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PubMed1987

High concentration of cholecystokinin neurons in the newborn human entorhinal cortex.

Numerous cholecystokinin (CCK)-immunoreactive cells are detected in the newborn human entorhinal cortex. They are located essentially in layer II and in the superficial part of layer III. Their shape and size indicate that they are interneurons. Most of them are vertically oriented and have beaded processes reaching layer I and the deep part of layer III. The cell type most frequently observed are bipolar cells with an ovoid cell body measuring 8-10 microns across and 15 microns in length. No CCK immunoreactivity is seen in the large stellate and pyramidal cells.

Age Factors↗
PubMedDate not supplied

The dopaminergic innervation of monkey entorhinal cortex.

Dopamine has been implicated in the pathophysiology of schizophrenia, and the entorhinal cortex (ERC) is thought to be a site of structural pathology in this disorder. However, relatively little is known about the dopaminergic (DA) innervation of ERC in the primate brain. In this study, immunohistochemical methods and antibodies directed against tyrosine hydroxylase (TH) and dopamine were used to determine the organization of DA axons in the ERC of macaque monkeys. The anti-TH antibody used in this study appeared predominantly to identify DA axons, as demonstrated by its failure to label fibers that were immunoreactive with an antibody against dopamine-beta-hydroxylase in double-labeling experiments. In addition, the regional and laminar distributions of TH-immunoreactive fibers were strikingly similar to those labeled with the anti-dopamine antibody. With both antibodies, cytoarchitectonically identified subdivisions of monkey ERC (Amaral et al., 1987) differed in both the density and laminar distribution of labeled fibers. Immunoreactive processes exhibited a substantial rostral-to-caudal gradient of decreasing density across subdivisions of ERC, and the density of labeled fibers also decreased from medial to lateral in the rostral but not in the caudal subdivisions of ERC. The laminar distribution of labeled fibers differed both between and within subdivisions. For example, in the olfactory and rostral subdivisions of ERC, the superficial layers contained a very high density of immunoreactive processes, whereas in the intermediate region, three bands of labeled fibers were seen in layers I, III-IV, and VI. In addition, radial columns of fibers interdigitated with areas of decreased density were present between layers I and III. Although the overall density of labeled fibers was greater in lateral than in the caudal subdivisions of ERC, these regions had similar laminar distribution patterns. In these areas of monkey ERC, labeled processes were highest in density in deep layer I, and homogeneously distributed in the other cortical layers. These findings demonstrate that the DA innervation of monkey ERC is complex, and follows laminar- and subdivision-specific patterns. These patterns of distribution suggest the possible interactions that DA axons may have with other elements of ERC circuitry, and may provide insight into the possible functional roles of dopamine in ERC in both normal and disease states.

Animals↗
PubMedDate not supplied

[Characteristics of the cortical input of the hippocampus. Functional differences in the lateral and medial entorhinal cortex].

Extracellular investigation in unanaesthetized rabbits revealed low reactivity of the lateral entorhinal cortex neurones (lEC, field 28b) to visual and auditory stimuli. Only 25% of cells responded to them by diffuse long-latency reactions, while in medial EC (mEC, field 28a) 70% of neurones responded to these stimuli with short-latency patterned reactions. The neurones of lEC were selectively responsive to different somatosensory stimuli. Among reactions short-latency on-effects were observed. In some cells application of these stimuli switched on rhythmic bursts of spikes (frequency about 3-4 Hz) or regular activity of pacemaker type. The lEC neurones responded by short-latency driving to electrical stimulation of prefrontal cortex, while mEC neurones were responsive to stimulation of posterior non-primary neocortical areas. The data are discussed in the light of recent morphological findings on cortico-cortical connections of EC.

Animals↗
PubMedDate not supplied

Preserved number of entorhinal cortex layer II neurons in aged macaque monkeys.

The perforant path, which consists of the projection from the layer II neurons of the entorhinal cortex to the outer molecular layer of the dentate gyrus, is a critical circuit involved in learning and memory formation. Accordingly, disturbances in this circuit may contribute to age-related cognitive deficits. In a previous study, we demonstrated a decrease in N-methyl-D-aspartate receptor subunit 1 immunofluorescence intensity in the outer molecular layer of aged macaque monkeys. In this study, we used the optical fractionator, a stereological method, to determine if a loss of layer II neurons occurred in the same animals in which the N-methyl-D-aspartate receptor subunit 1 alteration was observed. Our results revealed no significant differences in the number of layer II neurons between juvenile, young adult, and aged macaque monkeys. These results suggest that the circuit-specific decrease in N-methyl-D-aspartate receptor subunit 1 reported previously occurs in the absence of structural compromise of the perforant path, and thus may be linked to an age-related change in the physiological properties of this circuit.

Aging↗
PubMed2005

Entorhinal cortex involvement in human mesial temporal lobe epilepsy: an electrophysiologic and volumetric study.

PURPOSE: Several studies have demonstrated diminution in the volume of entorhinal cortex (EC) ipsilateral to the pathologic side in patients with temporal lobe epilepsy (TLE). The relation between the degree of EC atrophy and the epileptogenicity of this structure has never been directly studied. The purpose of the study was to determine whether atrophy of the EC evaluated by the quantitative magnetic resonance imaging (MRI) method is correlated with the epileptogenicity of this structure in TLE. METHODS: Intracerebral recordings (SEEG method) of seizures from 11 patients with mesial TLE were analyzed. Seizures were classified according to patterns of onset: pattern 1 was the emergence of a low-frequency, high-amplitude rhythmic spiking followed by a tonic discharge, and pattern 2 was the emergence of a tonic discharge in the mesial structures. A nonlinear measure of SEEG signal interdependencies was used to evaluate the functional couplings occurring between hippocampus (Hip) and EC at seizure onset. MRI volumetric analysis was performed by using a T(1)-weighted three-dimensional gradient-echo sequence in TLE patients and 12 healthy subjects. RESULTS: Significant interactions between Hip and Ec were quantified at seizure onset. The EC was found to be the leader structure in most of the pattern 2 seizures. Volumetric measurements of EC demonstrated an atrophy in 63% of patients ipsilateral to the epileptic side. A significant correlation between the strength of EC-Hip coupling and the degree of atrophy was found. In addition, in those patients that had a normal EC volume, the EC was never the leader structure in Ec-Hip coupling. CONCLUSIONS: These results validate the potential role of volumetry to predict the epileptogenesis of the EC in patients with hippocampal sclerosis and MTLE.

Adolescent↗
PubMed1996

The distribution of two calcium binding proteins, calbindin D-28K and parvalbumin, in the entorhinal cortex of the adult mouse.

The immunohistochemical localization of two specific calcium binding proteins, parvalbumin (PV) and calbindin D-28K (CB), were examined in the entorhinal cortex (EC) of the adult mouse. The PV and CB immunoreactivities exhibited a conspicuous regional and laminar distribution in the EC. The overall immunostaining pattern of PV and CB appeared to be complementary in the EC, especially in the medial entorhinal area (MEA). In the dorsal MEA, although layer 2 showed intense PV and CB immunostaining, the PV immunoreactivity was denser in layers 3, 5 and 6a than in layers 4 and 6b, whereas the CB immunoreactivity was denser in layers 4 and 6b than in layers 3, 5 and 6a. Moreover, we recognized the dorsoventral gradation of the PV and CB staining that is, in the dorsal to ventral direction, the intensity of the PV immunostaining in layers 2, 3, 5 and 6a gradually decreased whereas that of the CB immunostaining in those layers gradually increased. In addition, a similar dorsoventral gradation was also observed in the number of PV immunoreactive (PV-IR) and CB-IR neurons in layer 3. In layer 2 of the MEA, the CB-IR neurons were clustered, while displaying a patch-like pattern which could not be recognized in either Nissl staining or PV staining. In contrast, layer 2 of the LEA was separated into two sublayers, the superficial sublayer 2a and the deeper sublayer 2b; both of these sublayers consisted of cell clusters recognized by Nissl staining. These sublayers showed a prominent difference in their CB immunoreactivity; the cells in the layer 2a clusters were CB negative, whereas the cells in the layer 2b clusters were CB-IR. Furthermore, we also recognized a particular region at the most medial part of the MEA, where layer 2 was different from the other portion of the MEA regarding CB immunoreactivity and the cells containing another calcium binding protein, calretinin, were clustered in layer 3. Both the adjacent section technique and the fluorescent double-staining technique clearly revealed that a relatively large number of presumable interneurons contained both PV and CB immunoreactivities. Furthermore, the three neuron groups that were immunoreactive for both PV and CB, immunoreactive for PV alone and immunoreactive for CB alone were heterogeneous in their structural features such as shape and size, and no particular difference was found in their structural features among these three groups.

Age Factors↗
PubMed1996

Involvement of entorhinal cortex or parietal cortex in long-term spatial discrimination memory in rats: retrograde amnesia.

Twenty-four rats assigned to 1 of 3 matched groups (control, entorhinal cortex [EC], and parietal cortex [PC]) were trained on 6 successive discrimination problems (2 in an 8-arm for pretraining and 4 in a 12-arm radial maze for training per se). The training on the 12-arm maze started 6, 4, 2, and 0.5 weeks before surgery. On the day after the rats learned the last problem, they were given surgery according to groups. Postoperative retention was measured by presenting 16 trials per session for each of the problems during 4 sessions. Results indicate that the EC lesions produced a retention deficit for problems learned immediately and up to 4 weeks before surgery, but not for the problem acquired 6 weeks before the lesions. The PC lesions produced a significant retrograde amnesia that was not temporally graded. Results demonstrate that the EC and PC make important, albeit distinct, contributions to spatial memory storage and retrieval in rats.

Amnesia, Retrograde↗
PubMed1999

Effects of combined medial septal area, fimbria-fornix and entorhinal cortex tetrodotoxin inactivations on passive avoidance response consolidation in the rat.

On the basis of previous experimental evidence, it has been concluded that the entorhinal cortex (EC), the fimbria-fornix (FF) complex and medial septal area (MSA) do not take part in the consolidation phase of passive avoidance response (PAR) memorization. On the other hand, a mnemonic role during consolidation of at least two of these structures has been argued, based on several considerations. In order to ascertain whether the EC and FF are still involved in PAR memorization during consolidation, the coupled fully reversible functional tetrodotoxin (TTX) inactivation of MSA, FF and EC was performed in rats having undergone a PAR training. In Experiment 1 MSA, FF and EC were inactivated pair-wise (FF and EC always bilaterally). Permanently cannulated animals were injected stereotaxically with TTX (5 ng in 0.5 microliter saline) or saline (0.5 microliter) immediately following PAR acquisition. It was shown that combined FF-EC inactivation induced PAR retention impairment, whereas FF-MSA and EC-MSA inactivation was not followed by amnesic effects. Having obtained a positive result, in Experiment 2 the combined FF-EC inactivation was performed at different post-acquisition delays (0.25 h, 1.5 h, 6 h), so as to assess the duration of their involvement in PAR consolidation. It was shown that only the coupled inactivation performed at the shortest post-acquisition delay was followed by amnesic effects. Thus EC and FF play a definite role during early consolidation. The results are discussed in relation to EC, FF, MSA, and hippocampal involvement in PAR memorization, as reported in previous studies, and to their connectivity.

Animals↗
PubMed2005

Fundamental differences in spontaneous synaptic inhibition between deep and superficial layers of the rat entorhinal cortex.

We have previously shown that there are clear differences between spontaneous excitatory synaptic currents recorded in layers V and II of the rat entorhinal cortex (EC) in vitro, and have suggested that these might contribute to a more pronounced susceptibility of the deeper layer to epileptogenesis. In the present study, we have made a detailed comparison of spontaneous synaptic inhibition between the two layers by recording spontaneous inhibitory synaptic currents (sIPSCs) using whole-cell patch-clamp techniques in EC slices. Pharmacological studies indicated that sIPSCs were mediated exclusively by gamma-aminobutyric acid (GABA)(A) receptors. There was little difference in average amplitudes, rise or decay times of sIPSCs in layer II compared with layer V. However, in the former, events occurred at 4-5 times the frequency seen in the latter, and frequencies of </=40 Hz were not uncommon. When activity-independent, miniature IPSCs were isolated in tetrodotoxin (TTX), the frequency in layer V was more than halved, but in layer II only a small reduction was seen, and the frequency remained very high. In terms of kinetics, while averaged sIPSCs in each layer were very similar, detailed comparison of individual sIPSCs within layers revealed distinct differences, possibly reflecting inputs from different subtypes of interneurons or inputs at different somatodendritic locations. In layer V, sIPSCs could be divided into three groups, one with slow rise and decay kinetics and a second with fast rise kinetics, further distinguished into two groups by either fast or slow decay kinetics. The distinction between events in layer II was simpler, one group having both fast rise and decay times and the second with both parameters much slower. Finally, IPSCs could occur in high-frequency bursts in both layers, although these were much more prevalent in layer II. The results are discussed in terms of the overall level of background inhibition in the two layers, as well as how this might relate to their susceptibilities to epileptogenesis.

Anesthetics, Local↗
PubMed2004

Different time course for the memory facilitating effect of bicuculline in hippocampus, entorhinal cortex, and posterior parietal cortex of rats.

Several lines of evidence indicate that gamma-aminobutyric acid (GABA) type A (GABA(A)) receptors regulate memory consolidation. Here we studied the effect on consolidation of the selective antagonist of GABA(A) receptors, bicuculline, given into several regions of the cortex at different times after one-trial step-down inhibitory avoidance (0.5 mA, 2-s footshock). Rats were bilaterally implanted with cannulae aimed at the CA1 region of the dorsal hippocampus, entorhinal cortex or posterior parietal cortex, three areas known to be involved in the memory consolidation of this task. At different times after training, bicuculline (0.5 microg/side) was infused into the above mentioned structures. Bicuculline increased memory retention when administered either immediately or 1.5h after training into CA1, and both immediately and 3h after training in the entorhinal or parietal cortex. Thus, in agreement with previous findings using other drugs, the response was biphasic in these latter structures. This suggests that GABAergic mechanisms normally downregulate, memory processing by inhibiting on-going activities necessary for consolidation at the times in which bicuculline was effective in each structure. Based on previous findings, in the hippocampus, such activity involves a number of receptors and signaling pathways in the first 1.5h after training. In the entorhinal and parietal cortex memory-related activities include the participation of protein kinase A and extracellularly regulated kinase (ERK) twice, right after training and then again 3h later.

Animals↗
PubMed1975

Time-dependent changes in commissural field potentials in the dentate gyrus following lesions of the entorhinal cortex in adult rats.

Previous neuroanatomical work has shown that lesions of the entorhinal cortex in adult rats cause the commissural projections to spread from their normally restricted locus in the inner molecular layer approximately 40-50 mum into the outer molecular layer (that is, into the zone deafferented by the lesion). In the present study we measured the effects of the entorhinal lesion on the distribution of short-latency potentials elicited by commissural stimulation in the molecular layer. Studies with animals tested at various times after the lesion and with a preparation that permitted recording from the same rat at several post-lesion intervals both indicated that the commissural response spread 100-150 mum towards the deafferented outer molecular layer, while the maximum response spread 50-100 mum. These effects were first detectable by 9 days after the lesion and were fully developed by 15 days post-lesion. These findings suggest that the growth of the commissural system seen after entorhinal lesions results in the rapid formation of functional terminals and are discussed in relationship to the behavioral consequences of brain lesions.

Animals↗
PubMed2005

Lateral entorhinal cortex lesions rearrange afferents, glutamate receptors, increase seizure latency and suppress seizure-induced c-fos expression in the hippocampus of adult rat.

The entorhinal cortex (EC) provides the predominant excitatory drive to the hippocampal CA1 and subicular neurones in chronic epilepsy. Here we analysed the effects of one-sided lateral EC (LEC) and temporoammonic (alvear) path lesion on the development and properties of 4-aminopyridine-induced seizures. Electroencephalography (EEG) analysis of freely moving rats identified that the lesion increased the latency of the hippocampal seizure significantly and decreased the number of brief convulsions. Seizure-induced neuronal c-fos expression was reduced in every hippocampal area following LEC lesion. Immunocytochemical analysis 40 days after the ablation of the LEC identified sprouting of cholinergic and calretinin-containing axons into the dentate molecular layer. Region and subunit specific changes in the expression of ionotropic glutamate receptors (iGluRs) were identified. Although the total amount of AMPA receptor subunits remained unchanged, GluR1(flop) displayed a significant decrease in the CA1 region. An increase in NR1 and NR2B N-methyl-d-aspartate (NMDA) receptor subunits and KA-2 kainate receptor subunit was identified in the deafferented layers of the hippocampus. These results further emphasize the importance of the lateral entorhinal area in the spread and regulation of hippocampal seizures and highlight the potential role of the rewiring of afferents and rearrangement of iGluRs in the dentate gyrus in hippocampal convulsive activity.

4-Aminopyridine↗
PubMed2006

Selective involvement of the lateral entorhinal cortex in the control of the olfactory memory trace during conditioned odor aversion in the rat.

Evidence from the effect of aspiration lesions of the entorhinal cortex (EC) has shown that this region is involved in conditioned odor-aversion (COA) learning--that is, the avoidance of an odorized tasteless solution the ingestion of which precedes toxicosis--by rendering COA tolerant to long odor-toxicosis delay. The present study examined whether neurotoxic lesions restricted to the lateral or medial parts of the EC, in comparison with large aspiration lesions, were sufficient to produce this effect. Male Long-Evans rats received odor-intoxication pairing with either a short (5-min) or long (120-min) delay between the presentation of the odor and toxicosis. All groups, including sham-lesioned controls, showed COA at the 5-min odor-toxicosis delay interval, but only rats with lateral EC damage displayed COA at the longer delay. These data show that the lateral EC is part of the substrate involved in the control of the olfactory memory trace during COA.

Animals↗
PubMed2003

Nerve growth factor attenuates hippocampal cholinergic deficits and operant learning impairment in rats with entorhinal cortex lesions.

In the present study we investigated whether continuous intraventricular nerve growth factor (NGF) infusion could ameliorate hippocampal cholinergic deficits and learning impairment following entorhinal cortex lesions. Rats with such lesions received continuous intraventricular infusions of NGF or vehicle. Unlesioned rats with a sham operation were studied as controls. After learning sessions, a dialysis probe was implanted in the CA3 hippocampal region. In addition, brain sections were stained for synaptophysin immunoreactivity. In rats undergoing surgical procedures similar to those in the behavioral study, brains were processed for acetylcholinesterase (AChE) histochemistry. NGF-treated rats showed partial amelioration of lesion-associated hippocampal acetylcholine (ACh) efflux deficits and fixed-interval schedule learning impairment compared with vehicle-treated rats. Histochemical, immunohistologic, and microdensitometric analyses confirmed greater density of AChE-positive fibers and synaptophysin immunoreactivity in CA3, in NGF-treated rats relative to vehicle-treated rats, although not as great as in sham-operation rats, indicating partial recovery in NGF-treated rats. These results suggest that enhanced performance of the learning task with NGF treatment was related to improved hippocampal cholinergic function: specifically, increased cholinergic neurotransmission resulting from NGF effects on cholinergic neurons and presynaptic terminals.

Acetylcholine↗
PubMed2001

Cholinergic modulation of synaptic physiology in deep layer entorhinal cortex of the rat.

We have recently shown that cholinergic effects on synaptic transmission and plasticity in the superficial (II/III) layers of the rat medial entorhinal cortex (EC) are similar, but not identical, to those in the hippocampus (Yun et al. [2000] Neuroscience 97:671-676). Because the superficial and deep layers of the EC preferentially convey afferent and efferent hippocampal projections, respectively, it is of interest to compare cholinergic effects between the two regions. We therefore investigated the physiological effects of cholinergic agents in the layer V of medial EC slices under experimental conditions identical to those in the previous study. Bath application of carbachol (0.5 microM) induced transient depression of field potential responses in all cases tested (30 of 30; 18.5% +/- 2.3%) and rarely induced long-lasting potentiation (only 3 of 30; 20.4% +/- 3.2% in successful cases). At 5 microM, carbachol induced transient depression only (20 of 20, 48.9% +/- 2.8%), which was blocked by atropine (10 microM). Paired-pulse facilitation was enhanced during carbachol-induced depression, suggesting presynaptic action of carbachol. Long-term potentiation (LTP) could be induced in the presence of 10 microM atropine by theta burst stimulation, but its magnitude was significantly lower (9.1% +/- 4.7%, n = 15) compared to LTP in control slices (22.4% +/- 3.9%, n = 20). These results, combined with our previous findings, demonstrate remarkably similar cholinergic modulation of synaptic transmission and plasticity across the superficial and deep layers of EC.

Acetylcholine↗
PubMed1990

Kainate receptors in the rat hippocampus: a distribution and time course of changes in response to unilateral lesions of the entorhinal cortex.

The response of kainate receptors to deafferentation and subsequent reinnervation following unilateral entorhinal cortex lesions was studied in the rat hippocampus using quantitative in vitro autoradiography. The binding levels of [3H]kainic acid (KA) and changes in the distribution of KA sites were investigated in the dentate gyrus molecular layer (ML) and in various terminal zones in the CA1 field at 1, 3, 7, 14, 21, 30, and 60 d postlesion. The data from both the ipsilateral and contralateral hippocampus were compared with those from unoperated controls. The first changes in KA receptor distribution were observed 21 d postlesion when the dense band of KA receptors occupying the inner one-third of the ML expanded into the denervated outer two-thirds of the ipsilateral ML. The spreading of the KA receptor field into previously unoccupied zones continued 30 and 60 d postlesion. At these time points, the zone enriched in [3H]KA binding sites became significantly (on average 50%) wider than in unoperated controls. No changes were observed in either the distribution or binding levels in other hippocampal areas or in the contralateral hippocampus at any studied time point. Saturation analysis of binding in the ipsilateral ML 60 d postlesion revealed changes in the maximum number of receptor sites (Bmax) without changes in KA receptor affinity (Kd). The data suggest that the elevation of the [3H]KA binding in the outer two-thirds of the ML reflects an increase in the number of both low and high affinity receptor binding sites. The pattern of KA receptor redistribution was similar to the well-characterized pattern of sprouting of commissural/associational systems from the inner one-third into the outer two-thirds of the ML after entorhinal lesions (Zimmer, 1973; Lynch et al., 1975). This supports the hypothesis (Geddes et al., 1985) that the KA receptor response observed in the present study reflects postlesion reorganization of inputs within the denervated ML and may be relevant to functional recovery of the damaged circuits.

Animals↗
PubMed2001

Reciprocal connections between the entorhinal cortex and hippocampal fields CA1 and the subiculum are in register with the projections from CA1 to the subiculum.

The topology of the connections between the entorhinal cortex (EC), area CA1, and the subiculum is characterized by selective and restricted origin and termination along the transverse or proximodistal axis of CA1 and the subiculum. In the present study, we analyzed whether neurons in CA1 and the subiculum that receive EC projections are interconnected and give rise to return projections to EC, such that they terminate deep in the area of origin of the EC-to-CA1/subiculum projections. Both for the lateral and medial subdivision of EC, the projections to CA1/subiculum, as well as the projections from CA1 to the subiculum and back to EC, are rather divergent. Interestingly, we only rarely observed evidence for the presence of "reentry loops," i.e., cells in layer III of EC giving rise to projections to interconnected neurons in CA1 and the subiculum, while the targeted CA1 neurons also projected back to the deep layers of the area of origin of the pathway in EC. We conclude that although fibers originating from a restricted part of EC distribute extensively in a divergent way along the longitudinal axis of CA1 and the subiculum, only restricted portions of the latter two areas, receiving inputs from the same entorhinal area, are interconnected. Moreover, only a small percentage of the CA1 neurons that project to the correspondingly innervated subicular neurons give rise to projections that return to the deep layers of the originating part of EC. The present findings are taken to indicate that the EC-hippocampal circuitry functionally comprises many parallel-organized specific "reentry loops."

Animals↗
PubMed2004

Plasticity in the entorhinal cortex suppresses memory for contextual fear.

Several studies have delineated a role for the hippocampus in fear conditioning. However, in this task, the role of the entorhinal cortex (EC), the main input-output structure for the hippocampus, is uncertain. The extracellular signal-regulated kinase (ERK) cascade has been shown to be a molecular correlate for long-term memory, and its activity is required for various types of memory storage, including fear memory. In this study, we show that ERK activity in the EC increased 90 min after fear conditioning. Post-training intra-EC infusion of ERK cascade inhibitors (PD098059, UO126) at 40 min, but not at 10 min, resulted in increased freezing to the context, but not to the tone, during a 48 hr retention test. Interestingly, both PD098059- and UO126-infused animals also demonstrated anticipatory freezing in the context, freezing maximally at the time the shock was given during training. This anticipatory behavior was also seen in naive animals receiving additional training. Together, these results suggest that ERK-mediated plasticity in the EC normally suppresses context-specific fear memory, especially the temporal nature of the freezing response, and that blocking this plasticity mimics the effects of additional training.

Animals↗