolated stimulation of muscle afferents and of low-threshold cutaneous afferents shortened SP duration. However, PES of the contralateral median nerve had no effect on SPs. Amplitudes of MEPs did not change significantly in any condition. Inhibitory control of motor output circuitries seems to be distinctly modulated by peripheral somatosensory and visual afferent information. We conclude that somatosensory information has privileged access to inhibitory interneuronal circuits within the primary motor cortex.     

Intracortical inhibition of lower limb motor-evoked potentials after paired transcranial magnetic stimulation

The aim of the present study was to determine the characteristics of intracortical inhibition in the motor cortex areas representing lower limb muscles using paired transcranial magnetic (TMS) and transcranial electrical stimulation (TES) in healthy subjects. In the first paradigm (n=8), paired magnetic stimuli were delivered through a double cone coil and motor evoked potentials (MEPs) were recorded from quadriceps (Q) and tibialis anterior (TA) muscles during relaxation. The conditioning stimulus strength was 5% of the maximum stimulator output below the threshold MEP evoked during weak voluntary contraction of TA (33+/-5%). The test stimulus (67+/-2%) was 10% of the stimulator output above the MEP threshold in the relaxed TA. Interstimulus intervals (ISIs) from 1-15 ms were examined. Conditioned TA MEPs were significantly suppressed (P<0.01) at ISIs of less than 5 ms (relative amplitude from 20-50% of the control). TA MEPs tended to be only slightly facilitated at 9-ms and 10-ms ISIs. The degree of MEP suppression was not different between right and left TA muscles despite the significant difference in size of the control responses (P<0.001). Also, conditioned MEPs were not significantly different between Q and TA. The time course of TA MEP suppression, using electrical test stimuli, was similar to that found using TMS. In the second paradigm (n=2), the suppression of TA MEPs at 2, 3, and 4 ms ISIs was examined at three conditioning intensities with the test stimulation kept constant. For the pooled 2- to 4-ms ISI data, relative amplitudes were 34+/-6%, 61+/-5%, and 98+/-9% for conditioning intensities of 0.95, 0.90, and 0.85x active threshold, respectively (P<0.01). In conclusion, the suppression of lower limb MEPs following paired TMS showed similar characteristics to the intracortical inhibition previously described for the hand motor area.     

Putative projection of phrenic afferents to the limbic cortex in humans studied with cerebral-evoked potentials

Respiratory sensations may rely in part on cortical integration of respiratory afferent information. In an attempt to study such projections, we recorded evoked potentials at scalp and cervical sites in 10 normal volunteers undergoing transcutaneous phrenic stimulation (0.1-ms square pulses, intensity liminal for diaphragmatic activation, series of 600 shocks at 2 Hz). A negative cerebral component of peak latency (12.79 +/- 0.54 ms; N13) was constant, and a negative spinal component (7.09 +/- 1.04 ms; N7) could also be recorded, all results being reproducible over time. Monitoring of cardiac frequency, skin anesthesia, and stimulation adjacent to the phrenic nerve made the phrenic origin of N7 and N13 the foremost hypothesis. Increasing stimulation frequency and comparison with median nerve stimulation provided arguments for the neural nature of the signals and their cerebral origin. Recordings from intracerebral electrodes in a patient showed a polarity reversal of the evoked potentials at the level of the cingulate gyrus. In conclusion, phrenic stimulation could allow one to study projections of phrenic afferents to the central nervous system in humans. Their exact site and physiological meaning remain to be clarified.     

Spatio-temporal subthreshold receptive fields in the vibrissa representation of rat primary somatosensory cortex

Spatio-temporal subthreshold receptive fields in the vibrissa representation of rat primary somatosensory cortex. J. Neurophysiol. 80: 2882-2892, 1998. Whole cell recordings of synaptic responses evoked by deflection of individual vibrissa were obtained from neurons within adult rat primary somatosensory cortex. To define the spatial and temporal properties of subthreshold receptive fields, the spread, amplitude, latency to onset, rise time to half peak amplitude, and the balance of excitation and inhibition of subthreshold input were quantified. The convergence of information onto single neurons was found to be extensive: inputs were consistently evoked by vibrissa one- and two-away from the vibrissa that evoked the largest response (the "primary vibrissa"). Latency to onset, rise time, and the incidence and strength of inhibitory postsynaptic potentials (IPSPs) varied as a function of position within the receptive field and the strength of evoked excitatory input. Nonprimary vibrissae evoked smaller amplitude subthreshold responses [primary vibrissa, 9.1 +/- 0.84 (SE) mV, n = 14; 1-away, 5. 1 +/- 0.5 mV, n = 38; 2-away, 3.7 +/- 0.59 mV, n = 22; 3-away, 1.3 +/- 0.70 mV, n = 8] with longer latencies (primary vibrissa, 10.8 +/- 0.80 ms; 1-away, 15.0 +/- 1.2 ms; 2-away, 15.7 +/- 2.0 ms). Rise times were significantly faster for inputs that could evoke action potential responses (suprathreshold, 4.1 +/- 1.3 ms, n = 8; subthreshold, 12.4 +/- 1.5 ms, n = 61). In a subset of cells, sensory evoked IPSPs were examined by deflecting vibrissa during injection of hyperpolarizing and depolarizing current. The strongest IPSPs were evoked by the primary vibrissa (n = 5/5), but smaller IPSPs also were evoked by nonprimary vibrissae (n = 8/13). Inhibition peaked by 10-20 ms after the onset of the fastest excitatory input to the cortex. This pattern of inhibitory activity led to a functional reversal of the center of the receptive field and to suppression of later-arriving and slower-rising nonprimary inputs. Together, these data demonstrate that subthreshold receptive fields are on average large, and the spatio-temporal dynamics of these receptive fields vary as a function of position within the receptive field and strength of excitatory input. These findings constrain models of suprathreshold receptive field generation, multivibrissa interactions, and cortical plasticity.     

Effects of interstimulus interval on somatosensory evoked magnetic fields (SEFs): a hypothesis concerning SEF generation at the primary sensorimotor cortex

Cerebral responses evoked by peripheral stimuli are known to depend critically on the interstimulus interval (ISI). Here we report on the effects of ISI on somatosensory evoked magnetic fields (SEFs) to right median nerve stimulation, obtained in 9 healthy adults with ISIs of 0.15 0.3, 1,3 and 5 s. At the contralateral (left) primary sensorimotor cortex (SMI), the first cortical response, N20m, was stable between the ISIs 0.3 and 5 s, but slightly attenuated at the shortest ISI of 0.15 s. In contrast, the P35m and P60m deflections were very sensitive to changes of the ISI, declining steadily with shortening of the ISI throughout the entire range. These deflections were frequently undetectable at the shortest ISI of 0.15 s. Concomitant with the reductions of P35m and P60m, an N45m deflection was enhanced toward the short ISIs. Responses from second somatosensory cortex (SII) and posterior parietal cortex (PPC) were seen only with ISIs of 1 s or greater, being strongest at the 5 s ISI. Based on known effects of the ISI on intracellular evoked potentials, we present the following tentative model for the generation mechanism of the SMI response: N20m represents early excitatory postsynaptic potentials (EPSPs), P35m early inhibitory postsynaptic potentials (IPSPs), N45m secondary EPSPs and P60m late IPSPs in pyramidal neurones of area 3b. For practical purposes, SEFs from SMI can be obtained with short ISIs, while responses from SII and PPC require an ISI of at least 1 s.     

Diaphragm EMG measured by cervical magnetic and electrical phrenic nerve stimulation

The purpose of the study was to compare electrical stimulation (ES) and cervical magnetic stimulation (CMS) of the phrenic nerves for the measurement of the diaphragm compound muscle action potential (CMAP) and phrenic nerve conduction time. A specially designed esophageal catheter with three pairs of electrodes was used, with control of electrode positioning in 10 normal subjects. Pair A and pair B were close to the diaphragm (pair A lower than pair B); pair C was positioned 10 cm above the diaphragm to detect the electromyogram from extradiaphragmatic muscles. Electromyograms were also recorded from upper and lower chest wall surface electrodes. The shape of the CMAP measured with CMS (CMS-CMAP) usually differed from that of the CMAP measured with ES (ES-CMAP). Moreover, the latency of the CMS-CMAP from pair B (5.3 +/- 0.4 ms) was significantly shorter than that from pair A (7.1 +/- 0.7 ms). The amplitude of the CMS-CMAP (1.00 +/- 0.15 mV) was much higher than that of ES-CMAP (0.26 +/- 0.15 mV) when recorded from pair C. Good-quality CMS-CMAPs could be recorded in some subjects from an electrode positioned very low in the esophagus. The differences between ES-CMAP and CMS-CMAP recorded either from esophageal or chest wall electrodes make CMS unreliable for the measurement of phrenic nerve conduction time.     

Neurotransmitter background of the anti-inflammatory effect evoked by activation of sensory nerve fibers

Intra-operative cortical and subcortical SEPs from the cerebral convexity and from the inter-hemispheric fissure were recorded following posterior tibial nerve (PTN) stimulation. Cortical and subcortical SEPs from the cerebral convexity after contra-lateral PTN stimulation consisted of N38 and P46, and their polarity reversed when the ipsi-lateral site was stimulated. On the other hand, cortical SEPs from the inter-hemispheric fissure always showed P38 and N46, whether the right or the left PTN was stimulated. Cortical and subcortical SEPs from the inter-hemispheric fissure showed clear cut polarity reversals. These findings provide good evidence for the existence of a tangential dipole oriented perpendicular to the inter-hemispheric fissure in the foot sensory area of the primary sensory cortex. SEPs recorded from the superficial part of the inter-hemispheric fissure showed smaller amplitudes and longer latencies than those of SEPs from the deeper regions. These findings suggest the existence of another dipole responsible for the generation of SEPs after PTN stimulation.     

Changes of relaxation times (T1, T2) and apparent diffusion coefficient after permanent middle cerebral artery occlusion in the rat: temporal evolution, regional extent, and comparison with histology

The quantitative NMR parameters T1, T2, rho, and apparent diffusion coefficient (ADC) were determined during the 7 h after middle cerebral artery occlusion in rats. In the normal caudate-putamen (CP), 869 +/- 145 ms and 72 +/- 2 ms for T1 and for T2, respectively, were found; the corresponding values for cortex were 928 +/- 117 ms and 73 +/- 2 ms. The ADC showed significant dependence on gradient direction: diffusion along x resulted in 534 +/- 53 microns 2/s (CP) and 554 +/- 62 microns 2/s (cortex), and along y in 697 +/- 58 microns 2/s (CP) and 675 +/- 53 microns 2/s (cortex). In the ischemic territory, a continuous increase over time of both relaxation times was observed in the CP, leading to an increase of 29 +/- 20% (T1) and 51 +/- 41% (T2) above control level. ADC dropped to 63 +/- 15% of control in the CP and to 74 +/- 4% of control in the temporal cortex. No significant change was noted in proton density during the observation period. Strongest ADC reduction was in the center of the ischemic territory (< or = 60% of control) surrounded by a region of lesser reduction (< or = 80% of control). During the early part of the study, the area of reduced ADC was larger than that of elevated relaxation times. Toward the end of the experiment, the area of increased relaxation times approached that of decreased ADC at < or = 80% of control. Good agreement of histological presentation of infarct with the total area of decreased ADC (< or = 80%) was demonstrated.     

Converging inputs to the entorhinal cortex from the piriform cortex and medial septum: facilitation and current source density analysis

Converging inputs to the entorhinal cortex from the piriform cortex and medial septum: facilitation and current source density analysis. J. Neurophysiol. 78: 2602-2615, 1997. The entorhinal cortex receives sensory inputs from the piriform cortex and modulatory inputs from the medial septum. To examine short-term synaptic facilitation effects in these pathways, current source density (CSD) analysis was used first to localize the entorhinal cortex membrane currents, which generate field potentials evoked by stimulation of these afferents. Field potentials were recorded at 50-micron intervals through the medial entorhinal cortex in urethan-anesthetized rats and the one-dimensional CSD was calculated. Piriform cortex stimulation evoked a surface-negative, deep-positive field potential component in the entorhinal cortex with mean onset and peak latencies of 10.4 and 18.4 ms. The component followed brief 100-Hz stimulation, consistent with a monosynaptic response. CSD analysis linked the component to a current sink, which often began in layer I before peaking in layer II. A later, surface-positive field potential component peaked at latencies near 45 ms and was associated with a current source in layer II. Medial septal stimulation evoked positive and negative field potential components which peaked at latencies near 7 and 16 ms, respectively. A weaker and more prolonged surface-negative, deep-positive component peaked at latencies near 25 ms. The early components were generated by currents in the hippocampal formation, and the late surface-negative component was generated by currents in layers II to IV of the entorhinal cortex. Short-term facilitation effects in conscious animals were examined using electrodes chronically implanted near layer II of the entorhinal cortex. Paired-pulse stimulation of the piriform cortex at interpulse intervals of 30 and 40 ms caused the largest facilitation (248%) of responses evoked by the second pulse. Responses evoked by medial septal stimulation also were facilitated maximally (59%) by a piriform cortex conditioning pulse delivered 30-40 ms earlier. Paired pulse stimulation of the medial septum caused the largest facilitation (149%) at intervals of 70 ms, but piriform cortex evoked responses were facilitated maximally (46%) by a septal conditioning pulse 100-200 ms earlier. Frequency potentiation effects were maximal during 12- to 18-Hz stimulation of either the piriform cortex or medial septum. Occlusion tests suggested that piriform cortex and medial septal efferents activate the same neurons. The CSD analysis results show that evoked field potential methods can be used effectively in chronically prepared animals to examine synaptic responses in the converging inputs from the piriform cortex and medial septum to the entorhinal cortex. The short-term potentiation phenomena observed here suggest that low-frequency activity in these pathways during endogenous oscillatory states may enhance entorhinal cortex responsivity to olfactory inputs.     

Stability of the input-output properties of chronically implanted multiple contact nerve cuff stimulating electrodes

The objective of this investigation was to measure the input-output (I-O) properties of chronically implanted nerve cuff electrodes. Silicone rubber spiral nerve cuff electrodes, containing 12 individual platinum electrode contacts, were implanted on the sciatic nerve of seven adult cats for 28-34 weeks. Measurements of the torque generated at the ankle joint by electrical stimulation of the sciatic nerve were made every 1-2 weeks for the first 6 weeks post-implant and every 3-5 weeks between 6 weeks and 32 weeks post-implant. In three implants the percutaneous lead cable was irreparably damaged by the animal within 4 weeks after implant and further testing was not possible. One additional lead cable was irreparably damaged by the animal at 17 weeks post-implant. The three remaining implants functioned for 28, 31, and 32 weeks. Input-output curves of ankle joint torque as a function of stimulus current amplitude were repeatable within an experimental session, but there were changes in I-O curves between sessions. The degree of variability in I-O properties differed between implants and between different contacts within the same implant. After 8 weeks, the session to session changes in the stimulus amplitude required to generate 50% of the maximum torque (I50) were smaller (15+/-19%, mean +/- s.d.) than the changes in I50 measured between 1 week and 8 weeks post-implant (34+/-42%). Furthermore, the I-O properties were more stable across changes in limb position in the late post-implant period than in acutely implanted cuff electrodes. These results suggest that tissue encapsulation acted to stabilize chronically implanted cuff electrodes. Electrode movement relative to the nerve, de- and regeneration of nerve fibers, and the inability to precisely reproduce limb position in the measurement apparatus all may have contributed to the variability in I-O properties.     

Cortical activation during fast repetitive finger movements in humans: steady-state movement-related magnetic fields and their cortical generators

OBJECTIVE: To study the cortical physiology of fast repetitive finger movements. METHODS: We recorded steady-state movement-related magnetic fields (ssMRMFs) associated with self-paced, repetitive, 2-Hz finger movements in a 122-channel whole-head magnetometer. The ssMRMF generators were determined by equivalent current dipole (ECD) modeling and co-registered with anatomical magnetic resonance images (MRIs). RESULTS: Two major ssMRMF components occurred in proximity to EMG onset: a motor field (MF) peaking at 37+/-11 ms after EMG onset, and a postmovement field (post-MF), with inverse polarity, peaking at 102+/-13 ms after EMG onset. The ECD for the MF was located in the primary motor cortex (M1), and the ECD for the post-MF in the primary somatosensory cortex (S1). The MF was probably closely related to the generation of corticospinal volleys, whereas the post-MF most likely represented reafferent feedback processing. CONCLUSIONS: The present data offer further evidence that the main phasic changes of cortical activity occur in direct proximity to repetitive EMG bursts in the contralateral M1 and S1. They complement previous electroencephalography (EEG) findings on steady-state movement-related cortical potentials (ssMRCPs) by providing more precise anatomical information, and thereby enhance the potential value of ssMRCPs and ssMRMFs for studying human sensorimotor cortex activation non-invasively and with high temporal resolution.     

Fos expression in the prefrontal cortex and nucleus accumbens following exposure to retrospective timing tasks.

The dorsal striatum and prefrontal cortex have been implicated in interval timing. We examined whether performance of temporal discrimination tasks is associated with increased neuronal activation in these areas, as revealed by Fos expression, a marker for neuronal activation. In Experiment 1, rats were trained on a discrete-trials temporal discrimination task in which a light (22 cd/m2) was presented for a variable time, t (2.5–47.5 s), after which levers A and B were presented. A response on lever A was reinforced if t t > 25 s. A second group was trained on a light-intensity discrimination procedure, in which a light of variable intensity, i (3.6–128.5 cd/m2) was presented for 25 s. A response on lever A was reinforced if i i > 22 cd/m2. In Experiment 2, bisection procedures were used to assess temporal (200–800 ms, 22 cd/m2) and light-intensity (3.6–128.5 cd/m2, 400 ms) discrimination. The increase in proportional choice of lever B as a function of stimulus duration or intensity conformed to a two-parameter logistic equation. Fos expression in the prefrontal cortex and nucleus accumbens was higher in rats performing temporal discrimination tasks than in those performing light-intensity discrimination tasks, indicating greater neuronal activation in these areas during temporal discrimination tasks. Fos expression in the dorsal striatum did not differ between rats performing temporal and light-intensity discrimination tasks. These results suggest that the prefrontal cortex and nucleus accumbens are involved in temporal discrimination. (PsycINFO Database Record (c) 2011 APA, all rights reserved)     

Delayed development of spontaneous seizures and prolonged convulsive state in rats after massed stimulation of the anterior piriform cortex

We studied the short- and long-term epileptogenic effects of massed stimulation (MS) of the piriform cortex. Sprague-Dawley rats with electrodes implanted bilaterally in the anterior piriform cortex and the dorsal and ventral hippocampi underwent MS: electrical stimulation of the left piriform cortex every 5 min for 6 h (afterdischarge threshold, 60 Hz, 1 ms, 1 s). Animals were retested (5 stimulations) 3-4 times later at different time points to check for the kindled state. Our data showed that MS resulted in delayed development of severe epilepsy. The interval between MS and the first appearance of convulsive response (2 weeks) was characterized by deep refractoriness to seizure (silent period). Unexpectedly, dramatic seizure activity occurred 4-7 weeks after MS. This was manifested by (1) generalized tonic-clonic convulsions with multiple failings, which were elicited repeatedly during retest; (2) frequent progression of elicited generalized convulsions into a prolonged (> 8 min) postictal convulsive state expressed mainly by continuous partial seizures and even new bouts of generalized seizures, and (3) development of mild spontaneous seizures. We found that epileptiform activity predominated in the ventral hippocampus. Mossy fiber sprouting was also most pronounced in this area. We propose that the MS resulted in formation of pathological circuits which involve both piriform cortex and ventral hippocampus and lead to severe epilepsy.     

Effect of electrical stimulation of the central amygdaloid nucleus on the nociceptive neuron of the cortex (SI) in the cat

The effect of conditioning stimulation of the central amygdaloid nucleus (ACE) on the response of tooth pulp-driven (TPD) neurons in the first somatosensory cortex (SI) was investigated in cats anesthetized with N2O-O2 (2:1) and 0.5% halothane. The tooth pulp test stimulus was a single 30-450 microA rectangular pulse, and the conditioning stimuli of the ACE were trains of 33 pulses (300 microA) delivered at 330 Hz. The ACE conditioning stimulation markedly suppressed the response of the slow-type neurons with latencies of more than 20 ms without any effect on the discharges of fast-type TPD neurons and spontaneous discharges. This inhibition was 68.9 +/- 24.7% (mean +/- SD) of the control. These findings suggest that there are at least two pathways for the ascending pulpal (nociceptive) information to the SI, and that the ACE modulates the transmission of impulses in one of the pathways.