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C Trepel

Publications and source records attributed to C Trepel.

15 recordsLinked to original sources

Spatial frequency maps in cat visual cortex.

Neurons in the primary visual cortex (V1) respond preferentially to stimuli with distinct orientations and spatial frequencies. Although the organization of orientation selectivity has been thoroughly described, the arrangement of spatial frequency (SF) preference in V1 is controversial. Several layouts have been suggested, including laminar, columnar, clustered, pinwheel, and binary (high and low SF domains). We have reexamined the cortical organization of SF preference by imaging intrinsic cortical signals induced by stimuli of various orientations and SFs. SF preference maps, produced from optimally oriented stimuli, were verified using targeted microelectrode recordings. We found that a wide range of SFs is represented independently and mostly continuously within V1. Domains with SF preferences at the extremes of the SF continuum were separated by no more than (3/4) mm (conforming to the hypercolumn description of cortical organization) and were often found at pinwheel center singularities in the cortical map of orientation preference. The organization of cortical maps permits nearly all combinations of orientation and SF preference to be represented in V1, and the overall arrangement of SF preference in V1 suggests that SF-specific adaptation effects, found in psychophysical experiments, may be explained by local interactions within a given SF domain. By reanalyzing our data using a different definition of SF preference than is used in electrophysiological and psychophysical studies, we can reproduce the different SF organizations suggested by earlier studies.

Algorithms↗

Cholinergic modulation of neocortical long-term potentiation in the awake, freely moving rat.

The neocortex has proven resistant to LTP induction using standard in vitro and acute, in vivo preparations. Because the neocortex is widely thought to be involved in long-term information storage, this resistance raises questions about the validity of LTP as a memory model. Recently, we have shown that the neocortex of freely moving rats reliably supports LTP, provided that the stimulation is spaced and repeated over days. The following experiments were designed to evaluate the neuromodulatory role played by cholinergic systems in the induction of LTP in this preparation. Chronically implanted rats received either low- or high-intensity LTP-inducing tetani in combination with the administration of either a cholinergic agonist or antagonist injected systemically. Potentiation was evidenced as amplitude changes in both early and late components of the evoked field potential, the former including population spikes. The cholinergic agonist facilitated LTP induction in the late component of both high- and low-intensity groups. The cholinergic antagonist blocked LTP induction in the early component of the high-intensity group. The possibility that there are component-specific modulatory effects of cholinergic agents on the induction of neocortical LTP is discussed.

Action Potentials↗

Rapid extragranular plasticity in the absence of thalamocortical plasticity in the developing primary visual cortex.

Monocular deprivation during early postnatal development remodels the circuitry of the primary visual cortex so that most neurons respond poorly to stimuli presented to the deprived eye. This rapid physiological change is ultimately accompanied by a matching anatomical loss of input from the deprived eye. This remodeling is thought to be initiated at the thalamocortical synapse. Ocular dominance plasticity after brief (24 hours) monocular deprivation was analyzed by intrinsic signal optical imaging and by targeted extracellular unit recordings. Deprived-eye responsiveness was lost in the extragranular layers, whereas normal binocularity in layer IV was preserved. This finding supports the hypothesis that thalamocortical organization is guided by earlier changes at higher stages.

Animals↗

Long-term depression and depotentiation in the sensorimotor cortex of the freely moving rat.

Activity-dependent reductions in synaptic efficacy are central components of recent models of cortical learning and memory. Here, we have examined long-term synaptic depression (LTD) and the reversal of long-term potentiation (depotentiation) of field potentials evoked in sensorimotor cortex by stimulation of the white matter in the adult, freely moving rat. Prolonged, low-frequency stimulation (1 Hz for 15 min) was used to induce either depotentiation or LTD. LTD was expressed as a reduction in the amplitude of both monosynaptic and polysynaptic field potential components. Both LTD and depotentiation were reliably induced by stimulation of the ipsilateral white matter. Stimulation of the contralateral neocortex induced only a depotentiation effect, which decayed more rapidly than that induced by ipsilateral stimulation (hours vs days). Although ipsilateral LTD was effectively induced by a single session of low-frequency stimulation, multiple sessions of stimulation, either massed or spaced, induced LTD effects that were larger in magnitude and longer lasting. Previously, we showed that the induction of long-term potentiation in the neocortex of chronic preparations required multiple, spaced stimulation sessions to reach asymptotic levels. Here, we report that LTD also required multiple stimulation sessions to reach asymptotic levels, but massed and spaced patterns of low-frequency stimulation were equally effective.

Action Potentials↗

GABAergic modulation of neocortical long-term potentiation in the freely moving rat.

Although the neocortex has generally been considered resistant to the induction of long-term potentiation (LTP), we have recently shown that LTP can be reliably induced in the freely moving rat provided that the stimulation sessions are spaced and repeated. Here, we report that the induction of LTP in this preparation can be modulated by both GABAergic agonism and antagonism. The delivery of stimulation trains in the presence of the GABA(A) agonist diazepam blocked the induction of neocortical LTP, while the GABA(A) antagonist picrotoxin slowed the development of potentiation. When animals that had previously received high-frequency stimulation combined with diazepam were repotentiated, they showed greater resistance to LTP induction than animals that had received diazepam alone. These data suggest that the inhibitory circuits themselves may have potentiated. The demonstration that diazepam blocks neocortical LTP provides further support for the notion that LTP plays a role in memory formation.

Animals↗

Patchy distribution of NMDAR1 subunit immunoreactivity in developing visual cortex.

Development of ocular dominance columns is dependent on patterned retinal activity, and yet patterned activity alone cannot explain all aspects of cortical column development. Features intrinsic to the cortex have been proposed to interact with activity to guide the patterning of cortical columns (), and the NMDA receptor, because of its role in experience-dependent plasticity, is an obvious candidate. Using immunohistochemical techniques, we found a transiently patchy distribution of the NMDA receptor 1 (NMDAR1) subunit in kitten visual cortex. Regularly spaced patches of NMDAR1-immunoreactive neurons were found at the top of the cortical plate in the developing visual cortex at 2 weeks of age. At 4-5 weeks of age, the radial extent of the NMDAR1 patches spanned the supragranular layers, and by 12 weeks of age, this nonuniform pattern of NMDAR1 immunostaining was no longer apparent. Monocular visual experience prevented the expression of the NMDAR1 patches, but just 4 d of subsequent binocular visual experience was sufficient to promote expression of the patches. Furthermore, the NMDAR1 patches tended to be associated with the borders of ocular dominance columns. These results suggest that the degree of plasticity associated with NMDA-mediated mechanisms is elevated in local regions across the tangential extent of the visual cortex and that the NMDAR1 patches may participate in sculpting the overall arrangement of visual cortical columns.

Animals↗

Long-term potentiation in the neocortex of the adult, freely moving rat.

Neocortical preparations have proven highly resistant to the induction of long-term potentiation (LTP), and we have only recently determined the conditions sufficient for the induction of neocortical LTP in the adult, freely moving rat. The stimulation trains must be spaced and repeated over a period of days in order to reach asymptotic levels of potentiation. Here we show that, within these constraints, the neocortex is actually highly responsive. LTP could be induced with as few as one brief high frequency train per day or with extremely low-intensity stimulation trains. We also provide evidence for a critical role for N-methyl-D-aspartate (NMDA) receptor activation in LTP induction in this preparation, and demonstrate that this LTP is input-specific. Control pathways showed no potentiation effects. LTP was found in a monosynaptic and two polysynaptic components (average latencies to peak: 8.1, 15.2 and 20.0 ms) and in the superimposed population spikes. Although LTP could be induced with one train per day or with low-intensity trains, larger and longer-lasting potentiation effects could be induced by increasing the number of trains delivered per session, the number of sessions over which trains were delivered, or the pulse intensity of the trains. The LTP decayed slowly and was still evident 5 weeks later. Administration of the competitive NMDA antagonist 3-[(+/-)-2-carboxypiperazin-4-yl]-propyl-1-phosphonic acid blocked the induction of LTP in a dose-dependent fashion and appeared to unmask a depression of both the population spikes and a polysynaptic component. These results indicate that the neocortex is highly sensitive to LTP induction procedures, as long as the stimulation trains are spaced and applied over a period of days. They are also consistent with the view that the neocortex must operate with a slow learning rate to reduce interference effects in memory.

Aging↗

Changes in field potentials and membrane currents in rat sensorimotor cortex following repeated tetanization of the corpus callosum in vivo.

Repeated, daily tetanization of the corpus callosum induces lasting changes in sensorimotor cortex field potential responses, but the synaptic populations that mediate these responses and support long-term potentiation (LTP) have not been characterized. Current source density analyses of field responses were compared between control animals and those in which LTP was induced by 10 daily series of tetanizations. Tetanization and paired-pulse stimulation (100 ms interval) enhanced the duration of initial (approximately 3 ms onset) deep-negative population spike activity generated by a current sink in layer V that peaked repeatedly at a frequency of approximately 400 Hz. The early (approximately 10 ms to peak) surface-negative component of field responses was generated by a current sink in upper layer V and a source in layer VI. This monosynaptic component followed high stimulation frequencies, recovered quickly from the effects of anaesthesia, and was enhanced by both tetanization and paired-pulse stimulation. The late (approximately 20 ms to peak) surface-negative component was generated by a sink in upper layer V and a source deep in layer V, and was greatly enhanced by tetanization and paired-pulse stimulation. The late component did not follow high-frequency stimulation and recovered slowly from anaesthesia, suggesting that it is driven polysynaptically. Potentiation of monosynaptic thalamic and cortico-cortical afferents probably mediates enhancements of the early component and population spikes, while potentiation of polysynaptic afferents to layer V may contribute to growth in the late component.

Animals↗

Non-uniform distribution of the NMDAR1 receptor subunit in kitten visual cortex at the peak of the critical period.

PURPOSE: The development of columnar systems in the visual cortex, in particular ocular dominance columns, is dependent on experiential activity in conjunction with NMDA-mediated plasticity mechanisms. Recent experiments, however, have shown that certain aspects of the columnar organization of the visual cortex, such as the spacing of columns, are not changed by manipulations that affect the pattern of retinal activity. This raises the possibility that features intrinsic to the visual cortex may play a crucial role in the development of cortical columns and that a non-uniform distribution of NMDA receptors in the developing visual cortex could form the link between activity and intrinsic cortical modularity. METHODS: To examine this possibility we used immunohistochemical techniques to label the NMDAR1 receptor subunit protein in kitten visual cortex. The arrangement of the NMDAR1 subunit was visualized (using a monoclonal antibody) in flattened and coronal sections through visual cortex. The tangential and laminar distributions of NMDAR1 immunoreactivity (NMDAR1ir) were studied at the peak of the critical period for plasticity (4-5 weeks of age) in the developing kitten visual cortex. RESULTS: At the ages examined there was a non-uniform distribution of NMDAR1 immunoreactivity in the visual cortex. These patches of darker NMDAR1 label were found in layers 2/3 and extended up into layer 1. Thus, during development neurons expressing the NMDAR1 receptor subunit were distributed in a patchy fashion in the upper layers of the kitten visual cortex. CONCLUSIONS: This suggests that NMDA-mediated activity-dependent plasticity may not occur uniformly across the tangential extent of the visual cortex, and raises the possibility that the arrangement of NMDAR1 patches may guide the emergence of nascent columns in the developing visual cortex.

Animals↗

Intraseptal microinfusion of muscimol: effects on hippocampal formation theta field activity and phasic theta-ON cell discharges.

The effect of intraseptal microinfusions of the GABA-A agonist muscimol on spontaneously occurring or hypothalamically induced hippocampal formation (HPC) theta field activity and the simultaneously occurring discharge properties of CA1 pyramidal and dentate granule layer phasic theta-ON cells, was investigated in urethane-anesthetized rats. The microinfusion of 5.0-12.5 nmol of muscimol into the medical septum/vertical limb of the diagonal band of Broca (MS/vDBB) resulted in a progressive reduction (beginning 5 min postinfusion) in the power (amplitude) and finally the total loss of theta field activity. In contrast, theta field frequency remained unaffected during the entire postinfusion period that theta field activity was present. In the time immediately following the first 1-min intraseptal microinfusion of 5 nmol muscimol, (before changes in theta amplitude occurred) a brief period of increased phasic theta-ON cell excitability was noted. This was manifested as an increase in the number of discharges per rhythmic burst. Associated with the progressive reduction of the amplitude of theta field activity, phasic theta-ON cell discharge rates progressively decreased for a period beginning 5 min postinfusion of 5 nmol muscimol. Despite the progressive decrease in the number of discharges and a noticeable reduction in the degree of rhythmicity, phasic theta-ON cells maintained their preferred timing of discharges in relation to the phase of theta field activity, while the latter was present. Just prior to the complete abolishment of theta field activity, phasic theta-ON cells ceased discharging. During the period when theta field activity was replaced on low amplitude asynchronous activity, phasic theta-ON cells discharged in bursts correlated with every occurrence of sharp wave field activity. The results support the following conclusions: (1) the brief excitatory effect on HPC theta-ON cell discharges may be correlated pharmacologically with an initial brief increase in HPC ACh turnover. The reduction of phasic theta-ON cell discharges and theta field activity may be correlated with the longer lasting reduction of HPC ACh turnover, controlled by MS/vDBB GABA-A inputs to MS/vDBB cholinergic septohippocampal neurons, possibly along with a direct inhibition of the GABAergic septohippocampal projection; (2) the primary contribution of the MS/vDBB nuclei, as a nodal point in the ascending brainstem HPC synchronizing system, is the modulation of the amplitude of HPC formation theta field activity and secondarily to relay frequency-coded inputs from the posterior hypothalamic region (posterior and supramammillary nuclei); (3) HPC theta and sharp wave field activity represent functionally distinct neural inputs to the same population of phasic theta-ON cells located in both the CA1 pyramidal and dentate granule cell layers.

Animals↗

Arrest of seizure progression during electrical kindling in guinea-pigs with prior pentylenetetrazol-induced convulsions.

A number of comparative differences in the kindling phenomenon have been observed between guinea-pigs and rats. These differences likely reflect different mechanisms underlying brain plasticity. In this study, guinea-pigs were used to examine the kindling transfer phenomenon between peripheral pentylenetetrazol injection and electrical kindling of the amygdala. The changes in afterdischarge characteristics and behavioural seizures during electrical kindling were compared between animals that had experienced three PTZ-induced convulsions and PTZ-naive controls. We report that on the first electrical kindling session the PTZ-convulsed guinea-pigs displayed lower AD thresholds, enhanced AD durations and seizures, but that their seizures did not progress with repeated daily kindling stimulation.

Animals↗

Post-activation potentiation in the neocortex. IV. Multiple sessions required for induction of long-term potentiation in the chronic preparation.

The neocortex in chronically prepared rats is very resistant to the induction of long-term potentiation (LTP). In the first of two experiments described in this paper, we tried unsuccessfully to induce neocortical LTP within one session by coactivating basal forebrain cholinergic and cortical inputs to our neocortical recording site. In the second experiment, we tested a new procedure which involved the application of repeated conditioning sessions over several days. This procedure was suggested by our finding that kindling-induced potentiation (KIP) of cortical field potentials could be reliably triggered but was slow to develop. We administered 30 high frequency trains per day to the corpus callosum for 25 days. LTP in callosal-neocortical field potentials became clear after about 5 days of stimulation and reached asymptotic levels by about 15 days. After the termination of treatment, LTP persisted for at least 4 weeks, the duration of our post-stimulation test period. As in previous experiments on kindling-induced potentiation, the potentiation effects were clear in both early population spike components and in a late (probably disynaptic) component. The monosynaptic EPSP component was often depressed, but this may have been due to competing field currents generated by the enhanced population spike activity. We discuss these results in the context of theories emphasizing slower but more permanent memory storage in neocortex compared to the hippocampus.

Animals↗

Evolution of afterdischarge and seizure characteristics during electrical kindling of the guinea-pig.

Interspecies comparisons may help us understand the mechanisms which underlie brain plasticity. In this study, we examined the electrical kindling phenomenon in the amygdala, piriform and perirhinal regions of the guinea-pig. The changes in afterdischarge (AD) characteristics and behavioural seizures were assessed under different stimulation intervals and parameters as well as under reduced inhibitory neurotransmitter systems. We report that the guinea-pigs displayed a number of similarities with other species, such as the progressive increases in AD characteristics and seizure behaviours, but also a number of differences, such as the behavioural manifestations of the seizures, failing to reach a fully generalized tonic-clonic seizure and an apparent insensitivity to both low-frequency stimulation and reduced GABA and catecholamine levels.

Animals↗

Extrinsic modulation of theta field activity in the entorhinal cortex of the anesthetized rat.

Field recordings of the entorhinal cortex (EC) were studied and compared to those recorded concomitantly in the dentate region of the hippocampal formation (HPC) in the urethane anesthetized rat. The EC, like the HPC, showed two main variations of spontaneous field activity: a desynchronized, large amplitude irregular activity and a synchronized, rhythmic, slow frequency field activity (RSA or theta). Corroborating previous research, a phase reversal was seen across layer II of the EC and when recorded superficial to this layer, EC theta was phase-locked to that recorded from the HPC (dentate). Entorhinal cortex (and HPC) theta could be evoked by the application of moderate tail pinches (sensory stimulation), by pharmacological treatments enhancing cholinergic transmission, and by electrical stimulation of the posterior hypothalamus. Spectral analysis revealed that in all cases, theta was produced coherently across the two limbic structures. Entorhinal cortex (and HPC) production of theta could be abolished by pharmacological treatments disrupting cholinergic transmission, and by reversible procaine inactivation of the medial septal region. Therefore, it was concluded that limbic theta is modulated spontaneously, and with sensory and hypothalamic stimulation through the activity of cells in the medial septal region via muscarinic neurotransmission. It was also hypothesized that the activation of cells in the posterior hypothalamus linearly codes the frequency, and to a lesser extent the power, of EC and HPC theta. Given these findings and the coincidence and coherence of the occurrence of theta across the EC and HPC, it was postulated that it occurs via a parallel mechanism in the two areas.

Anesthesia↗

Blockade and disruption of neocortical long-term potentiation following electroconvulsive shock in the adult, freely moving rat.

Although the neocortex has been considered to be highly resistant to the induction of long-term potentiation (LTP), we have recently shown that spaced and repeated stimulation of white matter afferents reliably induces neocortical LTP in the freely moving rat. The following study examined the effects of maximal electroconvulsive shock (MES) stimulation on the induction of LTP in the chronically prepared rat. MES stimulation was applied at different intervals following LTP-inducing trains over a 10 day period. High-frequency LTP-inducing stimulation resulted in amplitude changes in both early (9.28 ms to peak) and late (20.81 ms to peak) components of the evoked EPSP, as well as of the population spikes. There was a window of time following high-frequency stimulation within which MES could interrupt the induction of LTP MES stimulation applied immediately, or 1 h after, LTP-inducing trains prevented the induction of LTP LTP was not blocked, however, when the MES stimulation was applied 6 h after the LTP-inducing trains. MES stimulation applied to a fully potentiated animal transiently attenuated both the population spike and polysynaptic measures, but both components recovered within 24 h. These data support the idea of a consolidation gradient for neocortical LTP similar to that seen in behavioural studies.

Animals↗