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At least 19 recordsLinked to original sources

PubMed1991

Morphological correlates of pyramidal cell adaptation rate in the electrosensory lateral line lobe of weakly electric fish.

1. Extracellular HRP injections into the nucleus praeeminentialis dorsalis (NPd) of Apteronotus leptorhynchus retrogradely labeled a population of electrosensory lateral line lobe (ELL) efferent cells, deep basilar pyramidal cells, that differ morphologically from the previously described basilar and nonbasilar pyramidal cells. These neurons are found deep in the ELL cellular layers; they have small cell bodies and very short sparsely branching apical dendritic trees. The previously described basilar and nonbasilar pyramidal cells are larger, have extensive apical dendrites and are found more superficially. 2. Axon terminals of the deep basilar pyramidal cells were recorded from in the NPd and labeled with lucifer yellow. These NPd afferents have high, regular spontaneous firing rates, and respond tonically to changes in electric organ discharge amplitude. 3. Deep basilar pyramidal cell bodies were recorded from and labeled in the ELL, and these showed the same physiological responses as did the NPd afferent fibers. 4. In addition, basilar pyramidal cells were found which had spontaneous activity patterns and adaptation characteristics intermediate to those typical of the superficial basilar pyramidal cells and the deep basilar pyramidal cells. The size of the pyramidal cells' apical dendritic trees and the placement of their somata within the dorsoventral extent of the ELL cellular layers are highly correlated with the neurons' physiological properties.

Adaptation, Physiological↗

PubMed1992

Different kinds of axon terminals forming symmetric synapses with the cell bodies and initial axon segments of layer II/III pyramidal cells. III. Origins and frequency of occurrence of the terminals.

The cell bodies of the layer II/III pyramidal cells in rat visual cortex receive three morphologically distinct types of axon terminals. These axon terminals all form symmetric synapses and have been termed large, medium-sized, and dense axon terminals. The present study shows that each of these different kinds of axon terminals contains gamma-aminobutyric acid (GABA) which suggests that they are inhibitory. From an analysis of the profiles of 50 cell bodies it is calculated that the average layer II/III pyramidal cell has 65 axosomatic synapses, of which 43 are formed by medium-sized terminals, 10 by large terminals, and 12 by dense terminals. Comparison of these different kinds of axon terminals with labelled axon terminals of known origin suggests that the medium-sized terminals are derived from smooth multipolar cells with unmyelinated axons, and that at least some of the dense terminals originate from bipolar cells that contain vasoactive intestinal polypeptides. The source of the large axon terminals is not known, but it is suggested that they originate from multipolar non-pyramidal cells with myelinated axons. Since the initial axon segments of these same neurons receive GABAergic axon terminals from chandelier cells, at least four different types of neurons provide inhibition to the cell bodies and axons of layer II/III pyramidal cells. This serves as an illustration of the complexity of the neuronal circuits in which pyramidal cells are involved.

Animals↗

PubMed1992

Calbindin-D28K and ischemic damage of pyramidal cells in rat hippocampus.

An antibody against rat calbindin-D28K, a calcium-binding protein present at high concentration in certain neurons of the central and peripheral nervous systems, was used to determine the progression of the pathological events in the rat hippocampus following experimental cerebral ischemia. Calbindin-D28K immunoreactivity is present in dentate granule cells and in the CA1-CA2 pyramidal cells. CA1 subfield contains a higher proportion of calbindin-D28K-positive pyramidal cells than does the CA2 subfield and CA1 cells are more immunoreactive than the CA2 cells. The pyramidal cells of the CA1 and CA2 subfields are vulnerable to ischemia. The cells in the CA1 became necrotic within 3-4 days after ischemia while those of the CA2 became necrotic within 2 days. There was a concomitant decrease in calbindin-D28K immunoreactivity in the whole hippocampal regio superior after ischemia which peaked 3 days postischemia. The difference in CA2 and CA1 vulnerability seemed to be inversely correlated with the calbindin-D28K contents of the CA2 and CA1 pyramidal cells. The decrease in the calbindin-D28K contents of these neurons was accompanied by cell damage. We therefore suggest that calbindin-D28K is an important factor for the survival of pyramidal cells in the hippocampal formation after ischemia.

Animals↗

PubMed1976

[Quantitative study of primitive pyramidal cells in rat anterior cingular cortex].

In the present paper the primitive pyramidal cells of the Vthlayer of the anterior cingulate cortex in adult male white rats were analyzed quantitatively and compared statisticaly with large pyramidal cells of the same region. The number of dendrites, the total lengths of dendrites, the number of spines and the density of spines -- according to the order of dendrites -- show similarity between the primitive pyramidal cells and the large pyramidal cells the latter one exhibit the higher values. The curves of distribution of the various density of spines along the apical main dendrite of both cell types are similar in shape, too. The lengths of the dendritic fields and their basal spines-values are without significant distinction for both cell types, however there are more dendritic fields in large pyramidal cells. Refered to a complete pyramidal neuron they can say: there are significantly higher values in large pyramidal cells for the number of dendrites and their total lengths, the total number of spines, the number of branching sites sites and free endings. However the density of spines of the complete neuron has no significant differences between primitive and large pyramidal cells.

Animals↗

PubMed1991

Local circuit synaptic interactions between CA1 pyramidal cells and interneurons in the kainate-lesioned hyperexcitable hippocampus.

Following kainate (KA)-induced lesions of subfield CA3--a lesion relevant to human temporal lobe epilepsy--remaining pyramidal cells in CA1 display synchronous hyperexcitability associated with a loss of synaptic inhibition. Despite this loss, inhibitory interneurons in CA1 remain viable, and the density and function of GABAergic receptors on the CA1 pyramidal cells are maintained at approximately normal levels. To further evaluate inhibition in this system, the authors examined interactions between pyramidal cells and inhibitory interneurons in paired intracellular recordings. Recordings were carried out in rat hippocampal slices 2-4 weeks following bilateral intraventricular KA injections. The frequency of synaptic interactions between CA1 basket cells and pyramidal cells was lower in hyperexcitable slices than in controls; both synapses in the recurrent inhibitory circuit appeared to be involved. No recurrent excitatory interactions were seen between pyramidal cell pairs in lesioned or normal slices. The weakened interconnections between pyramidal cells and interneurons are consistent with the decreased inhibition previously found in this model. Unexpectedly, strong stimulation, which may directly activate local inhibitory circuitry, was effective in reducing hyperexcitability in KA-lesioned slices. These data suggest that development of recurrent excitatory connections among CA1 hippocampal pyramidal cells contribute little to tissue excitability, and support the hypothesis that a functional uncoupling between inhibitory interneurons and CA1 pyramidal cells is responsible for the seizure-like activity typical of KA-lesioned hippocampus. The data are also consistent with the hypothesis that in the KA model, the structural circuitry needed for inhibition in CA1 is maintained, and can be functionally activated by appropriate stimuli.

Animals↗

PubMed1991

Excitatory responses to serotonin (5-HT) in neurons of the rat piriform cortex: evidence for mediation by 5-HT1C receptors in pyramidal cells and 5-HT2 receptors in interneurons.

As a prerequisite to pharmacological analysis of the excitatory effects of serotonin (5-HT) on piriform pyramidal cells and interneurons, this study first examined the physiological characteristics of these two cell types. Intracellular recordings confirmed that the subpopulation of 5-HT-activated cells located at the border of layers II and III are indeed interneurons. Voltage clamp recordings in pyramidal cells showed that the increase in excitability produced by 5-HT in these cells was the result of voltage- and Ca(2+)-dependent outward currents with the characteristics of IM and IAHP. Pharmacological studies were designed to discriminate 5-HT2 from 5-HT1C responses in interneurons and pyramidal cells of piriform cortex. The 5-HT antagonist spiperone, which has a much higher affinity for 5-HT2 receptors than for 5-HT1C receptors, blocked the excitatory effect of 5-HT at lower concentrations in interneurons (IC50 = 31 nM) than in pyramidal cells (IC50 = 2.1 microM). Similarly, ritanserin, a drug which also has a higher affinity for 5-HT2 than 5-HT1C receptors, blocked the effect of 5-HT at lower concentrations in interneurons (IC50 = 400 nM) than in pyramidal cells (IC50 = 8.1 microM). In contrast, LY 53857, an antagonist with higher affinity for 5-HT1C than for 5-HT2 receptors, blocked the effect of 5-HT at lower concentrations in pyramidal cells (IC50 = 26 nM) than in interneurons (IC50 = 364 nM). The 5-HT1C partial agonist/5-HT2 antagonist mCPP produced agonist-like effects in only 66% of pyramidal cells tested indicating that not all pyramidal cells may express 5-HT1C receptors. In that both spiperone and ritanserin have higher affinity for 5-HT2 receptors than for 5-HT1C receptors and LY 53857 has a higher affinity for 5-HT1C receptors than for 5-HT2 receptors, these data suggest that in piriform cortex excitatory effects of 5-HT are mediated by 5-HT1C receptors in pyramidal cells an by 5-HT2 receptors in interneurons.

Animals↗

PubMed1992

Excitatory inputs to layer V pyramidal cells of rat primary visual cortex revealed by acetylcholine activation.

Cells in layers II-III or VI were activated by microdrop application of acetylcholine (ACh), while monitoring the intracellular response of layer V pyramidal cells. This enabled the tracing of functional connections between the cells of layers II-III or VI with those of layer V. ACh activation of layer II-III or VI cells resulted in a small depolarization of these cells, accompanied by a burst of excitatory postsynaptic potentials (EPSPs) from layer V pyramidal cells. These effects of ACh were blocked by tetrodotoxin (TTX), suggesting the involvement of action potentials in their production. The input resistance of layer V pyramidal cells during and after the EPSP burst was not significantly different from control values, further suggesting an indirect effect of ACh on layer V pyramidal cells. Isolation of the supragranular layer, by horizontal cutting, did not prevent the EPSP burst evoked by ACh application to the lower layer VI, suggesting a direct input from layer VI to layer V pyramidal cells. ACh applied near pyramidal cells in layers II-III, V or VI caused transient hyperpolarization associated with a decrease in input resistance followed by a large depolarization, an increase in input resistance, and action potential discharges. The ACh-mediated hyperpolarization and the train of action potentials of layer II-III pyramidal cells were blocked by TTX. Thus the ACh-activated cells in layers II-III and VI make an excitatory synaptic contact with layer V pyramidal cells, producing the EPSP burst observed in layer V.

Acetylcholine↗

PubMed1976

[Quantitative study of dendritic tree of large (regular) pyramidal cells of lamina V in rat anterior cingular cortex].

At three month old male rats the dendritic trees of 36 large pyramidal cells in the Vth layer of the anterior cingulate cortex were analyzed quantitatively by means of the Golgi-Kopsch method. 12 pyramidal cells were localized at the medial border of the regio praecentralis (neocortex), 12 cells were localized in the adjacent mesoarchicortex, 12 cells were localized in the mesoarchicortex, which are three subregions of the anterior cingulate cortex. By means of a varianz-analysis the values of the three subregions were compared, in order to verify a supposed gradient of differentiation. 1. In the three subregions basal the number and the branching behaviour of the dendrites are greater than apical. The pyramidal cells of the neocortex and of the mesoneocortex have significantly more basal dendrites of the 1st, 2nd, 3rd, and 4th order than those of the mesoarchocortex. There are significantly more apical dendrites of the 1st and 2nd order at pyramidal cells of the neocortex compared with the two other subregions. 2. The total lengths of the dendritic branches are in proportion to the dendritic numbers of the corresponding orders. There are following tendencies for the three subregions: the number and length of apical dendrites decrease with the increasing number of order, basally, however, the number and length first increase and than decrease. 3. The total length of all basal dendrites of a pyramidal cell is largest in the mesoneocortex, than follows the neocortex, least values they find in the mesoarchicortex. There are significant differences between every one of the three subregions. The values of the total dendritic tree of a pyramidal cell (total dendritic length, total number of dendrites, volume of the dendritic tree, number of branching sites and free endings, total apical dendritic length) show significant differences between neocortex and mesoarchicortex as well as between mesoneocortex and mesoarchicortex. There are no significant differences between noecortex and mesoneocortex. The values of the total dendritic tree demonstrate that neocortex and mesoneocortex have a similar organization, while the lamina V-pyramidal cells of the mesoarchicortex indicate a significantly smaller and less branched dendritic tree.

Animals↗

PubMed1991

Pyramidal cells in rat temporoauditory cortex project to both striatum and inferior colliculus.

A retrograde fluorescent double-labeling technique was employed to examine whether the cortico-striate fibers are collaterals of the corticofugal fibers directed to the inferior colliculus in the rat. Following injections of two different fluorescent tracers into the striatum and the inferior colliculus, double-labeled cells were found in layer V pyramidal cells of the temporal cortex. These double-labeled cells were located mostly in the area corresponding to the rat primary auditory cortex, and constituted 6.4% of the pyramidal cells projecting to the inferior colliculus. This study has revealed the existence of a common innervation of the basal ganglia and the auditory system by the pyramidal cell of the auditory cortex.

Amidines↗

PubMed1979

Neocortical pyramidal cells: a model with dendritic calcium conductance reproduces repetitive firing and epileptic behavior.

A computer model of a neocortical pyramidal cell has been constructed using ideas similar to those used for hippocampal pyramidal cells. This model has been applied to the study of (a) repetitive firing, and (b) the paroxysmal depolarizing shift (PDS), an important intracellular event during seizures. Although calcium spikes have not been demonstrated directly in neocortical cells, we have postulated (by analogy with hippocampal pyramidal cells) a dendritic calcium conductance and a 'slow potassium' conductance modulated by intracellular calcium ion. With these dendritic ionic conductances, the model is able to reproduce the following experimental features of neocortical pyramidal cells: the afterdepolarization and succeeding afterhyperpolarization after an antidromic spike, and the f-I (firing rate-injected current) curve. Some of the differences between 'fast' and 'slow' pyramidal tract neurons (PTNs) -- narrower spikes and a steeper f-I curve in the fast PTNs -- may be explained by differences in Hodgkin-Huxley potassium kinetics between the two kinds of cell. The same model which faithfully reproduces repetitive firing behavior also reproduces (given appropriate synaptic inputs) the following intracellular events recording during epileptic seizures: (a) a burst of action potentials superimposed on and followed by a PDS, and (b) rapid repetitive firing succeeded by an IPSP. Thus, a single set of parameters can reporduce both normal physiological behavior and 'epileptic' behavior: the particular behavior seen depending on how the cell is stimulated. This overall result is the same as for our model of the CA1 hippocampal cell. It suggests that certain acutely acting epileptogenic agents, e.g. penicillin, may act by increasing synaptic input (perhaps both excitatory and inhibitory) to pyramidal cells, rather than by altering their membrane properties. As in our CA1 hippocampal cell model, bursting seems to be a phenomenon generated by the apical dendrite.

Biophysical Phenomena↗

PubMed1991

Development of calcium current subtypes in isolated rat hippocampal pyramidal cells.

1. Patch-clamp techniques were used to record from acutely dissociated rat hippocampal pyramidal cells of different postnatal ages to study the development, kinetics of activation and inactivation, and pharmacology of various components of whole-cell calcium current. 2. In both adult and immature pyramidal cells, the threshold of activation for Ca2+ current from the holding potential of -50 mV was about -35 mV. The current was non-inactivating near threshold, and slowly inactivating with stronger depolarizations. 3. In adult pyramidal cells, hyperpolarizing pre-pulses (-85 mV, 3 s) increased the peak amplitude of current, but had little effect on the amplitude of sustained current or on the threshold. In immature cells, hyperpolarizing pre-pulses (-85 mV, 3 s) revealed an additional component of Ca2+ current that had a threshold for activation around -60 mV, and inactivated rapidly and completely at potentials between -60 and -35 mV. This low-threshold Ca2+ current was found in all cells less than 12 days of age, and in no cells older than 29 days of age. 4. No difference was observed between the Ca2+ currents elicited from CA3 or CA1 pyramidal cells. 5. The time course of decay for inactivating Ca2+ currents in adult cells at -20 mV was well fit with a single exponential of roughly 120 ms time constant. In immature cells, the addition of a second, faster time constant (roughly 25 ms) was required to describe the decay of the inactivating current adequately. The persistent Ca2+ current elicited from the holding potential of -50 mV decayed with a time constant of roughly 750 ms. The rate of inactivation for all Ca2+ current components was faster with stronger depolarizations. Inactivating Ca2+ currents contributed a significantly larger percentage of the total Ca2+ current in immature than adult cells. 6. Steady-state inactivation of the low-threshold Ca2+ current in immature cells was described by the Boltzmann equation with half maximal inactivation at -76 mV and a slope factor of 6.8. Recovery from inactivation was exponential, with a time constant of 820 ms (at -85 mV). Steady-state inactivation of the high-threshold inactivating Ca2+ current in adult cells was described by the Boltzmann equation with half maximal inactivation at -78 mV and a slope factor of 9.9. 7. The low-threshold Ca2+ current in immature cells was blocked in a reversible and dose-dependent manner by amiloride (100-250 microM). Amiloride had no effect on high-threshold Ca2+ currents.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗

PubMed1991

Ectopic dendrites occur only on cortical pyramidal cells containing elevated GM2 ganglioside in alpha-mannosidosis.

In a variety of neuronal storage diseases, cortical pyramidal cells elaborate ectopic dendrites at the axon hillock. A feature common to all the diseases characterized by ectopic dendrites is an elevated level of GM2 ganglioside in cerebral cortex. In cats with one such disease, alpha-mannosidosis, the number of pyramidal cells bearing ectopic dendrites is small; the present study shows that GM2 ganglioside is stored only in those pyramidal neurons exhibiting ectopic dendrites. Using a Golgi-electron microscopy method with periodic acid-Schiff (PAS) staining, we first established that pyramidal cells bearing ectopic dendrites contained PAS+ membranous inclusions, consistent with storage of glycolipids. In contrast, those with smooth axon hillocks accumulated PAS- floccular inclusions, consistent with storage of oligosaccharides. Next, application of a monoclonal antibody against GM2 ganglioside revealed that subsets of both pyramidal and intrinsic neurons contained GM2-like immunoreactivity. Every GM2+ cell contained PAS+ membranous inclusions, indicating that pyramidal cells bearing ectopic dendrites stored GM2 ganglioside. In cats with alpha-mannosidosis induced by swainsonine, some pyramidal neurons showed GM2-like immunoreactivity after 4 weeks of treatment, whereas ectopic dendrites only became evident after 7 weeks of treatment. Thus, GM2 ganglioside accumulated in pyramidal neurons before ectopic dendrites emerged from the axon hillock. We propose that the reinitiation of dendrite growth on mature pyramidal cells is brought about by accumulated GM2 ganglioside.

Animals↗

PubMed1992

Reduction of GABAB inhibitory postsynaptic potentials by serotonin via pre- and postsynaptic mechanisms in CA3 pyramidal cells of rat hippocampus in vitro.

The action of serotonin (5-HT) on GABAergic synaptic transmission was investigated with intracellular recordings in CA3 pyramidal cells of rat hippocampal slices. Local application of 5-HT (500 microM) hyperpolarized CA3 pyramidal cells, decreased cellular input resistance, and reduced slow afterhyperpolarizations. Serotonin attenuated the late (GABAB) component of polysynaptic inhibitory postsynaptic potentials (IPSPs; 47% of control) without affecting the early (GABAA) component. During bath application of the excitatory amino acid antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) (20 microM) and 2-amino-5-phosphonovalerate (AP-5) (40 microM), 5-HT similarly decreased the amplitude of the late (GABAB) component (17% of control) of monosynaptic IPSPs but did not affect the early (GABAA) component. The mean reversal potentials of poly- and monosynaptic IPSPs were unaffected by 5-HT. The conductance increases associated with the late component of poly- and monosynaptic IPSPs were reduced by 5-HT. Hyperpolarizing responses evoked in CA3 pyramidal cells by somatic applications of gamma-aminobutyric acid (GABA) were unaffected by 5-HT. During bath application of bicuculline (20-50 microM), hyperpolarizing responses elicited by dendritic GABA application were reduced by 5-HT (71% of control). The effect of 5-HT on these direct GABAB hyperpolarizations (29% decrease in response) does not appear sufficient to fully account for the effect of 5-HT on late GABAB IPSPs (53-83% decrease in response). Therefore, 5-HT may reduce GABAB IPSPs in CA3 pyramidal cells 1) by a postsynaptic action on pyramidal cells and 2) by a selective presynaptic action on GABAergic interneurons mediating the GABAB IPSP. This presynaptic action of 5-HT does not appear to involve excitatory afferents onto inhibitory interneurons.

Animals↗

PubMed1991

Apical dendritic depolarizations and field interactions evoked by stimulation of afferent inputs to rat hippocampal CA1 pyramidal cells.

The relationship between orthodromic extracellular field potentials and intradendritic depolarizations in apical dendrites of CA1 pyramidal neurons was investigated using the in vitro slice preparation of rat hippocampus. Orthodromic synaptic field potentials evoked by stimulation of afferent inputs in stratum radiatum or stratum oriens were used to measure extracellular voltage gradients generated over the pyramidal cell axis. Extracellular gradients were of opposite polarity over the region of pyramidal cell apical dendrites in stratum radiatum. The stratum radiatum-evoked gradient was negative towards the apical dendrites and the stratum oriens-evoked gradient negative towards the cell body layer, with gradients reaching values of up to 50 mV/mm over the apical dendritic axis. Intradendritic recordings obtained greater than 150 microns from stratum pyramidale directly measured the subthreshold apical dendritic excitatory postsynaptic potentials evoked by stratum radiatum or stratum oriens stimulation. These ground-referenced recordings were then compared to the transmembrane potential calculated by subtraction of the corresponding extradendritic field potential. Both stratum radiatum and stratum oriens stimulation evoked graded excitatory postsynaptic potentials that could be recorded in apical dendritic impalements up to 265 microns from stratum pyramidale. The calculated transmembrane potential of the stratum radiatum-evoked excitatory postsynaptic potential had a significantly greater rate of rise, peak amplitude, and rate of decay than that of the ground-referenced excitatory postsynaptic potential. In contrast, the rates of rise and decay of the transmembrane potential of the stratum oriens-evoked excitatory postsynaptic potential were reduced with respect to the ground-referenced recording. The peak amplitude of the stratum oriens-evoked transmembrane potential, however, varied according to the polarity of the corresponding extradendritic population spike response recorded in stratum radiatum. These data reveal that synaptic activation of either basal or apical dendrites of CA1 pyramidal cells evokes a depolarization that can be recorded over a substantial region of the apical dendritic arbor. Furthermore, extradendritic field potentials evoked by stimulation of these inputs produce opposite effects on the transmembrane potential of apical dendrites. The magnitude of the accompanying extracellular voltage gradients suggest that these shifts in transmembrane potential reflect ephaptic interactions at the apical dendritic level of pyramidal cells.

Animals↗

PubMed1992

Comparison of 5-hydroxytryptamine1A-mediated hyperpolarization in CA1 and CA3 hippocampal pyramidal cells.

5-hydroxytryptamine (5-HT) hyperpolarizes hippocampal pyramidal cells in both areas CA1 and CA3 through an increase in potassium conductance. The receptor mediating the hyperpolarization in CA1 has been characterized as the 5-HT1A receptor, but has not been identified in area CA3. Intracellular recording techniques were used to record from CA1 and CA3 pyramidal cells in a hippocampal slice preparation. 5-HT agonists and antagonists were applied in known concentrations by bath perfusion. Antagonists were tested alone and for their ability to block the hyperpolarization elicited by 5-HT. The 5-HT1 agonist 5-carboxyamidotryptamine and 5-HT were full agonists and the 5-HT1A-selective ligand 8-hydroxydipropyl-aminotetralin hydrobromide was a partial agonist in both CA3 and CA1. The rank order potency was 5-carboxyamidotryptamine > 8-hydroxydipropyl-aminotetralin hydrobromide > 5-HT for both regions. The agonists were a half-log unit less potent and the maximum response elicited by 5-carboxyamidotryptamine and 5-HT was greater in area CA3 than in area CA1. The selective 5-HT1A antagonist BMY 7378 and the 5-HT1A/2 antagonist spiperone were competitive in area CA1, but insurmountable in area CA3. Other 5-HT antagonists that were not effective in blocking the 5-HT-mediated hyperpolarization included ketanserin, odansetron and BRL 24924. Based on these results, we conclude that the hyperpolarization elicited by 5-HT in areas CA1 and CA3 is mediated by the 5-HT1A receptor. However, there are significant differences in the nature of the 5-HT1A receptor-mediated hyperpolarization that may be attributed to differences in receptor-effector number, receptor-effector coupling and/or the structure of the recognition site.

Animals↗

PubMed1992

Ontogenesis of the pyramidal cell of the mammalian neocortex and developmental cytoarchitectonics: a unifying theory.

The prenatal development of the mammalian neocortex has been analyzed, with the rapid Golgi method, in a variety of experimental animals (hamster, mouse, rat, and cat) and in humans. A new developmental conception of the structural organization of the mammalian neocortex is discussed. Neocortical development begins with the establishment of the primordial plexiform layer (PPL) which precedes and is a prerequisite for the subsequent formation of the cortical plate (CP). The formation of the CP occurs, in its entirety, within the PPL. During its development, three fundamental neuronal events occur: migration, early differentiation, and late maturation. All migrating neurons, travelling on radial glial fibers, reach layer I, develop an apical dendrite, and establish contacts with its elements. These newly differentiated neurons assume similar morphology resembling embryonic pyramidal cells. As such, an early differentiation stage common to all neurons of the CP is established. During the late maturation stage, all CP neurons acquire their specific phenotypic structural and functional features. Only pyramidal neurons retain and expand their original connections with layer I while other neuronal types lose these connections. The pyramidal cell is redefined in developmental terms: the neocortex's pyramidal cell is both structurally and functionally locked into position between layer I and the cortical depth of its soma. During mammalian evolution pyramidal cells are forced to structurally and functionally elongate their apical dendrite outwardly to accommodate an increasing amount of information without losing either their original anchorage to layer I or their cortical depth. This unique property of pyramidal neurons is considered to be a mammalian innovation. Based on these observations, a unifying developmental cytoarchitectonic theory applicable to all mammals is proposed. The theory considers the CP to be a mammalian innovation and to represent a single, stratified, and expanding telencephalic nucleus. The theory envisions the mammalian neocortex as an open biological system capable of progressive expansion by the recruitment and transformation of primitive neurons from upper layer II into pyramidal cells. Hence, the number of pyramidal cell strata increases over the course of mammalian phylogeny. The developmental roles of layer I in the migration of neurons, formation of the CP, unique morphology of pyramidal cells, and overall structural organization of the mammalian neocortex are emphasized.

Animals↗

PubMed1992

NMDA receptor-mediated depolarizing action of proline on CA1 pyramidal cells.

This study investigated the actions of proline on CA1 hippocampal pyramidal cells with use of slice preparations. Bath-applied L-proline first induced these cells to fire multiple orthodromic population spikes in response to a single stimulus and then blocked their response to both orthodromic and antidromic stimulation. These effects could be explained by postsynaptic depolarization followed by depolarization block. Grease-gap studies confirmed that L-proline depolarizes CA1 pyramidal cells. D-Proline was inactive in these tests. Excitatory amino acid antagonists reduced depolarizing responses to proline and N-methyl-D-aspartate (NMDA) in parallel. Mn2+ failed to attenuate proline-evoked depolarizations at concentrations that substantially inhibited synaptic transmission, but at a higher concentration it reduced responses to both proline and NMDA. These results suggest that proline depolarized CA1 pyramidal cells mainly by activating postsynaptic NMDA receptors. The neuroexcitatory and neurotoxic actions of proline in the hippocampus may contribute to the seizures and mental retardation associated with hyperprolinemia.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1992

Kindling enhances sensitivity of CA3 hippocampal pyramidal cells to NMDA.

Kindling is a form of experimental epileptogenesis in which periodic electrical stimulation of a brain pathway induces a permanently hyperexcitable state. Previous studies suggested that kindling might be explained, at least in part, by an increased sensitivity of brain neurons to NMDA receptor agonists. This possibility was investigated with the use of grease-gap preparations for assaying the depolarizing responses of CA3 and CA1 hippocampal pyramidal cells to amino acid excitants. When studied 1-2 months after the last evoked seizure, CA3 pyramidal cells from kindled rats were five- to sixfold more sensitive to NMDA than CA3 pyramidal cells from controls. A similar, though smaller, effect of stimulation was observed 1 d after the last evoked seizure. The greater potency of NMDA in kindled rats can probably be explained by enhanced expression of NMDA receptors in the presence of a receptor reserve. The stimulation protocol did not alter the ability of Mg2+ to reduce NMDA potency. It also affected neither the response of CA3 pyramidal cells to AMPA [(RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate] nor the response of CA1 pyramidal cells to NMDA or AMPA. In area CA3, the potency of NMDA, but not of AMPA, declined 2.5-4-fold over the 1-2 month experimental period, apparently as a result of increasing age. This age-related loss of sensitivity to NMDA was completely prevented by kindling. These findings suggest that kindling prevents a loss of NMDA receptor function in CA3 pyramidal cells that normally occurs during early adulthood. Such a change could contribute to maintenance of the kindled state.

Aging↗