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Electrophysiology and morphology of the developing hippocampus of fetal rabbits.

The pyramidal neurons of fetal rabbit hippocampus were studied using intracellular electrophysiological techniques in in vitro slice preparations. Correlative light and electron microscopic analyses were carried out on hippocampus during the 21st through the 29th day of fetal gestation. In intracellular experiments, neurons with all-or-none action potentials and near-adult level resting potentials were found even in the youngest preparations. Synaptic activity, however, was rare until about 24 days of gestation. CA1 neurons showed primarily excitatory synaptic potentials during fetal development, whereas CA3 neurons displayed both inhibitory and excitatory postsynaptic potentials at early stages. Anatomical studies suggested that pyramidal cell precursors were still dividing and migrating at 21 days; by 29 days, cellular migration was completed, and cellular intercommunication in the form of synapses was increasing. These experiments demonstrate that fetal central nervous system (CNS) material can be studied electrophysiologically without growing tissue in culture. Our results suggest that the newly differentiated hippocampal neurons have a limited repertoire of activities. Such data may provide a link between in vivo studies of postnatal CNS development and cell and tissue culture investigations of the properties of immature neurons.

Action Potentials↗

Synaptic transmission: long-lasting potentiation by a postsynaptic mechanism.

Slow decreases of ionic conductance across neuronal cell membranes, which generate slow synaptic potentials, can increase the effectiveness of synaptic transmission. Slow conductance decreases sufficient magnitude increase the amplitude of monosynaptic fast excitatory postsynaptic potentials in B cells of the bullfrog sympathetic ganglion. By this postsynaptic mechanism, activation of one synaptic pathway can cause an increase in transmission, lasting several minutes, across another synapse. This may provide an important mechanism for synaptic integration and control of neuronal interaction.

Animals↗

Mechanisms of depolarizing inhibition at the crayfish giant motor synapse. I. Electrophysiology.

1. Mechanisms of depolarizing synaptic inhibition were investigated at the crayfish giant motor synapse with the use of two-electrode current- and voltage-clamp techniques. Depolarizing inhibitory postsynaptic potentials (d-IPSPs) of between 5 and 15 mV in amplitude are produced there in the motor giant motoneuron (MoG) by motor giant inhibitor (MoGI) interneurons. 2. Three mechanisms of inhibition are activated by the d-IPSP: inactivation of a voltage-sensitive inward current (probably sodium), activation of the delayed rectifier, and reverse bias of the electrically rectifying giant motor synapse (GMS). These mechanisms supplement the inhibition produced by a gamma-aminobutyric acid (GABA)-mediated increase in postsynaptic conductance. 3. The d-IPSP is produced by a fast-rising increase in postsynaptic membrane conductance that peaks at 10 microS and lasts nearly 100 ms. 4. An 8-ms, 10-mV depolarizing prepulse inactivated 90% of the inward current evoked by a subsequent step to 33 mV above rest potential, which was -70 mV. d-IPSPs having similar amplitudes should have similar effects on the inward current evoked by an excitatory postsynaptic potential (EPSP). 5. The input resistance of MoG decreased by greater than 60% when the cell was depolarized to 11 mV above rest. This resistance change corresponds to delayed rectification, which should also contribute to the increase in input conductance during a d-IPSP. 6. Depolarization of MoG by 10 mV reduced the excitatory postsynaptic current through the GMS by up to 30%. The reduction in synaptic current occurs because postsynaptic depolarization reduces the transynaptic driving force and increases the reverse bias of the electrically rectifying synapse.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Angiotensin II blockade of long-term potentiation at the perforant path--granule cell synapse in vitro.

Field recordings of evoked excitatory postsynaptic potentials (pEPSPs) were carried out in the granule cell stratum moleculare following stimulation of the perforant path in rat hippocampal slices. Under control conditions tetanic stimulation produced long-term potentiation (LTP) as measured by an increase in the initial slope of the pEPSPs that lasted for at least 1 h. LTP experiments were repeated with 0.5, 5.0, 50, or 500 nM angiotensin II (AII) present in the bath at the time of tetanization. Induction of LTP was blocked by 50 nM AII; however, normal baseline responses were not affected. At the highest dose tested, 500 nM, a decrease in the amplitude and slope of baseline pEPSPs was observed. When the AII AT1 receptor antagonist losartan was present in the bath AII inhibition of LTP was blocked. The application of losartan alone had no effect on LTP expression. These findings support previous results from in vivo studies demonstrating that activation of AT1 receptors in the dentate gyrus blocks the induction of LTP at the perforant path-granule cell synapse.

Analysis of Variance↗

Synaptic inputs and action potentials of magnocellular neuropeptidergic cells: intracellular recording and staining in slices of rat hypothalamus.

Excitatory postsynaptic potentials (EPSPs) and action potentials of magnocellular neuropeptidergic cells (MNCs) in the paraventricular (PVN) and supraoptic nuclei (SON) were studied with intracellular recording in coronal slices of rat hypothalamus. The fluorescent dye Lucifer Yellow (LY) was injected intracellularly and the cells were subsequently identified as magnocellular (somata greater than 15 x 15 micrometer). These cells generally had a large cytoplasm-to-nucleus ratio. In PVN it was frequently possible to trace filled dendrites to the ependyma of the third ventricle, and occasionally dendritic spines could be seen. Electrical stimuli in areas dorsolateral and ventrolateral to the fornix column evoked EPSPs in some anatomically identified MNCs of PVN, which indicates that presynaptic fibers innervating MNCs approach PVN from this region. Short-latency (less than 1 msec) spikes could be evoked in many MNCs of PVN by stimulation near SON, which is consistent with the known projection to the neurohypophysis of many MNCs. Action potentials in MNCs of PVN and SON had significantly longer durations at one-third spike height (mean +/- S.D. = 2.06 +/- 0.6 msec) than hippocampal CA1 pyramidal cells (1.17 +/- 0.29 msec). This suggests that neuroendocrine cells in mammals and some lower vertebrates and invertebrates are similar in this regard.

Action Potentials↗

Long lasting functional alterations in the rat dentate gyrus following entorhinal cortex lesion: a current source density analysis.

The functional consequences of lesions of the entorhinal cortex of rats were studied by analysing laminar distributions of stimulus induced field potentials in the dentate gyrus with a subsequent current source density analysis. Stimulation of the inner molecular layer elicits large excitatory postsynaptic potentials with small if any population spikes in the stratum granulare both in normal and lesioned animals. In lesioned animals middle molecular layer stimulation causes large excitatory sinks in the stratum moleculare without generation of population spikes in stratum granulare, while the same stimulation in slices from normal animals readily induces population spikes. The current source density analysis revealed a shift of current sinks induced by stimulation of either the inner or the middle molecular layer to common site. The N-methyl-D-aspartate receptor contribution to the current sink and source was found to be more prominent after middle molecular layer stimulation in comparison to inner molecular layers stimulation in the control group, while such a distinction could not be made in the lesioned group. Activation of mossy fibers did not reveal any significant differences between normal and lesioned animals. Following entorhinal cortex lesion sprouting of remaining afferents (e.g. commissural fibers) into the termination zones of the degenerated perforant path has been reported suggesting a compensatory replacement of excitatory synaptic input. However, persistent transneuronal dendritic alterations of neurons in the dentate gyrus have been observed which might result in altered dentate gyrus function. Our findings suggest that the reorganization process after entorhinal cortex lesion does not lead to full functional compensation of the lost perforant path input, resulting in an altered balance between excitation and inhibition.

Animals↗

Effects of histamine on dentate granule cells in vitro.

Hippocampal slices from rat brain were exposed to histamine and related substances in a perfusion chamber. Granule cells of the dentate gyrus were studied with conventional extra- and intracellular recording and a single electrode voltage clamp. Histamine caused, through activation of H(2)-receptors, a small depolarization, an increase in the number of synaptic and action potentials, a block of the long lasting (but not the early) component of spike afterhyperpolarizations and a reduction of the accommodation of action potential firing. These effects were mimicked by forskolin (suggests activation of adenylate cyclase). In voltage clamp, histamine blocked a long lasting calcium-dependent outward tail current without any reduction of inward current. Thus histamine selectively blocks the late calcium-dependent potassium current in dentate granule cells which receive histaminergic input from the posterior hypothalamus. Histamine also reduces the field excitatory postsynaptic potential evoked by perforant path stimulation. These actions allow for a powerful modulation of excitatory signals and an effective regulation of hippocampal excitability.

Action Potentials↗

Inhibitory processes in development of seizure activity in hippocampal slices.

The possibility that changes in inhibitory processes are necessary for development of seizure activity was examined using guinea pig hippocampal slices. After repeated tetanic stimulation to the stratum radiatum in region CA3, seizure discharges were evoked in the stratum pyramidale by test stimuli. The latency of the seizure discharges was shortened and the duration was prolonged progressively with the number of tetanic stimulations. The latency ranged from 30 to 100 ms and it was decreased successively as the distance between the recording site and the site of tetanic stimulation was decreased. This suggests that the foci of the seizure discharges existed near the site of tetanic stimulation. In neurons within the foci, inhibitory postsynaptic potentials and the suppressing action of alveus stimulation on glutamate-induced single cell discharges remained unchanged during development of seizure activity, although excitatory postsynaptic potentials were potentiated. In addition, no marked changes were detected in the input resistance, resting membrane potential and the amplitude, threshold and afterhyperpolarization of action potentials. These results suggest that suppression of inhibitory processes do not necessary for tetanus-induced seizure activity.

Action Potentials↗

Developmental changes in NMDA and non-NMDA receptor-mediated synaptic potentials in rat neocortex.

1. In vitro slices of frontal neocortex were prepared from rat pups 3-14 days of age. Whole-cell patch-clamp recordings were obtained from layer II-III cortical neurons, and measurements of passive membrane properties were made. The development of evoked synaptic excitation and inhibition was also examined with the use of current- and voltage-clamp techniques. 2. Pharmacological separation of excitatory synaptic activity into both N-methyl-D-aspartate (NMDA) and non-NMDA receptor-mediated components was accomplished by application of D(-)2-amino-5-phosphonovaleric acid (APV), D(-)2-amino-7-phosphonoheptanoic acid (AP7), and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). Inhibitory synaptic events were described according to their reversal potentials and modulation by the GABAA receptor antagonist bicuculline methiodide (BMI). 3. Pups were grouped into three categories on the basis of age: postnatal day (PN) 3-5, PN 6-8, and PN 9-14. In slices from PN 3-5 pups, neurons exhibited high input resistances (Rn) and relatively low resting membrane potentials (RMP). Rns decreased, and RMPs became more negative with development. At all ages studied, current-voltage relationships measured in current clamp were relatively linear, with inward rectification observed in some neurons at hyperpolarized membrane potentials. Neurons in each group were capable of firing overshooting action potentials. 4. Local stimulation in layer IV-V at 0.033 Hz elicited depolarizing excitatory postsynaptic potentials (EPSPs) in neurons from all three age groups. In PN 3-5 neurons, EPSPs were characterized by a long duration and latency to peak. By PN 6-8, EPSPs had decreased significantly in both duration and latency-to-peak. Some neurons responded with a single-component EPSP, whereas others exhibited multicomponent EPSPs consisting of distinct early and late components. In PN 3-5 neurons, increasing the frequency of stimulation from 0.033 to 1 Hz resulted in an overall decrease in the amplitude of the entire EPSP, whereas in PN 6-8 neurons the main decrease was observed in the late EPSP. 5. Excitatory postsynaptic currents (EPSCs) recorded in both PN 3-5 and PN 6-8 neurons were shorter in duration than corresponding EPSPs and consisted of both early and late components. Early EPSCs routinely increased in amplitude with hyperpolarization at all ages. In PN 3-5 neurons, the voltage dependence of late EPSCs was variable. By PN 6-8, late EPSCs always exhibited a region of reduced amplitude from -45 to -90 mV. The reversal potential for both early and late EPSCs was near +10 mV.(ABSTRACT TRUNCATED AT 400 WORDS)

2-Amino-5-phosphonovalerate↗

Regulation of synaptic strength at mixed synapses: effects of dopamine receptor blockade and protein kinase C activation.

Previous studies of the mixed excitatory synapses between eighth nerve afferents and the lateral dendrite of the goldfish Mauthner (M-) cell have shown that synaptic strength is enhanced for an hour or longer following either repeated brief tetanizations or local extracellular applications of dopamine. Both the initial electrotonic coupling potential, mediated via current flow through gap junctions, and the subsequent chemically mediated excitatory postsynaptic potentials (EPSPs) are potentiated. Different second messenger pathways are implicated in the postsynaptic induction of these potentiations, with a Ca2+ influx presumably triggering the activity dependent long-term potentiations (LTP) and dopamine acting via a cAMP dependent pathway. Experiments performed to determine whether the LTP involves a stimulus-induced release of dopamine or requires a background level of dopamine receptor activation suggest neither is the case, as tetanization in the presence of a D1 receptor antagonist, which blocks the dopamine effects, produced an LTP comparable to that in the absence of the blocker. The effects of Ca2+ are presumably not due to protein kinase C (PKC) activation, since phorbol esters had no effect on the mixed excitatory synaptic responses, although they did enhance the frequency of spontaneously occurring inhibitory PSPs.

Animals↗

Activation of Metabotropic Glutamate Receptors in Conjunction with Postsynaptic Depolarization Triggers a Long-Term Depression of the N-Methyl-D-Aspartate Receptor-Mediated Synaptic Potential in the Rat Hippocampus.

The mechanism responsible for long-term depression (LTD) of pharmacologically isolated N-methyl-D-aspartate (NMDA) receptor-mediated excitatory postsynaptic potential (EPSP(NMDA)) was studied. Intracellular recordings were made from CA1 cells of rat hippocampal slices in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (10 &mgr;M) and picrotoxin (50 &mgr;M), which block non-NMDA and GABA(A) receptors, respectively. Intracellular injections of depolarizing pulses (500 ms, 0.3-0.7 nA) at 1 Hz for 5 min in the absence of synaptic stimulation caused a persistent increase in the amplitude of EPSP(NMDA). However, coupling postsynaptic depolarization with synaptic activity induced LTD. The EPSP(NMDA) LTD could be blocked by L-2-amino-3-phosphonopropionic acid (50 &mgr;M) or (RS)-alpha-methyl-4-carboxyphenylglycine (200 &mgr;M), specific antagonists for metabotropic glutamate receptors (mGluR). Furthermore, application of trans-1-aminocyclopentane-1,3-dicarboxylic acid (t-ACPD, 50 &mgr;M), a specific mGluR agonist, in conjunction with postsynaptic depolarizing elicited LTD. In contrast, the mGluR agonists quisqualate or t-ACPD when given alone produced a sustained enhancement of EPSP(NMDA). Finally, coupled depolarization did not evoke LTD in slices pretreated with the protein kinase C (PKC) inhibitor calphostin c (60 nM). The present results demonstrate that activation of mGluR is necessary for the induction of LTD of EPSP(NMDA) and suggest that NMDA receptors are subject to bidirectional regulation by mGluR. Furthermore, the induction of LTD is likely to involve the stimulation of PKC. Copyright 1995 S. Karger AG, Basel

Journal Article↗

Adenosine inhibits a GABAB receptor-mediated hyperpolarizing postsynaptic potential in neurons of rat septal nuclei.

Intracellular recordings were made from neurons of rat dorsolateral septal nucleus (DLSN), in vitro. Adenosine and 2-chloroadenosine (1-500 microM) hyperpolarized DLSN neurons and blocked the excitatory postsynaptic potential (EPSP) and the late hyperpolarizing potential (LHP) in the presence of bicuculline. Adenosine did not depress the glutamate-induced potential. Bath-application of adenosine depressed the baclofen-induced potential in 60% of the neurons. Adenosine also inhibited the LHP in the remaining 40% of neurons, while it did not depress the baclofen-induced potential in these neurons. These results indicate that adenosine inhibits the EPSP pre-synaptically whereas it inhibits the LHP both pre- and postsynaptically in rat septal nuclei.

Adenosine↗

Phasic bursts in rat magnocellular neurosecretory cells are not intrinsically regenerative in vivo.

Vasopressinergic hypothalamic magnocellular neurosecretory cells fire in phasic bursts. Burst initiation involves summation of postsynaptic potentials to generate action potentials. Action potentials are each followed by a nonsynaptic depolarizing after-potential that summates temporally to generate a plateau potential and so sustain activity throughout the burst. It is unknown whether this plateau potential exceeds spike threshold in vivo to cause intrinsic regenerative firing or simply approaches threshold to increase the probability that excitatory postsynaptic potentials will trigger further action potentials. Here we show that pharmacological blockade of ionotropic glutamatergic transmission by microdialysis application of kynurenic acid into the supraoptic nucleus of anaesthetized rats prevents spontaneous bursts and bursts (after-discharge) evoked by short trains of antidromically stimulated action potentials in magnocellular neurosecretory cells. Even during prolonged depolarization induced by 1 m NaCl infusion, kynurenic acid microdialysis application still blocked after-discharge. The ability of kynurenic acid to block after-discharge during osmotic stimulation was not caused by an unmasking of inhibitory postsynaptic potentials as kynurenic acid was equally effective in the presence of the ionotropic gamma-aminobutyric acid receptor antagonist, bicuculline, nor did it result from inhibition of plateau potential amplitude as this was unaffected by kynurenic acid and bicuculline in vitro, as was after-discharge evoked in vitro. We conclude that phasic bursts are nonregenerative in vivo but rather require continued excitatory synaptic input activity superimposed upon a subthreshold plateau potential to sustain burst activity.

Action Potentials↗

Excitatory amino acid receptors mediate slow synaptic transmission in turtle cerebellum.

In the isolated turtle cerebellum intracellular recordings from Purkinje cell dendrites and somata reveal novel slow excitatory synaptic potentials evoked by activation of climbing fiber (CF) or parallel fiber (PF) inputs. Classical fast excitatory synaptic responses to CF and PF stimulation are followed by large, slow excitatory postsynaptic potentials (sEPSPs) which are associated with an increase in conductance and are enhanced by hyperpolarization. Both sEPSPs are blocked by the excitatory amino acid (EAA) antagonist kynurenate, but not by DL-2-amino-5-phosphonovalerate (AP-5). The EAA receptor antagonist L-amino-4-phosphonobutyric acid (L-AP-4) reversibly blocked the PF-sEPSP without affecting the CF-sEPSP. Two novel slow synaptic potentials mediated by excitatory amino acid receptors can therefore be observed in turtle cerebellum which may play an important role in synaptic integration.

Action Potentials↗

2-Deoxyglucose-induced long-term potentiation of monosynaptic IPSPs in CA1 hippocampal neurons.

In previous experiments on excitatory synaptic transmission in CA1, temporary (10-20 min) replacement of glucose with 10 mM 2-deoxyglucose (2-DG) consistently caused a marked and very sustained potentiation (2-DG LTP). To find out whether 2-DG has a similar effect on inhibitory synapses, we recorded pharmacologically isolated mononosynaptic inhibitory postsynaptic potentials (IPSPs; under current clamp) and inhibitory postsynaptic currents (IPSCs; under voltage clamp); 2-DG was applied both in the presence and the absence of antagonists of N-methyl-D-aspartate (NMDA). In spite of sharply varied results (some neurons showing large potentiation, lasting for >1 h, and many little or none), overall there was a significant and similar potentiation of IPSP conductance, both for the early (at approximately 30 ms) and later (at approximately 140 ms) components of IPSPs or IPSCs: by 35.1 +/- 10.25% (mean +/- SE; for n = 24, P = 0.0023) and 36.5 +/- 16.3% (for n = 19, P = 0.038), respectively. The similar potentiation of the early and late IPSP points to a presynaptic mechanism of LTP. Overall, the LTP was statistically significant only when 2-DG was applied in the absence of glutamate antagonists. Tetanic stimulations (in presence or absence of glutamate antagonists) only depressed IPSPs (by half). In conclusion, although smaller and more variable, 2-DG-induced LTP of inhibitory synapses appears to be broadly similar to the 2-DG-induced LTP of excitatory postsynaptic potentials previously observed in CA1.

2-Amino-5-phosphonovalerate↗

Altered synaptic transmission in dentate gyrus of rats reared in complex environments: evidence from hippocampal slices maintained in vitro.

Pre- and postsynaptic responses to activation of medial perforant path (MPP) axons were examined in hippocampal slices taken from rats reared for 3-4 wk in relatively complex (EC) or individual cage (IC) environments. Three types of extracellular field potentials were recorded in the infrapyramidal blade of the dentate gyrus: 1) granule cell population spikes (PSs), which reflect the number and synchrony of discharging granule cells (2), 2) population excitatory postsynaptic potentials (EPSPs), which reflect the amount of excitatory synaptic current flow into dendrites (28), and 3) presynaptic fiber volleys (FVs), which reflect the number of activated axons (28). Stimulation of the MPP evoked significantly larger PSs in slices taken from EC rats. There was no significant effect of rearing environment on PS/EPSP relationships. The slopes of EPSPs recorded at the site of synaptic activation in the dentate molecular layer and at the major current source in the dentate granule cell layer were significantly greater in slices taken from EC rats. The presynaptic FV was recorded at the site of synaptic activation in the molecular layer. FV amplitude did not differ significantly as a function of rearing environment. To examine possible differences in tissue impedance, granule cells were activated by stimulating granule cell axons in the dentate hilus and recording the antidromic PS in the granule cell layer. Antidromic PS amplitude was not significantly affected by rearing environment. The relative permanence of the experience-dependent alterations in synaptic transmission was assessed by comparing slices taken from rats that had been reared for 4 wk in complex environments followed by 3-4 wk in individual cages with those from rats reared for 7-8 wk in individual cages. There were no significant differences in MPP synaptic transmission between these groups of animals. The results suggest that experience in a relatively complex environment is associated with greater MPP synaptic transmission arising from an increased synaptic input to granule cells; the greater MPP synaptic transmission associated with behavioral experience can occur independent of behavioral state, influences from extrahippocampal brain regions and intrahippocampal inhibitory activity; and the experience-dependent synaptic alterations in the dentate gyrus are transient, in contrast to experience-dependent morphological alterations described in occipital cortex. The possible relationship of these alterations to the phenomenon of long-term enhancement is discussed.

Afferent Pathways↗

Activation of metabotropic glutamate receptor type 2/3 suppresses transmission at rat hippocampal mossy fibre synapses.

1. The effects of metabotropic glutamate receptor (mGluR) agonists on excitatory transmission at mossy fibre-CA3 synapses were studied in rat hippocampal slice preparations using both extracellular and whole-cell clamp recording techniques. 2. Application of a novel and potent mGluR2/mGluR3-specific agonist (2S,1'R,2'R,3'R)-2-(2,3-dicarboxycyclopropyl)glycine (DCG-IV, 0.1 microM) reversibly suppressed field excitatory postsynaptic potentials evoked by mossy fibre stimulation. DCG-IV at the same concentration did not affect other glutamatergic excitatory transmissions at the commissural/associational input to CA3 or at the Schaffer collateral/commissural input to CA1 regions. 3. This suppressing effect of DCG-IV on mossy fibre transmission was dose dependent and partly antagonized by a competitive mGluR antagonist (+)-methyl-4-carboxylphenylglycine (1 mM). 4. The field potential changes induced by pressure application of glutamate (0.1 mM) to the stratum lucidum of the CA3 region was unaffected by 0.1 microM DCG-IV. 5. In whole-cell clamp experiments, 0.1 microM DCG-IV suppressed excitatory postsynaptic currents evoked by mossy fibre stimulation without inducing detectable inward current in CA3 neurons, and paired-pulse facilitation was enhanced by DCG-IV application. 6. These results suggest that mGluR2/mGluR3 are specifically expressed at mossy fibre synapses in the hippocampal CA3 region, and activation of the receptor suppresses synaptic transmission by an action on a presynaptic site.

Animals↗

Identification of neurons producing long-term potentiation in the cat motor cortex: intracellular recordings and labeling.

Intracellular, in vivo recordings were used to identify and subsequently to label neurons in the cat motor cortex in which long-term potentiation (LTP) was induced. Thirty-nine motor cortical neurons that produced excitatory postsynaptic potentials (EPSPs) in response to microstimulation in areas 1-2 (SI) or in area 5a (SIII) were studied. Amplitudes of EPSPs produced in response to test stimulation (1 Hz) were recorded before and after tetanic stimulation (200 Hz, 20 seconds). In 25/39 cells (64%), EPSP amplitudes were significantly increased following the tetanic stimulation (65 +/- 51% average increase), and remained at the potentiated level as long as stable recordings could be maintained (20 +/- 18 minutes, maximum = 90 minutes). LTP was induced exclusively in cells that produced monosynaptic EPSPs in response to area 1-2 or area 5a stimulation. Of the 39 analyzed cells, 13 were labeled by intracellular injections of 5% biocytin. Neurons in which LTP was induced included both pyramidal and nonpyramidal cells and were located exclusively in layers II or III of the motor cortex; cells in deeper cortical layers were not potentiated. These findings indicate that various corticocortical inputs can increase the efficacy of synaptic transmission in a subset of motor cortical neurons. We propose that this plasticity in synaptic transmission constitutes one of the bases of motor learning and memory.

Animals↗