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At least 55 records · Page 3Linked to original sources
PubMed1989

GABAergic inhibition shapes temporal and spatial response properties of pyramidal cells in the electrosensory lateral line lobe of gymnotiform fish.

1. The amplitude-coding pyramidal neurons of the first-order nucleus in weakly electric gymnotiform fish (Eigenmannia), the electrosensory lateral line lobe (ELL), exhibit 2 major physiological transformations of primary afferent input. Pyramidal cells rapidly adapt to a step change in amplitude, and they have a center/surround receptive-field organization. This study examined the physiological role of GABAergic inhibition on pyramidal cells. GABAergic synapses onto the somata of pyramidal cells primarily originate from granule-cell interneurons along with descending input. 2. Pyramidal cells fall into two physiologically distinct categories: E units, which are excited by a rise in stimulus amplitude, and I units, which are inhibited by a rise in stimulus amplitude. Microiontophoretic application of bicuculline methiodide onto both types of pyramidal cells increased the time constant of adaptation, defined as the time required for the neuron's response to decay to 37% of its maximum value, by 70-90%. The peak firing rate of E units to a step increase in stimulus amplitude increased by 49%, while the firing rate of I units did not change significantly. 3. Bicuculline application demonstrated that GABAergic inhibition may contribute to the strict segregation of E and I response properties. In the presence of bicuculline, many E units (normally excited only by stimulus amplitude increases) became excited by both increases and decreases; many I units (normally excited only by amplitude decreases) also became excited to increases. 4. The size of the excitatory receptive-field of E units was not affected by bicuculline, although response magnitude increased. The inhibitory surround increased in spatial extent by 175% with bicuculline administration. Neither the size of the I unit receptive-field center nor the response magnitude changed in the presence of bicuculline. The antagonistic surround of I units, however, increased by 49%. 5. The anatomy of the ELL is well understood (see Carr and Maler 1986). The physiological results obtained in this study, along with the results of Bastian (1986a, b), further our understanding of the functional role of the ELL circuitry. Our results suggest that spatial and temporal response properties of pyramidal cells are regulated by different but interacting inhibitory interneurons, some of which use GABA as a neurotransmitter. The activity of these interneurons is in turn controlled by descending feedback systems.

Action Potentials↗
PubMed1989

Differential effects of methionine5-enkephalin on hippocampal pyramidal cells and interneurons.

While the excitatory action of opioids and opiate drugs upon pyramidal neurons in the hippocampus is well known, the mechanism by which this excitation is achieved is still argued. A popular hypothesis is that opiates reduce the activity of inhibitory interneurons, thereby indirectly exciting the pyramidal cells. To validate this idea, it is necessary to show that opiates selectively affect the population of interneurons. The present study therefore examined the effects of met-enkephalin upon pyramidal cells and interneurons located in area CA1. Extracellular action potentials were recorded using multibarrelled micropipettes. Drugs were applied locally by either pressure micro-ejection or microiontophoresis. Met-enkephalin (10(-5) M) elevated the spontaneous discharge of pyramidal cells, while interneurons were inhibited. The responses of both types of cell were blocked by the opiate antagonist naloxone. When the synaptic connections between the pyramidal cells and interneurons were disrupted by local application of magnesium or bicuculline, met-enkephalin had no effect on the pyramidal cells. However, neither magnesium nor bicuculline altered the enkephalin-induced inhibition of theta neurons. These results support the hypothesis that opioids of the enkephalin subclass, excite pyramidal cells in the hippocampus through a disinhibition mechanism.

Action Potentials↗
PubMed1989

A grease-gap method for studying the excitatory amino acid pharmacology of CA1 hippocampal pyramidal cells.

A grease-gap method for studying the pharmacology of CA1 hippocampal pyramidal cells was developed with use of rat hippocampal slices that included only area CA1 and the retrohippocampal area. These slices were transferred to a two-compartment superfusion chamber and the pyramidal cell bodies in area CA1 were separated from their axons in the subiculum with a grease barrier. The CA1 pyramidal cells were depolarized relative to their axons by superfusion with N-methyl-D-aspartate (NMDA), (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA), kainate and L-glutamate. NMDA was unusually potent in the CA1-subiculum slice compared to other preparations. The NMDA receptor antagonists D(-)-2-amino-5-phosphonovalerate (D-AP5), phencyclidine and Mg2+ shifted the NMDA dose-response curve to the right in a parallel manner. Similarly, the quisqualate receptor antagonist pentobarbitone shifted the AMPA dose-response curve to the right. Schild plots for these antagonists had slopes insignificantly different from 1. These results are consistent with the presence of a substantial NMDA receptor reserve on CA1 pyramidal cells. They are also in line with the high density of excitatory amino acid receptors on CA1 hippocampal pyramidal cells and with the known pharmacological properties of these receptors. Grease-gap studies on the CA1-subiculum slice fill the need for a means of obtaining quantitative pharmacological data on CA1 pyramidal cells.

2-Amino-5-phosphonovalerate↗
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↗
PubMed1984

The pharmacology of cholinergic excitatory responses in hippocampal pyramidal cells.

The pharmacology of excitatory cholinergic responses in CA1 pyramidal cells was examined in detail using intracellular recording from the hippocampal slice preparation. Acetylcholine (ACh), carbachol, muscarine and pilocarpine depolarized the membrane potential with an associated increase in input resistance. In addition, these agonists increased cell firing and depressed the afterhyperpolarization (AHP) that is due to a calcium-activated potassium conductance. The weak effects of ACh (20-200 microM) were considerably enhanced by addition of eserine (1-10 microM). All excitatory effects were completely antagonized by atropine (0.1-1 microM) but unaffected by dihydro-beta-erythroidine (DHBE) and gallamine (1-50 microM). In contrast to the muscarinic agonists, the nicotinic agonists nicotine and dimethylphenylpiperazinium (DMPP) had no excitatory effects on CA1 pyramidal cells. Phenyltrimethylammonium (PTMA), at high concentrations did depolarize cells and depress the AHP but these effects were antagonized by atropine and not DHBE or gallamine. The action of the analogue of cyclic GMP, 8-bromo-cyclic GMP, although variable, mimicked the membrane effects of ACh in some cells and depressed the AHP in most cells. Intracellular injection of cyclic GMP routinely depressed the AHP. In summary, we have demonstrated two cholinergic responses of hippocampal pyramidal cells that are mediated purely by muscarinic receptors. We could find no evidence to support a mixed-type receptor or the involvement of nicotinic receptors in the excitation of hippocampal pyramidal cells to cholinergic agents.

Acetylcholine↗
PubMed1989

Comparison of opioid and GABA receptor control of excitability and membrane conductance in hippocampal CA1 pyramidal cells in rat.

Opioids are thought to increase the excitability of hippocampal pyramidal cells by decreasing release of neurotransmitter from inhibitory interneurons. This study compared the actions of the opioid agonist normorphine, and the GABA receptor antagonist bicuculline, on the responses of CA1 pyramidal cells to afferent stimulation. Both normorphine and bicuculline increased the sensitivity of pyramidal cells to presynaptic stimulation, increased the number of population spikes and action potentials elicited, increased the duration of the excitatory postsynaptic potential (EPSP) and reduced the change in input conductance during the early inhibitory postsynaptic potential (IPSP). Unlike bicuculline, normorphine also decreased the change in conductance during the late inhibitory postsynaptic potential. The decreased change in the conductance of pyramidal cells caused by normorphine during both early and late inhibitory postsynaptic potentials supports the hypothesis that opioids decrease the release of GABA from inhibitory interneurons. In addition to reducing GABA-mediated changes in conductance, both normorphine and bicuculline unmasked a D-APV-sensitive conductance, measured during the early inhibitory postsynaptic potential. These results demonstrate that activation of opioid receptors enhances the excitability of CA1 pyramidal cells by decreasing GABA-mediated early and late inhibitory postsynaptic potentials and by unmasking NMDA receptors.

2-Amino-5-phosphonovalerate↗
PubMed1986

Lesions to Schaffer collaterals prevent ischemic death of CA1 pyramidal cells.

The contribution of excitatory inputs to CA1 pyramidal cell death after ischemia was examined using rats with unilateral destruction of CA3 pyramidal cells. Intracerebroventricular injection of L-alpha-kainic acid (KA) was performed before the induction of transient forebrain ischemia. Five days after ischemic insult, pyramidal cells and L-glutamate binding sites in the CA1 region ipsilateral to the KA injection were preserved in spite of neuronal necrosis and a significant decrease in L-glutamate receptor density in the contralateral CA1 region, indicating the critical role of Schaffer collaterals in delayed neuronal death.

Animals↗
PubMed1987

The neuronal composition of area 17 of rat visual cortex. IV. The organization of pyramidal cells.

In area 17 of the rat visual cortex, most of the apical dendrites of the large layer V pyramidal cells aggregate into oriented clusters, each containing three or more such dendrites. These clusters are not randomly distributed, but have a basic hexagonal packing distribution in which the mean center-to-center spacing is 55-60 microns. The majority of medium-size pyramidal cells of layer V also add their apical dendrites to the clusters. As these clusters pass through layer IV they remain intact, and successively layer III and finally layer II pyramids add their apical dendrites to them. Perhaps because the pyramidal cells in layer II/III are so numerous, some of their apical dendrites form independent groups. Apical dendrites of the small pyramidal neurons in layers VIa and IV seem not to specifically add to the clusters. Instead, apical dendrites of layer VIa pyramids form into contiguous fascicles and sheets, which pass around the groups of layer V pyramidal cell bodies to ascend to layer IV, where most of them form their apical tufts. Layer IV pyramidal cell apical dendrites behave somewhat similarly. These apical dendrites have to pass between the cell bodies of the lower layer III pyramidal cells. To do this, some join the clusters, but others form independent bundles. It is suggested that the pyramidal cells whose apical dendrites are clustered represent vertically oriented neuronal modules whose activity is synchronized, and that different combinations of these modules are excited by afferents to the cortex to provide the bases for the various kinds of functional columns.

Animals↗
PubMed1986

Intrahippocampal injection of kainic acid produces significant pyramidal cell loss in neonatal rats.

Previous reports have indicated that pyramidal cells in the developing rat hippocampal formation are not destroyed by intraventricular or intraperitoneal administration of kainic acid. We examined the neurotoxic properties of kainic acid and ibotenic acid following intrahippocampal injection in neonatal rats and found significant pyramidal cell death following injection of 1.0 microgram kainic acid in 6, 7 and 9-day-old pups. At doses 2.5 or five times this amount, significant pyramidal cell loss was obtained in 5-day-old rats as well. The susceptibility of pyramidal neurons to kainic acid increased as a function of age. The developing hippocampus was considerably more vulnerable to ibotenic acid compared with kainic acid, in contrast to the order of potency reported in adult rats. The increased sensitivity of CA3 pyramidal cells parallels the development of the mossy fiber innervation to the dendrites of these cells supporting the twofold mechanism suggested by Coyle for kainic acid neurotoxicity; that is, a direct cytotoxic action via postsynaptic receptors as well as increased sensitivity due to the presence of excitatory inputs.

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↗
PubMed1981

Synaptic excitation may activate a calcium-dependent potassium conductance in hippocampal pyramidal cells.

In hippocampal CAl pyramidal cells, orthodromic synaptic excitation is followed by an early hyperpolarization mediated by gamma-aminobutyric acid (GABA) and a late non-GABA-mediated hyperpolarization that has properties consistent with an increase in potassium conductance. Depolarizations produced by iontophoretically applied glutamate are followed by hyperpolarizations that have features in accordance with an increase in potassium conductance. The hyperpolarizations are independent of chloride and resistant to tetradotoxin but are blocked by a low-calcium, high-cobalt medium. Voltage clamping the glutamate depolarization does not reduce the subsequent hyperpolarization, indicating that the hyperpolarization results from a direct increase in calcium conductance produced by glutamate, rather than from activation of voltage-sensitive calcium channels. A single transmitter, possibly acting on one type of receptor and channel, may initiate both excitation and inhibition in the same postsynaptic cell.

Animals↗
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↗
PubMed1982

Cholinergic pharmacology of mammalian hippocampal pyramidal cells.

Responses of CAl pyramidal cells to cholinergic compounds were recorded with intracellular microelectrodes in guinea-pig hippocampal slices. Perfusion of slices with medium containing the muscarinic antagonists atropine or scopolamine (10(-7)-10(-6)M) blocked all actions of acetylcholine. Properties of control neurons and those from separate populations of neurons impaled in slices exposed to muscarinic blocking agents were compared. 1-2 h of perfusion with atropine-containing media significantly decreased membrane input resistance from 37.6 +/- 8.7 (S.D.) M omega (n = 74) to 21.9 +/- 7.7 (S.D.) M omega (n = 24) without producing significant changes in membrane potential. Muscarinic antagonists also reduced or eliminated the anomalous inward rectification normally seen in hippocampal pyramidal neurons. Exposure of slices to 10(-5)-10(-6)M eserine for about 1 h produced changes in neuronal membrane input resistance and potential and slow after hyperpolarizations similar to those elicited by application of acetylcholine. Bethanechol mimicked the actions of acetylcholine but was effective at lower concentrations and had longer lasting effects on afterhyperpolarizations. Nicotine produced an excitatory response in only one of 7 neurons. These experiments demonstrate that the actions of acetylcholine on hippocampal CAl neurons result from interaction with muscarinic receptors. Acetylcholine has modulatory effects on cell membrane properties which may be mediated through tonic release mechanisms.

Acetylcholine↗
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↗
PubMed1985

Gap junctions between non-pyramidal cell dendrites in the rat hippocampus (CA1 and CA3 regions): a combined Golgi-electron microscopy study.

Non-pyramidal cells in the rat hippocampus were examined with a combined Golgi-electron microscopic method. The somata of non-pyramidal cells were ovoid, about 15 X 30 micron, and several smooth and/or varicose dendrites extended from them. With electron microscopy, Golgi-impregnated gold-toned non-pyramidal cells showed distinctive fine structural features. The somata displayed large nuclei and an extensive perikaryal cytoplasm. The nuclei showed extensive cytoplasmic invaginations, little heterochromatin, conspicuous nucleoli, and intranuclear rods composed of filamentous bundles. The perikaryal cytoplasm was rich in cell organelles such as well-developed cisternae of rough endoplasmic reticulum and Golgi apparatus, and numerous clusters of free ribosomes and mitochondria. Many synaptic boutons, most of which formed asymmetrical synapses, impinged upon the somata and dendrites. Gap junctions were seen on varicose dendrites of Golgi-impregnated non-pyramidal cells. These gap junctions were patch-like, about 0.1-0.6 micron in diameter, and situated in the stratum radiatum or stratum oriens of the CA1 and CA3 regions 70-230 micron from the soma. They displayed a characteristic cytoplasmic semidense material undercoating the junctional membranes. The gap junctions were usually formed between impregnated and unimpregnated varicose dendrites. Thirteen of a total of 22 gap junctions involving the impregnated dendrites were situated singly, whereas the remaining nine were on four impregnated dendrites in clusters of two or three side by side. In the latter cases, two pairs of junctions were formed between pairs of dendrites running parallel to each other, and each of the other two pairs was formed among three dendrites, appearing to make a dendritic network bridged by gap junctions. One gap junction was seen between two impregnated dendrites originating from two identified Golgi-impregnated non-pyramidal cells. These observations revealed unequivocally that non-pyramidal cells in the hippocampus form gap junctions with one another on their dendrites.

Animals↗
PubMed1989

An after-hyperpolarization of medium duration in rat hippocampal pyramidal cells.

1. In hippocampal pyramidal cells, action potentials are followed by three after-hyperpolarizations (AHPs): a fast AHP (fAHP) lasting 2-5 ms, a medium AHP (mAHP) lasting 50-100 ms, and a slow AHP (sAHP) lasting more than 1 s. The mechanism underlying the mAHP was studied in CA1 cells (n = 46) in rat hippocampal slices, using injection of depolarizing current to elicit discharge. 2. The current underlying the mAHP was studied by single-electrode voltage clamp in two ways. Either the voltage clamp was activated following a burst of spikes, thus recording the early tail current underlying the mAHP (hybrid clamp), or, after blocking the spikes with tetrodotoxin, the early tail current following a depolarizing voltage clamp command (to -20 to -45 mV for 100-400 ms) was measured. In both cases, the early tail current (measured at -60 mV) showed the following characteristics: (a) it decayed exponentially with a time constant of about 50 ms; (b) it was substantially reduced by the muscarinic agonist carbachol (40-50 microM); (c) it was moderately reduced (by 20% or less) by Ca2+-free medium and Ca2+ channel blockers (Cd2+, Mn2+), which abolished the fAHP and the sAHP; (d) it was partly blocked by tetraethylammonium (TEA, 1-10 mM) both before and during Ca2+ channel blockade; (e) it was resistant to noradrenaline (5-10 microM), which blocked the sAHP, and to apamin (100 nM). 3. The mAHP itself, recorded under current clamp, showed properties corresponding to those of the early tail current. 4. Unlike the current underlying the sAHP, which was reduced and reversed by hyperpolarization, the early tail current appeared to be reduced only at potentials down to -80 mV, and to increase at more negative potentials. The early tail current and mAHP-like undershoot at hyperpolarized potentials was blocked by external Cs+, but not by carbachol, in contrast to the early tail current and mAHP at -60 mV. 5. It was concluded that two currents contribute to the mAHP: IM (a voltage-gated muscarine-sensitive K+ current) and IC (a Ca2+-dependent TEA-sensitive K+ current). TEA reduced both the IM (5 mM) and the IC (1 mM) component of the mAHP. When the cell is hyperpolarized, a third current, IQ (a Ca+-sensitive mixed Na+-K+ inward current activated by hyperpolarization), masks the reversal of the mAHP by causing a depolarizing sag which resembles the decay of the mAHP.

Action Potentials↗
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↗