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PubMed1986

Effects of histamine on hippocampal pyramidal cells of the rat in vitro.

The actions of bath applied histamine on CA1 pyramidal cells were investigated in hippocampal slices of the rat. Histamine caused a) a slight depolarization but no significant change in resting membrane conductance; b) an abbreviation of long afterhyperpolarizations after single action potentials, bursts of action potentials or TTX resistant spikes; c) a loss of accommodation of firing. In the presence of TEA or barium, histamine prolonged and increased the size and number of the slow TTX resistant spikes. A depolarizing plateau which follows such spikes was also increased by histamine, but the population spike was increased. The frequency of spontaneous chloride dependent potentials, which reflect interneurone firing, was also increased. These effects considerably outlasted histamine application and were mimicked by the H2-agonist impromidine but not the H1-agonist thiazolethylamine, and blocked by the H2-antagonists cimetidine and metiamide but not the H1-antagonists mepyramine or the beta-antagonist propranolol. It is concluded that histamine, by activating H2-receptors, antagonizes a calcium mediated potassium conductance in hippocampal pyramidal cells without affecting calcium current. By this mechanism histaminergic afferent fibres could effectively regulate cortical responsiveness by selectively potentiating large excitatory inputs of target neurones.

Animals↗
PubMed1988

Water-maze learning and effects of cholinergic drugs in mouse strains with high and low hippocampal pyramidal cell counts.

Morphological differences have been found in inbred strains of mice in the number and volume of pyramidal cells in Ammon's horn of the hippocampus. Among the mouse strains surveyed, NZB/BINJ (NZB) and C57BL/10J (B10) are most divergent in both total volume and total number of neurons. These genetically derived differences were exploited to determine hippocampal involvement in the acquisition of a spatial water maze. Genetic differences in hippocampal cell number were related to the acquisition of this spatial task. Mice with small numbers of hippocampal pyramidal cells, the B10 strain, acquired a water-maze task more slowly than either NZB mice or (NZBxNZW) F1 (NZBWF) animals. In addition, strain differences in responsivity to cholinergic manipulations were found. B10 mice were more sensitive than NZB or NZBWF mice to both the disruptive effects of scopolamine and the facilitory effects of physostigmine on swim maze learning. Although other inherited differences undoubtedly exist between these strains as is apparent in other mouse lines, these data suggest a prominent role for the hippocampus in the learning of spatially oriented behavior. Furthermore, this behavior appears to be responsive to cholinergic manipulations.

Animals↗
PubMed1987

Phorbol esters broaden the action potential in CA1 hippocampal pyramidal cells.

Intracellular recordings were made from CA1 pyramidal cells in rat hippocampal slices. Single action potentials were elicited by injection of brief current pulses. Bath application of phorbol esters (4 beta-phorbol-12,13-diacetate, 0.3-5 microM; or 4 beta-phorbol-12,13-dibutyrate, 5-10 microM) broadened the action potential in each of the cells tested (n = 9). The broadening reflected slowing of the repolarization, whereas the upstroke of the spike was unchanged. This effect may enhance transmitter release from synaptic terminals, and contribute to enhancement of synaptic transmission through activation of protein kinase C, a mechanism which has been associated with long term potentiation.

Action Potentials↗
PubMed1986

Facilitating and nonfacilitating synapses on pyramidal cells: a correlation between physiology and morphology.

Pyramidal cells in piriform cortex receive excitatory inputs from two different sources that are segregated onto adjacent segments of their apical dendrites. The present studies show that excitatory postsynaptic potentials (EPSPs) evoked by primary olfactory tract afferents that terminate on distal apical segments display paired shock facilitation whereas ESPSs evoked by intrinsic association fibers that terminate on proximal apical segments do not. An ultrastructural comparison of the presynaptic elements of these two fiber systems has revealed that the facilitating olfactory tract afferent synapses have a much lower packing density of synaptic vesicles than do the nonfacilitating association fiber synapses. Further, a search of the literature has revealed that where both morphological and physiological data are available for the same synapses, this same correlation appears to apply. We propose a hypothesis to account for this correlation based on synaptic vesicles to buffer internal calcium and the biochemical characteristics of preterminal calcium-dependent mechanisms affecting the number of vesicles available for release.

Animals↗
PubMed1978

Identification of pyramidal cells as the critical elements in hippocampal neuronal plasticity during learning.

The activity of single neurons recorded from rabbit hippocampus during classical conditioning of the nictitating membrane reflex was studied. All cells were first categorized according to their responses after fornix stimulation--i.i., antidromic activation, orthodromic activation, or no activation. The majority of cells that were antidromically activated--pyramidal cells--showed a highly positive correlation between the pattern of unit discharge and the topography of the nicititating membrane response within trial periods. Units that were orthodromically driven by fornix stimulation tended to inhibit during the presentation of trial stimuli, whereas most non-activated cells maintained low spontaneous levels of activity at all times. Thus, the major output neurons of the hippocampus appear to be the neuroanatomical substrate for the large and rapidly developing neuronal plasticity induced by this classical conditioning paradigm.

Action Potentials↗
PubMed1986

Giant multivesicular bodies in the rat hippocampal pyramidal cells after chronic alcohol consumption.

Multivesicular bodies (MVBs) with diameters up to 4.5 microns were observed in the hippocampal pyramidal cells of rats submitted to chronic alcohol consumption. A significant increase in the volumetric density (Vv) of these organelles was found in CA1 pyramidal cells. Transitional forms of MVBs towards lysosomes were seen. A failure in MVB's enzymatic hydrolytic mechanisms, due to the prolonged alcohol aggression, could underlie its formation.

Alcoholism↗
PubMedDate not supplied

Altered pyramidal cell dendritic development in the motor cortex of lead intoxicated neonatal rats. A Golgi study.

Neonatal Long-Evans rat pups were given the standard dose, 600 mg of lead acetate per kg of body weight every 24 hours beginning one day after birth until a cumulative dose of 2400 mg/kg (4 doses) had been administered via stomach intubation. Blood lead levels in lead treated rats averaged 526.35 micrograms/dl at 10 days of age. Blood lead values in age-matched controls averaged 0.079 microgram/dl. The body weights of the lead treated rats were not significantly different than control rats at 30 days of age. The brain weights were significantly greater than those of control rats at 30 days. Camera lucida drawings of pyramidal cells from motor cortex of control rats contained significantly (54%) more secondary and tertiary branches extending laterally from the primary apical dendrite than pyramidal cells of lead treated rats. The dendritic branches were numbered according to their branching point away from the soma. There was a significant reduction in the number of 4, 5, 6, and 7th order branches extending from the apical dendrite and 3 and 4th order branches extending from the basal dendrites in the leaded-rats. The mean dendritic length was reduced by 19% in basal dendrites and by 28% in apical dendrites. Measurements of dendritic material by the Scholl method revealed 17% reduction in the basal dendrites and a 36% reduction in the apical dendritic material in treated rats. These results suggest that neonatal lead exposure alters the dendritic development of pyramidal cells of rat motor cortex.

Animals↗
PubMed1986

The dendritic origins of penicillin-induced epileptogenesis in CA3 hippocampal pyramidal cells.

Experiments were performed in order to identify the sites of epileptiform burst generation in rat hippocampal CA3 pyramidal cells. A subsequent slow field potential was studied, which is associated with afterdischarge generation. Laminar field potential and current source-density (CSD) methods were employed in hippocampal slices exposed to penicillin. Simultaneous intracellular and extracellular field recordings from the CA3 pyramidal cell body layer showed that whenever an epileptiform burst was recorded extracellularly, individual CA3 neurons underwent an intense depolarization shift. In extracellular records a slow negative field potential invariably followed epileptiform burst generation. In approximately 10% of slices, synchronous afterdischarges rode on the envelope of this negative field potential. Intracellularly a depolarizing afterpotential followed the depolarization shift and was coincident with the extracellular slow negative field potential. A one-dimensional CSD analysis performed perpendicular to the CA3 cell body layer showed that during epileptiform burst generation large current sinks occur simultaneously in the central portions of both the apical and basilar dendrites. The average distance of the peak amplitude for these sinks from the center of the cell body layer was 175 +/- 46.8 microns and 158 +/- 25.0 microns, respectively. A large current source was recorded in the cell body layer. Smaller current sources were observed in the distal portions of the dendritic layers. During the postburst slow field potential a current sink was recorded at the edge of the cell body layer in stratum oriens--a region referred to as the infrapyramidal zone. Simultaneous with the current sink recorded there, smaller sinks were often observed in the dendritic layers that appeared to be "tails" or prolongations of the currents underlying burst generation. Two-dimensional analyses of these field potentials were performed on planes parallel and perpendicular to the exposed surface of the slice. Isopotential contours showed that the direction of extracellular current is mainly orthogonal to the CA3 laminae. Correction of CSD estimates made perpendicular to the cell body layer for current flowing in the other direction did not alter the location of computed current sources and sinks. In order to show that the dendritic currents associated with epileptiform burst generation were active sinks, tetrodotoxin (TTX) was applied locally to the dendrites where the current sinks were recorded.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Excitatory effects of ACPD receptor activation in the hippocampus are mediated by direct effects on pyramidal cells and blockade of synaptic inhibition.

1. Phosphoinositide hydrolysis-linked excitatory amino acid (EAA) receptors (ACPD receptors) are selectively activated by the glutamate analogue trans-1-amino-1,3-cyclopentanedicarboxylic acid (trans-ACPD). Regional analysis of trans-ACPD-induced phosphoinositide hydrolysis indicates that this response is greater in the hippocampus than in other brain regions. Therefore we designed a series of studies aimed at testing the hypothesis that activation of this receptor modulates synaptic function in the hippocampal region. 2. We report that trans-ACPD dramatically altered field population spikes at each of the three major synapses in the hippocampal trisynaptic circuit at concentrations that are effective in activating phosphoinositide hydrolysis. At the perforant path-dentate gyrus synapse, bath application of trans-ACPD resulted in a decrease in the amplitude of field population spikes. In contrast, trans-ACPD markedly enhanced field population spike amplitude at the mossy fiber-CA3 synapse and the Schaffer collateral-CA1 synapse. In area CA1, but not area CA3, trans-ACPD also induced generation of multiple population spikes. 3. Simultaneous field potential recordings from the s. pyramidale and s. radiatum in area CA1 revealed that the effect of trans-ACPD on population spikes in this region was not accompanied by an increase in the initial slope of the field EPSP. This suggests that the effect of trans-ACPD was not mediated by a presynaptic action but must be mediated by direct effects on CA1 pyramidal cells or by a decrease in synaptic inhibition. 4. trans-ACPD had a number of direct excitatory effects on CA1 pyramidal cells. These included 1) cell depolarization (with an increase in input resistance), 2) inhibition of the slow afterhyperpolarization, and 3) blockade of spike frequency adaptation. trans-ACPD also had effects on CA1 pyramidal cells that were not excitatory in nature. These included an increase in the threshold for initiation of calcium spikes and an increase in interspike interval during prolonged current injection. None of these effects were mimicked by an ACPD analogue that does not activate the ACPD receptor (trans-methanoglutamate), nor were they blocked by kynurenate, a nonselective EAA receptor antagonist that does not block the ACPD receptor.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acids↗
PubMed1983

Influence of the medial septal nucleus on the excitability of the commissural path-CA1 pyramidal cell synapse in the hippocampus of freely moving mice.

Changes in the excitability of the commissural path-CA1 pyramidal cell synapse were studied by varying the interval between the application of a conditioning pulse in the medial septal nucleus and a test pulse in the contralateral hippocampus in freely moving mice. The results showed that septal prestimulation results in marked changes in the excitability of pyramidal cells (population spikes) without any associated changes in the averaged evoked excitatory post synaptic potentials. Thus, as a result of septal stimulation, population spikes were first potentiated for interpulse intervals ranging from 10 to 30 ms; this was followed by inhibition at intervals between 40 and 60 ms and then by another phase of hyperexcitability between 100 and 160 ms. Possible mechanisms underlying this phenomenon are discussed and these successive changes in excitability are compared to the phase-locked ones which occur spontaneously during theta waves.

Afferent Pathways↗
PubMed1982

Convergence of associational and commissural pathways on CA1 pyramidal cells of the rat hippocampus.

The interaction of the commissural and associational systems to the CA1 region of the hippocampus was studied by recording extracellular field potentials and single unit activity in anesthetized rats. Associational fibers were activated by stimulating the stratum oriens of the CA1 region contralateral to recording: this stimulation activated the Schaffer collaterals by antidromically firing the pyramidal cells of the CA3 region on the side of recording. Commissural fibers were stimulated where they emerge from CA3 region. Both pathways excited both the basal and apical dendrites of the CA1 pyramidal cells. Commissural activation in stratum oriens was more efficient than associational path stimulation, while the opposite was seen in stratum radiatum. Responses elicited by associational path activation had their peak negativity 100--150 micrometers deeper in stratum radiatum than commissurally evoked responses. Both pathways were able to discharge pyramidal neurons. Both homonymous and heteronymous double pulse stimulation showed response facilitation. Simultaneous activation of both pathways induced a greater amplitude population spike than predicted by algebraic summation of the independent responses. Over 80% of the responsive CA1 cells could be fired by either pathway. These results show a considerable convergence of the commissural and associational pathways on CA1 pyramidal cells, although their predominant locus of excitation might be different.

Action Potentials↗
PubMed1991

Inactivation kinetics of calcium current of acutely dissociated CA1 pyramidal cells of the mature guinea-pig hippocampus.

1. The process of inactivation of the Ca2+ current of acutely dissociated pyramidal cells from the CA1 subfield of mature guinea-pig hippocampus was characterized. The decline of the current after rapid activation could be approximated well by the sum of two exponentials (time constants approximately 200 ms and 2 s) and a constant offset. 2. The time constants of inactivation exhibited a voltage dependence consistent with a voltage-dependent mechanism. However, under conditions which normally counteract Ca(2+)-dependent inactivation (viz. intracellular bis(O-aminophenoxy)-ethane-N,N,N',N'-tetraacetic acid (BAPTA) and external Ba2+) all three showed a U-shaped inactivation curve, characteristic of Ca(2+)-dependent inactivation. 3. The rate of inactivation was found to increase with current at a given voltage; however, increasing external divalent ion concentrations did not accelerate inactivation. 4. Calcium imaging experiments, using the Ca(2+)-sensitive probe, Fura-2, were performed to estimate the accumulation of Ca2+ in the presence of 10 mM-intracellular BAPTA. Under these conditions voltage steps which induced maximal Ca2+ currents lead to free Ca2+ concentrations of less than 500 nM in the bulk of the cytoplasm. 5. Elevation of the intracellular free Ca2+ concentration to above 1 microM suppressed all the components of the Ca2+ current. However, even at a concentration of 3 microM-Ca2+ the U-shaped inactivation curve persisted. 6. Substitution of Ca2+ for Ba2+ led to an acceleration of inactivation through an increase in the proportion of the fast process of inactivation and an acceleration of both the fast and slow rates of inactivation. 7. During the slow decline of Ca2+ current ('run-down') the proportion of all three components remained approximately constant and there was little change in the rate of inactivation. 8. On the basis of the results I suggest that inactivation results fro a dual process of voltage- and Ca(2+)-dependent inactivation. Ca(2+)-dependent inactivation seems to result from the accumulation of Ca2+ close to the channel mouth. 9. The macroscopic properties of the Ca2+ channel are consistent with the existence of one channel type in the CA1 pyramidal cells.

Animals↗
PubMed1991

Cerebral ischemia induces transient intracellular redistribution and intranuclear translocation of the raf proto-oncogene product in hippocampal pyramidal cells.

In this report we describe changes in the intracellular redistribution of raf serine/threonine protein kinase (product of the raf proto-oncogene family) in hippocampal neurons following cerebral ischemia in Mongolian gerbils. For immunohistochemical localization studies polyclonal antisera specific for each of the A, B, and Raf-1 isotypes of raf, as well as a pan-raf antisera, were employed. Of these, only sera recognizing B-raf, as well as the general v-raf (raised against the conserved C-terminal region) were positive, indicating that B-raf is the major isotype in this neuronal region. Three different ischemic models were used (repeated 3 times for two min and single 5 or 15 min occlusions, of the common carotid arteries) to demonstrate that ischemic insult causes redistribution of raf protein kinase into the cell nucleus of hippocampal neurons. Increased amounts of raf protein in the nuclei of pyramidal cells following ischemia was confirmed by Western blot analysis of isolated nuclear fractionations. Moreover, an elevation in the level of nuclear raf protein also was detected in the contralateral (i.e. non-occluded hemisphere) neurons of CA1 and CA3 subfields 4 days after the ischemic insult indicating a possible transsynaptic increase in the amount of raf protein along with redistribution. The intranuclear translocation of the immunoreactive material started from the perinucleolar rim and with time extended throughout the nucleus. Enhanced levels and altered redistribution of the raf polypeptide in the nuclei of pyramidal cells of the CA3 subfield appears to be reversible and returns to the normal level 12 days following the ischemic insult.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1984

Increased glucose metabolism during long-duration recurrent inhibition of hippocampal pyramidal cells.

The locally subnormal brain metabolism observed in some experiments utilizing the Sokoloff 2-deoxyglucose (2-DG) method has often been attributed to postsynaptic inhibition despite the fact that inhibitory postsynaptic potentials are themselves caused by energy-requiring mechanisms. To explore this issue, neurophysiologically confirmed long-duration recurrent inhibition of hippocampal pyramidal unit firing was induced by low frequency (2 to 4 Hz) stimulation of the fornix for 60 min following intravenous infusion of [14C]-2-DG. The resulting autoradiograms showed that long-duration suppression of pyramidal cell firing was accompanied by distinctly increased hippocampal 2-DG uptake, particularly in the stratum pyramidale, which contains a dense plexus of inhibitory interneuronal terminals upon pyramidal cells. Both the pyramidal inhibition and the increased 2-DG uptake were confined to the ipsilateral hippocampus in animals with previously severed fornices and hippocampal commissures. In a second series of rats, the excitatory entorhinohippocampal "perforant path" (PP) was stimulated at low frequency (2 to 9 Hz) following 2-DG administration. At 2 to 4 Hz, each PP stimulation resulted in a brief burst of pyramidal unit firing followed by short-duration firing suppression; this result was associated with paradoxically decreased 2-DG uptake in the ipsilateral stratum molecular. By contrast, 7 to 9 Hz entorhinal stimulation induced PP-mediated excitation immediately followed by powerful intrinsic hippocampal inhibition, evidenced by prolonged pyramidal unit suppression after each stimulation. This suppression was accompanied by increased 2-DG uptake in the dentate stratum molecular and hippocampal stratum pyramidale. Thus it appeared that even with entorhinal stimulation, hippocampal 2-DG uptake was more closely associated with long-duration recurrent inhibition than with transient pyramidal excitation. Therefore, although it still remains possible that regions of hypometabolism observed in some previous 2-DG studies may actually reflect mild inhibition, other mechanisms such as disfacilitation are more likely mechanisms for this metabolic pattern.

Animals↗
PubMedDate not supplied

The locomotor and exploratory activities in rats after lesion of hippocampal pyramidal cells with kainic acid.

The effect of single kainic acid (KA) intracerebroventricular(icv) injection on spontaneous locomotor, exploratory, basal and total activities in rats measured a different times was tested. Whereas at 3 hr after KA icv administration an increase of the total, basal and spontaneous activities of rats were observed, a great decrease of the exploratory activity was noted. KA at 24 hr after its administration depressed all types of rats activities. From 72nd hr after KA icv injection a significant increase in the total, exploratory and spontaneous locomotor activities without changes in the basal activity was observed. The above mentioned changes persisted up to 10-20 days after KA administration. The histological examinations showed evident neuropathologic changes in hippocampal stratum pyramidale. The most evident changes concerned the hippocampal areas CA3/CA4 and CA1. There were observed shrinking, narrowing and fragmentation of pyramidal cells. An intense progressive gliotic reaction was present among the fragmented cells, the layer of pyramidal cells being considerably diminished.

Animals↗
PubMed1990

Visibility of synaptically induced conductance changes: theory and simulations of anatomically characterized cortical pyramidal cells.

A recent report has provided evidence that there are no significant increases in the neuronal input conductance during the response of cortical cells in cat visual cortex to non-preferred visual stimuli (Douglas et al., 1988). A criticism of experiments of this kind is that changes in the membrane conductance occurring in the dendritic tree may not be visible from electrodes that impale the soma. Our paper describes theoretical and numerical results concerning the visibility of synaptically induced conductance changes from intracellular electrodes, in both ideal and anatomically well-characterized cortical neurons. Based on earlier work by Rall (1967), we here derive theoretical expressions for the change in input conductance at any location in a passive dendritic tree resulting from activation of a single synapse and obtain bounds for the effects of multiple synapses. We find that the conductance change measured at the cell body is always less than the sum of the synaptic conductance changes and that this observed conductance change does not depend on the synaptic reversal potential. For the case of an infinite dendritic cylinder, the change in input resistance due to a single synaptic input decays exponentially with distance of the synapse from the recording site. Numerical simulations of synaptic inputs that change approximately as fast as the membrane time-constant produce an increase in input conductance that is only slightly less visible than that of a constant input. We also compute the changes in somatic input conductance of 2 morphologically identified pyramidal cells from cat visual cortex during activity of a single inhibitory basket cell with known synaptic input locations. We find that the increase in conductance due to the activity of the inhibitory basket cells is clearly visible from the cell body of the pyramidal cells and that a 70% reduction in the amplitude of excitation is associated with at least a 30% increase in somatic input conductance, which would be visible in intracellular recordings. Taken together with the negative experimental evidence of Douglas et al. (1988), our results cast doubt on a large class of models of direction selectivity that rely on synaptically mediated inhibitory conductance increases to veto or block excitatory conductances increases.

Animals↗
PubMed1979

The effect of muscimol on hippocampal pyramidal cells.

The effects of muscimol on rabbit hippocampal pyramidal cell firing were studied and compared after iontophoretic, topical, and intravenous administration of the drug. All modes of application resulted in a bicuculline-sensitive, strychnine-insensitive, depression of the monosynaptically activated population spike evoked by micro-stimulation of the contralateral hippocampal field. These findings indicate that systemically administered muscimol selectively activates hippocampal GABA receptors suggesting that this compound may be useful for studying limbic system physiology.

Action Potentials↗
PubMed1981

Axonal ramifications of hippocampal Ca1 pyramidal cells.

Intracellular injections of Lucifer Yellow into CA1 pyramidal cells of the in vitro guinea pig hippocampal slice enabled us to examine in detail the morphology of the axons of these neurons. We also recorded the electrophysiological responses of these neurons to alvear stimulation. In our morphological examinations, we found that many axons bifurcate in the alveus, with the major branch projecting caudally toward the subiculum and the second, thinner branch projecting rostrally toward the fimbria. Either axons may bifurcate further to produce several axon branches which follow parallel paths in the alveus. These axons also have local collaterals which project into strata oriens and pyramidale. In addition, a very fine plexus of axonal processes was observed in stratum oriens located largely within the basal dendritic field of the parent cell. Our electrophysiological experiments demonstrated that neurons could be activated antidromically by stimulation of the alveus at sites both rostral ad caudal to the neuron. Weak alvear stimulation occasionally evoked small potentials which appeared similar to fast prepotentials. The local axonal ramifications may be involved in recurrent pathways mediating feedback inhibition and/or excitation. The axonal bifurcations also may provide a basis for understanding the origins of fast prepotentials elicited with antidromic stimulation.

Action Potentials↗