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PubMed1995

Transport of dendritic microtubules establishes their nonuniform polarity orientation.

The immature processes that give rise to both axons and dendrites contain microtubules (MTs) that are uniformly oriented with their plus-ends distal to the cell body, and this pattern is preserved in the developing axon. In contrast, developing dendrites gradually acquire nonuniform MT polarity orientation due to the addition of a subpopulation of oppositely oriented MTs (Baas, P. W., M. M. Black, and G. A. Banker. 1989. J. Cell Biol. 109:3085-3094). In theory, these minus-end-distal MTs could be locally nucleated and assembled within the dendrite itself, or could be transported into the dendrite after their nucleation within the cell body. To distinguish between these possibilities, we exposed cultured hippocampal neurons to nanomolar levels of vinblastine after one of the immature processes had developed into the axon but before the others had become dendrites. At these levels, vinblastine acts as a kinetic stabilizer of MTs, inhibiting further assembly while not substantially depolymerizing existing MTs. This treatment did not abolish dendritic differentiation, which occurred in timely fashion over the next two to three days. The resulting dendrites were flatter and shorter than controls, but were identifiable by their ultrastructure, chemical composition, and thickened tapering morphology. The growth of these dendrites was accompanied by a diminution of MTs from the cell body, indicating a net transfer of MTs from one compartment into the other. During this time, minus-end-distal microtubules arose in the experimental dendrites, indicating that new MT assembly is not required for the acquisition of nonuniform MT polarity orientation in the dendrite. Minus-end-distal microtubules predominated in the more proximal region of experimental dendrites, indicating that most of the MTs at this stage of development are transported into the dendrite with their minus-ends leading. These observations indicate that transport of MTs from the cell body is an essential feature of dendritic development, and that this transport establishes the nonuniform polarity orientation of MTs in the dendrite.

Animals↗
PubMed1955

Further study of soma, dendrite, and axon excitation in single neurons.

The present investigation continues a previous study in which the soma-dendrite system of sensory neurons was excited by stretch deformation of the peripheral dendrite portions. Recording was done with intracellular leads which were inserted into the cell soma while the neuron was activated orthodromically or antidromically. The analysis was also extended to axon conduction. Crayfish, Procambarus alleni (Faxon) and Orconectes virilis (Hagen), were used. 1. The size and time course of action potentials recorded from the soma-dendrite complex vary greatly with the level of the cell's membrane potential. The latter can be changed over a wide range by stretch deformation which sets up a "generator potential" in the distal portions of the dendrites. If a cell is at its resting unstretched equilibrium potential, antidromic stimulation through the axon causes an impulse which normally overshoots the resting potential and decays into an afternegativity of 15 to 20 msec. duration. The postspike negativity is not followed by an appreciable hyperpolarization (positive) phase. If the membrane potential is reduced to a new steady level a postspike positivity appears and increases linearly over a depolarization range of 12 to 20 mv. in various cells. At those levels the firing threshold of the cell for orthodromic discharges is generally reached. 2. The safety factor for conduction between axon and cell soma is reduced under three unrelated conditions, (a) During the recovery period (2 to 3 msec.) immediately following an impulse which has conducted fully over the cell soma, a second impulse may be delayed, may invade the soma partially, or may be blocked completely. (b) If progressive depolarization is produced by stretch, it leads to a reduction of impulse height and eventually to complete block of antidromic soma invasion, resembling cathodal block, (c) In some cells, when the normal membrane potential is within several millivolts of the relaxed resting state, an antidromic impulse may be blocked and may set up within the soma a local potential only. The local potential can sum with a second one or it may sum with potential changes set up in the dendrites, leading to complete invasion of the soma. Such antidromic invasion block can always be relieved by appropriate stretch which shifts the membrane potential out of the "blocking range" nearer to the soma firing level. During the afterpositivity of an impulse in a stretched cell the membrane potential may fall below or near the blocking range. During that period another impulse may be delayed or blocked. 3. Information regarding activity and conduction in dendrites has been obtained indirectly, mainly by analyzing the generator action under various conditions of stretch. The following conclusions have been reached: The large dendrite branches have similar properties to the cell body from which they arise and carry the same kind of impulses. In the finer distal filaments of even lightly depolarized dendrites, however, no axon type all-or-none conduction occurs since the generator potential persists to a varying degree during antidromic invasion of the cell. With the membrane potential at its resting level the dendrite terminals contribute to the prolonged impulse afternegativity of the soma. 4. Action potentials in impaled axons and in cell bodies have been compared. It is thought that normally the over-all duration of axon impulses is shorter. Local activity during reduction of the safety margin for conduction was studied. 5. An analysis was made of high frequency grouped discharges which occasionally arise in cells. They differ in many essential aspects from the regular discharges set up by the generator action. It is proposed that grouped discharges occur only when invasion of dendrites is not synchronous, due to a delay in excitation spread between soma and dendrites. Each impulse in a group is assumed to be caused by an impulse in at least one of the large dendrite branches. Depolarization of dendrites abolishes the grouped activity by facilitating invasion of the large dendrite branches.

Action Potentials↗
PubMedDate not supplied

Nonuniform alteration of dendritic development in the cerebral cortex following prenatal cocaine exposure.

Prenatal exposure to cocaine has the potential to modify normal brain development and result in behavioral dysfunction. We used a new animal model in which cocaine was administered intravenously during prenatal development in pregnant rabbits twice daily at low dosages. Analysis of brain development focused on two areas of the cerebral cortex, anterior cingulate and primary visual, in which dopamine afferents, a target of cocaine, are differentially distributed. All postnatal rabbits exposed to cocaine prenatally exhibited normal features of cortical organization, including thickness, lamination patterns, and cytoarchitectonic differentiation. General axonal and astroglial organization, assessed by neurofilament-H and glial fibrillary acidic protein immunostaining, also was unchanged in the cocaine-exposed animals. Analysis of dendritic organization was done using antibodies against microtubule-associated protein 2 (MAP2), which reveals mostly the larger apical shafts of cortical pyramidal cells. In the anterior cingulate cortex of adolescent rabbits exposed to cocaine in utero, there is a marked decrease in both dendritic bundling and typical long, straight MAP2-stained profiles. In normal animals, the long, bundled dendrites area readily traced in a single focal plane from layer III or V pyramidal cell somata to the pial surface in saline-treated animals. Instead, the drug-exposed animals contained many more short segments of MAP2-stained dendrites that could be viewed coursing in and out of the plane of focus in the sections. Apical dendrites in mature visual cortex appeared normal in the cocaine-exposed rabbits. Examination of MAP2 staining at various postnatal ages revealed that the dendritic changes expressed in the adolescent anterior cingulate cortex appeared less robust, but still evident at birth. By P10-14, dendritic modifications were similar to the adult. Counts of the number of MAP2-positive dendritic profiles crossing the layer II-III interface reached a nadir of 50% in the cocaine-exposed animals, indicative of a change in the organization of the apical dendrites compared to the control animals. Dendritic profiles of anterior cingulate neurons, filled by 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine percholate (Dil), confirmed that in the cocaine offspring, the dendrites coursed in an irregular, wavy manner from deep to superficial layers, suggestive of dendrites that were longer than normal, although cortical thickness was unchanged. The altered dendritic profiles also were seen in Golgi-impregnated neurons. The data indicate that prenatal exposure to cocaine can lead to specific alterations of neuronal growth that are long lasting. The lack of dendritic changes in visual cortex suggests that the drug does not modify development of cortical regions uniformly. This study also provides a new focus on the anterior cingulate cortex as a site in which aberrant structure-function relationships following prenatal cocaine exposure should be examined in both animal models and clinically.

Animals↗
PubMed1992

During HIV-1 infection most blood dendritic cells are not productively infected and can induce allogeneic CD4+ T cells clonal expansion.

We have considered the possibility that antigen-presenting cells of the dendritic cell lineage may be infected in vivo and spread HIV-1 at the time dendritic cells initiate the clonal expansion of antigen-specific T cells. Dendritic cells were isolated from 25 HIV-1-infected subjects (CDC stages II-IV). Fewer dendritic cells were recovered from most infected subjects. Reduced numbers of total non-T cells were also found in these patients, so that preferential loss of dendritic cells did not occur. Dendritic cell function was assessed by stimulatory capacity for allogeneic CD4+ T cells in the mixed leucocyte reaction (MLR). Potent MLR stimulator activity was retained in the dendritic cell-enriched populations from HIV-infected patients. Seven out of nine patients without AIDS (asymptomatic, lymphadenopathy or ARC) and three out of six patients with AIDS had proliferative responses equivalent to those induced by dendritic cells from controls. Dendritic cells from HIV+ subjects were able to initiate the expansion of allogeneic CD4+ T cell clones with cloning efficiency not different from controls and without evidence of cytopathic effect in the expanding CD4+ clones. In situ hybridization of the different mononuclear cell populations with a gag-specific riboprobe demonstrated positive cells in the T cell fractions of 12 of the 15 patients tested. None of the asymptomatic or ARC patients had riboprobe-positive cells in the dendritic cell-enriched populations. Four out of nine patients with AIDS had cells positive for HIV-1 expression in the dendritic cell-enriched fraction. However, the positive cells had the nuclear profile of lymphocytes, and by cytofluorography some residual low-density T cells were present. By limiting dilution and polymerase chain reaction (PCR), CD4+ lymphocytes carried HIV provirus in inocula of 500-5000 cells, while provirus could only be detected in 50,000 cells from the dendritic cell-enriched fraction. The latter signal may be due to the demonstrated levels of T cell contamination. Our data indicate that productive or latent HIV-1 infection of blood dendritic cells in vivo is rare, certainly no greater than in T lymphocytes, and that in vitro dendritic cell preparations from patients can expand CD4+ T cells efficiently and therefore may be able to expand T cells with immunotherapeutic activity.

CD4-Positive T-Lymphocytes↗
PubMed1980

A comparison of distal and proximal dendritic synapses on CAi pyramids in guinea-pig hippocampal slices in vitro.

1. In vitro slices of guinea-pig hippocampus have been employed to compare excitatory synapses located distally and proximally on the dendritic tree of CA1 pyramidal cells.2. The main orientation of unmyelinated afferent fibres was found to be parallel to each other and perpendicular to the dendritic axis.3. The density of boutons ending on dendritic spines was roughly similar throughout the greater part of the dendritic tree with an average of 42 +/- 7.2 synapses per 100 mum(2). Their number did, however, decrease in the distal fifth of the apical and in the distal third of the basal dendritic region in parallel with an increase of boutons on the dendritic shafts.4. Negative synaptic field potentials (extracellular field e.p.s.p.s) had their maximum in the region where activated afferent fibres terminated and showed reversal when recorded from sufficiently displaced positions along the dendritic axis. The field e.p.s.p. was preceded by a diphasic presynaptic fibre volley. By cutting all but a narrow bundle of afferent fibres selective activation of a small group of dendritic synapses was possible. Stimulation of fibres crossing tissue bridges (35-100 mum wide) evoked field e.p.s.p.s comparable in amplitude to those seen in slices without lesions. The size of the field e.p.s.p.s evoked via distal and proximal bridges was remarkably similar and linearly related to the size of the appropriate stimulus current and presynaptic volley.5. Selective activation of a small group of afferent fibres gave rise to large amplitude population spikes. Proximal and distal bridges were largely equipotent when they were equally wide. Above the threshold amplitude, the evoked population spikes were linearly related to both the presynaptic volley and the stimulus current. Constant current stimulation of fibres at all apical dendritic levels was equally effective in evoking population spikes, with the exception of the outer fifth of the tree where stimulation was unsuccessful. Input across distal or proximal bridges (400 or 50 mum from the soma) also gave the same high probability of discharge of single units (1.0 for thirty-five of thirty-six cells).6. An input across a narrow and distal bridge (35 mum), representing less than 5% of the fibres synapsing on the apical dendrite, was sufficient to give a firing probability of 1.0 for all cells tested (fifteen).7. For seventeen cells pairs of equally wide distal and proximal apical dendritic bridges were compared. Both inputs gave a mean probability of firing above 0.95 with stimulation strengths less than 2.5 times the spike threshold.8. Intracellular e.p.s.p.s had similar shapes following activation across distal and proximal dendritic bridges. The amplitude of neither type was significantly affected by hyperpolarization of the soma up to 25 mV. The half-width was prolonged to the same moderate degree for both inputs.9. The firing level for the action potential was similar for proximal and distal dendritic inputs and for spikes excited by depolarizing current pulses across the soma membrane.10. The apparent equipotentiality of synchronously activated distal and proximal dendritic synapses is discussed in the light of the known histology of the CA1 pyramidal cells.

Action Potentials↗
PubMed1989

Size and remoteness: two relatively independent parameters of dendrites, as studied for spinal motoneurones of the cat.

1. The spatial extent of motoneuronal dendrites was analysed using data from the fifty-two dendritic trees of four completely reconstructed cat motoneurones that had been labelled with intracellularly injected horseradish peroxidase. The cells belonged to m. triceps surae, and their physiological properties covered much of the known range for this muscle. 2. The percentage of total dendritic area extending beyond a radial somatofugal distance of 750 microns (PA750) was selected as an index of 'dendritic remoteness'. 3. The value of our standard remoteness index PA750 was well correlated with a number of other possible remoteness measures, such as the percentage of total dendritic area beyond 500 or 1000 microns or the percentage of cumulative dendritic length beyond 750 or 1000 microns. 4. Most of the dendritic parameters could be classified as belonging either to a cluster of remoteness-related properties or to a cluster of size-related properties. Remoteness-related properties were significantly correlated with PA750 but not with stem diameter. Size-related properties were significantly correlated with stem diameter but not with the remoteness index PA750. The remoteness-related properties included the mean somatofugal distance to branch points, the mean and maximum distance to terminal ending and, somewhat less distinctly, the mean length of terminal branches. The size-related properties included the total dendritic area, the cumulative dendritic length, and the total number of branch points and terminal endings. 5. The extent of area expansion at branch points and the overall extent of tapering were not systematically related to differences in remoteness. 6. The relative degree of remoteness was greater for medial than for lateral dendrites. 7. Even in the present limited sample of cells, there were marked and systematic differences between different neurones with respect to the relative remoteness of their dendrites. The slowest and most high-resistance motoneurone was the one with the most remote dendrites. On the whole there was, however, a considerable degree of independence between the variation in dendritic remoteness and the variation in physiologically determined properties (axonal conduction velocity, input resistance, after-hyperpolarization). 8. In the discussion it is suggested that differences in dendritic remoteness might lead to a selectivity between the various members of a given motoneurone pool with respect to their reception of topographically distributed systems of synapses. It is proposed that such differences might be of interest in relation to, for instance, the organization of innervation to motoneurones belonging to different task groups within the same muscle.

Animals↗
PubMed1992

Different firing patterns generated in dendrites and somata of CA1 pyramidal neurones in guinea-pig hippocampus.

1. Intracellular recordings, taken from CA1 pyramidal cells in guinea-pig hippocampal slices, were used to examine the origins of repetitive and burst firing in these cells. Single action potentials were elicited by depolarizing current injection at somatic recording sites. In contrast, current injection during intradendritic recordings initiated burst firing in the dendrites. Burst firing could be elicited in the soma by direct depolarization of distal apical dendrites (> 150 microns from the cell body layer) with large extracellular polarizing electrodes. 2. Intracellular recordings were taken simultaneously from the apical dendrites and pyramidal cell somata with the intention of impaling the same neurone with both electrodes. Paired dendrite-soma recordings confirmed that rhythmic single action potentials were generated at the cell soma, whereas bursts of action potentials were initiated in the distal apical dendrites (> 150 microns from the cell body layer). Fast spikes in the dendrite often triggered fast spikes in the soma, but not all fast spikes in the dendritic burst were 'relayed' to the soma. 3. In paired recordings, when a dendritic action potential failed to elicit a full somatic action potential, a 'd-spike' was commonly recorded in the soma. Somatic d-spikes were uniform all-or-none responses that could be shown, in some cases, to trigger the full somatic action potentials. 4. Attenuated spikes could be recorded in the dendrites, triggered by action potentials initiated at the cell soma. Dendritic responses to somatic stimulation sometimes varied in amplitude, but always showed a direct correspondence with somatic action potentials. 5. Dendritic recordings taken closer to the pyramidal cell bodies (< 150 microns from the cell body layer) showed a 'transitional' region where single action potentials rather than burst discharges could be evoked. After-potentials of these single spikes differed from those associated with somatic spikes in that proximal dendritic spikes had depolarizing after-potentials. The observed shift from after-hyperpolarization to depolarizing after-potentials in intradendritic recordings taken progressively further from the cell body corresponds to the change from repetitive to burst firing. 6. The results indicate that activity of the CA1 pyramidal cell soma, presumably a reflection of its output, can be either burst or repetitive firing. Somatic 'bursts,' unlike the burst discharges seen in the apical dendrites or the burst discharges reported in CA3 cells, are not initiated locally. Rather, they appear to be simply a rapid spike-for-spike response by the soma to the fast spikes that form part of the apical dendritic burst.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed2003

Regulation of backpropagating action potentials in mitral cell lateral dendrites by A-type potassium currents.

Dendrodendritic synapses, distributed along mitral cell lateral dendrites, provide powerful and extensive inhibition in the olfactory bulb. Activation of inhibition depends on effective penetration of action potentials into dendrites. Although action potentials backpropagate with remarkable fidelity in apical dendrites, this issue is controversial for lateral dendrites. We used paired somatic and dendritic recordings to measure action potentials in proximal dendritic segments (0-200 microm from soma) and action potential-generated calcium transients to monitor activity in distal dendritic segments (200-600 microm from soma). Somatically elicited action potentials were attenuated in proximal lateral dendrites. The attenuation was not due to impaired access resistance in dendrites or to basal synaptic activity. However, a single somatically elicited action potential was sufficient to evoke a calcium transient throughout the lateral dendrite, suggesting that action potentials reach distal dendritic compartments. Block of A-type potassium channels (I(A)) with 4-aminopyridine (10 mM) prevented action potential attenuation in direct recordings and significantly increased dendritic calcium transients, particularly in distal dendritic compartments. Our results suggest that I(A) may regulate inhibition in the olfactory bulb by controlling action potential amplitudes in lateral dendrites.

2-Amino-5-phosphonovalerate↗
PubMed1995

Long-term potentiation at the apical and basal dendritic synapses of CA1 after local stimulation in behaving rats.

1. We recorded the extracellular excitatory postsynaptic potentials (EPSPs) in CA1 in the freely behaving rats after stimulation of the apical dendritic and basal dendritic afferents. The apical dendritic population EPSP was negative at the apical dendritic layers and positive at stratum oriens and alveus. The basal dendritic population EPSP was negative at basal dendritic layer (stratum oriens) and positive at the cell body and apical dendritic layers. 2. We delivered various tetanic stimulus patterns in an attempt to elicit long-term potentiation (LTP) at the apical dendritic synapse of CA1 pyramidal cells. A 200-Hz high-frequency train (HF) 1 s in duration was more successful than theta-frequency primed bursts (PBs; 1 or 4 priming pulses followed by 10 or 4 pulses at 100 Hz) in eliciting LTP of the apical dendritic population EPSP, recorded either ipsilaterally or contralaterally. 3. Tetanus applied to the apical dendritic afferents occasionally elicited long-term depression (LTD) at an intensity lower than the LTP threshold. LTD persisted to > or = 1 day after a tetanus. 4. High-intensity tetanic stimulations often elicited hippocampal afterdischarges (ADs). If the AD duration was brief (< 15 s), apical dendritic LTP could follow the AD. However, if the AD duration was long, no apical dendritic LTP was observed. Tetanus that evoked an apical dendritic LTP typically evoked a short hippocampal AD < 15 s in duration. 5. LTP of the basal dendritic population EPSP was readily elicited either after an HF or a PB tetanus of low (1.5-2 times threshold) stimulus intensity.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1997

Modification of current transmitted from apical dendrite to soma by blockade of voltage- and Ca2+-dependent conductances in rat neocortical pyramidal neurons.

The axial current transmitted to the soma during the long-lasting iontophoresis of glutamate at a distal site on the apical dendrite was measured by somatic voltage clamp of rat neocortical pyramidal neurons. Evidence for voltage- and Ca2+-gated channels in the apical dendrite was sought by examining the modification of this transmitted current resulting from the alteration of membrane potential and the application of channel-blocking agents. After N-methyl-D-aspartate receptor blockade, iontophoresis of glutamate on the soma evoked a current whose amplitude decreased linearly with depolarization to an extrapolated reversal potential near 0 mV. Under the same conditions, glutamate iontophoresis on the apical dendrite 241-537 microm from the soma resulted in a transmitted axial current that increased with depolarization over the same range of membrane potential (about -90 to -40 mV). Current transmitted from dendrite to soma was thus amplified during depolarization from resting potential (about -70 mV) and attenuated during hyperpolarization. After Ca2+ influx was blocked to eliminate Ca2+-dependent K+ currents, application of 10 mM tetraethylammonium chloride (TEA) altered the amplitude and voltage dependence of the transmitted current in a manner consistent with the reduction of dendritic voltage-gated K+ current. We conclude that dendritic, TEA-sensitive, voltage-gated K+ channels can be activated by tonic dendritic depolarization. The most prominent effects of blocking Ca2+ influx resembled those elicited by TEA application, suggesting that these effects were caused predominantly by blockade of a dendritic Ca2+-dependent K+ current. When cells were impaled with microelectrodes containing ethylene glycol-bis(beta-amino-ethyl ether)-N,N',N'-tetraacetic acid to prevent a rise in intracellular Ca2+ concentration, blockade of Ca2+ influx altered the tonic transmitted current in different manner consistent with the blockade of an inward dendritic current carried by high-threshold-activated Ca2+ channels. We conclude that the primary effect of Ca2+ influx during tonic dendritic depolarization is the activation of a dendritic Ca2+-dependent K+ current. The hyperpolarizing attenuation of transmitted current was unaffected by blocking all known voltage-gated inward currents except the hyperpolarization-activated cation current (Ih). Extracellular Cs+ (3 mM) reversibly abolished both the hyperpolarizing attenuation of transmitted current and Ih measured at the soma. We conclude that activation of Ih by hyperpolarization of the proximal apical dendrite would cause less axial current to arrive at the soma from a distal site than in a passive dendrite. Several functional implications of dendritic K+ and Ih channels are discussed.

Animals↗
PubMed1998

Modeling action potential initiation and back-propagation in dendrites of cultured rat motoneurons.

Regardless of the site of current injection, action potentials usually originate at or near the soma and propagate decrementally back into the dendrites. This phenomenon has been observed in neocortical pyramidal cells as well as in cultured motoneurons. Here we show that action potentials in motoneurons can be initiated in the dendrite as well, resulting in a biphasic dendritic action potential. We present a model of spinal motoneurons that is consistent with observed physiological properties of spike initiation in the initial segment/axon hillock region and action potential back-propagation into the dendritic tree. It accurately reproduces the results presented by Larkum et al. on motoneurons in organotypic rat spinal cord slice cultures. A high Na+-channel density of Na = 700 mS/cm2 at the axon hillock/initial segment region was required to secure antidromic invasion of the somato-dendritic membrane, whereas for the orthodromic direction, a Na+-channel density of Na = 1,200 mS/cm2 was required. A "weakly" excitable (Na = 3 mS/cm2) dendritic membrane most accurately describes the experimentally observed attenuation of the back-propagated action potential. Careful analysis of the threshold conditions for action potential initiation at the initial segment or the dendrites revealed that, despite the lower voltage threshold for spike initiation in the initial segment, an action potential can be initiated in the dendrite before the initial segment fires a spike. Spike initiation in the dendrite depends on the passive cable properties of the dendritic membrane, its Na+-channel density, and local structural properties, mainly the diameter of the dendrites. Action potentials are initiated more easily in distal than in proximal dendrites. Whether or not such a dendritic action potential invades the soma with a subsequent initiation of a second action potential in the initial segment depends on the actual current source-load relation between the action potential approaching the soma and the electrical load of the soma together with the attached dendrites.

Action Potentials↗
PubMed1999

Mechanisms underlying burst and regular spiking evoked by dendritic depolarization in layer 5 cortical pyramidal neurons.

Apical dendrites of layer 5 pyramidal cells in a slice preparation of rat sensorimotor cortex were depolarized focally by long-lasting glutamate iontophoresis while recording intracellularly from their soma. In most cells the firing pattern evoked by the smallest dendritic depolarization that evoked spikes consisted of repetitive bursts of action potentials. During larger dendritic depolarizations initial burst firing was followed by regular spiking. As dendritic depolarization was increased further the duration (but not the firing rate) of the regular spiking increased, and the duration of burst firing decreased. Depolarization of the soma in most of the same cells evoked only regular spiking. When the dendrite was depolarized to a critical level below spike threshold, intrasomatic current pulses or excitatory postsynaptic potentials also triggered bursts instead of single spikes. The bursts were driven by a delayed depolarization (DD) that was triggered in an all-or-none manner along with the first Na+ spike of the burst. Somatic voltage-clamp experiments indicated that the action current underlying the DD was generated in the dendrite and was Ca2+ dependent. Thus the burst firing was caused by a Na+ spike-linked dendritic Ca2+ spike, a mechanism that was available only when the dendrite was adequately depolarized. Larger dendritic depolarization that evoked late, constant-frequency regular spiking also evoked a long-lasting, Ca2+-dependent action potential (a "plateau"). The duration of the plateau but not its amplitude was increased by stronger dendritic depolarization. Burst-generating dendritic Ca2+ spikes could not be elicited during this plateau. Thus plateau initiation was responsible for the termination of burst firing and the generation of the constant-frequency regular spiking. We conclude that somatic and dendritic depolarization can elicit quite different firing patterns in the same pyramidal neuron. The burst and regular spiking observed during dendritic depolarization are caused by two types of Ca2+-dependent dendritic action potentials. We discuss some functional implications of these observations.

Action Potentials↗
PubMed2006

Calcium spikes in basal dendrites of layer 5 pyramidal neurons during action potential bursts.

Patch-clamp recording from dendrites has lead to a significant increase in our understanding of the mechanisms underlying signal integration and propagation in neurons. The majority of synaptic input to neurons, however, is made onto small-diameter dendrites, currently beyond the scope of patch-clamp recording techniques. Here we use both calcium and voltage imaging to investigate propagation of action potentials (APs) in fine basal dendrites of cortical layer 5 pyramidal neurons. High-frequency (200 Hz) AP bursts caused supralinear increases in dendritic calcium at distal, but not proximal, basal locations. Supralinear increases in dendritic calcium were also observed at distal basal locations during AP trains above a critical frequency (approximately 100 Hz). Using voltage imaging, we show that single APs undergo significant attenuation as they propagate into basal dendrites, whereas AP bursts lead to generation of dendritic calcium spikes. Focal and bath application of 4-AP increased the amplitude of calcium transients evoked by APs at distal, but not proximal, locations, suggesting that A-type potassium channels regulate AP backpropagation into basal dendrites. Finally, we show that pairing EPSPs with AP bursts is an effective means of activating synaptic NMDA receptors in basal dendrites. The experimental observations on the role of A-type potassium channels in regulation of AP backpropagation in basal dendrites, as well as the generation of dendritic calcium spikes during AP bursts, were reproduced in a morphologically realistic neuronal model with uniform distributions of dendritic sodium, calcium, and potassium channels. Together, these findings have important implications for understanding dendritic integration and synaptic plasticity in cortical basal dendrites.

Action Potentials↗
PubMed2001

Cell-type specific dendritic contacts between retinal ganglion cells during development.

The extent of a neuron's dendritic field defines the region within which information is processed. The dendritic fields of functionally distinct ON and OFF center retinal ganglion cells (RGCs) form separate mosaics across the retina. Within each mosaic, neighboring dendritic fields overlap by a constant amount, sampling the visual field with the appropriate coverage. Contact-mediated lateral inhibition between neighboring RGCs has long been thought to regulate both the extent and overlap of dendritic fields during development. Here we show that dendro-dendritic contact exists between developing RGCs and occurs in a manner that would regulate the formation of ON and OFF mosaics separately. Dye-filled neighboring ON and OFF ferret alpha RGCs were reconstructed using multiphoton microscopy. At all neonatal ages examined, we observed dendro-dendritic contacts between RGCs of the same sign (ON/ON; OFF/OFF), but never between cells of opposite signs (ON/OFF). Terminal dendrites of one cell often touched a dendrite of its neighbor as they intersected. In some instances, the distal dendrite of one cell formed a fascicle with the proximal process of its neighbor. Alpha cells did not form contacts with neighboring beta cells of the same sign. Together, these observations suggest that dendro-dendritic contact between RGCs is cell-type specific. Dendritic contacts were observed even before the alpha cell arbors were completely stratified, suggesting that cell-cell recognition may take place early in their development. For each cell type, the relative overlap of dendritic fields was constant with age, despite a two-fold increase in field area. We suggest that dendro-dendritic contacts may be sites of intercellular signaling that could regulate local extension of dendrites to maintain the relative overlap of RGCs within a mosaic during development.

Animals↗
PubMed1987

Development and regulation of dendrites in the rat superior cervical ganglion.

Intracellular injection of HRP was used to study the postnatal development of dendrites in the rat superior cervical ganglion (SCG). This study had 2 goals: to describe the growth of dendrites during normal development and to determine the influence of preganglionic innervation on dendritic growth. At birth, ganglion cell morphology is relatively simple; cells have few dendritic branches and an average total dendritic length under 300 micron. In the first postnatal month there is a 4-fold increase in dendritic length and a marked increase in the complexity of branching. Dendrites continue to grow into adulthood; at each age studied (up to 16 months old), the dendritic geometries of SCG cells became progressively more extensive and complex. The influence of innervation on the development of dendrites was assessed by cutting the cervical sympathetic trunk (CST) within a day of birth; reinnervation was prevented by ligating and displacing the proximal end of the CST. During the first postnatal month, the cells in denervated ganglia showed an increase in dendritic length indistinguishable from that seen in unoperated control ganglia. The rate of growth after 1 month was somewhat slower in experimental animals than in controls; nevertheless, the dendrites of cells in denervated ganglia showed progressively larger arbors at each time point measured. These results indicate that in the SCG the majority of dendritic growth occurs postnatally, dendrites continue to grow in adult rats, and dendritic growth is largely independent of the presence of preganglionic innervation. The significance of these findings for the regulation of innervation in this part of the nervous system is discussed.

Animals↗
PubMed1985

Isolated follicular dendritic cells: cytochemical antigen localization, Nomarski, SEM, and TEM morphology.

The objectives of the present study were to determine the cytological features of isolated follicular dendritic cells (FDC), which distinguish them from other leukocytes or dendritic cell types. Consequently, we have developed methods for the fixation, peroxidase cytochemistry, and visualization of FDC, which are applicable to cytological evaluations by Nomarski optics, scanning, and transmission electron microscopy. A functionally supported identification of FDC in vitro was made possible by utilizing, in conjunction with the dendritic morphology, the cytochemically identifiable antigen, horseradish peroxidase (HRP), and the known capacity of FDC to sequester immune complexes (i.e. HRP-anti-HRP) on their plasma membranes. The observations showed that FDC constitute a relatively pleomorphic, nonphagocytic group, distinct from other dendritic type cells such as lymphoid dendritic cells, Langerhans cells, and interdigitating cells (LDC, LC, and IDC), as well as typical leukocytes. Morphologically distinct FDC were identified as cells either with filiform dendrites or with "beaded" dendrites. FDC possessed a single or sometimes a double, lymphocyte-size cell body, which contained an irregular, lobated nucleus, Golgi apparatus, numerous small vesicles, and some mitochondria. Mitochondria were not abundant in the dendritic processes. Filiform dendrites tended to branch and anastomose near the cell body and form a radiating "sunburst"-like pattern. On the average, dendrites measured 15-20 microns in length and 0.1-0.3 micron in diameter. Occasional dendrites were extremely elongated, reached several hundred microns in length, and terminated in an enlargement measuring nearly a micron in diameter. Other filiform dendrites usually had a club-shaped terminal enlargement. The microspheres of "beaded" dendrites ranged between 0.3 and 0.6 micron in diameter. The dendritic processes were also shown to have a highly ordered pattern of immune complex attachment on their surface, suggestive of a periodic arrangement of receptor sites.

Animals↗
PubMed1979

A technique for estimating total spine numbers on Golgi-impregnated dendrites.

The functional significance of dendritic spines and their morphological sensitivity to a wide spectrum of experimental manipulations and pathological states have led to a number of studies in which counts of dendritic spine number have been carried out. These studies have, for the most part, involved the enumeration of only those spines which protrude from the opaque shafts of Golgi-impregnated dendrites into the clear zones flanking the dendrite. Such counts, limited to only those spines which are visible, underrepresent the true total number of spines borne by the dendrites. The magnitude of underrepresentation correlates positively with dendritic shaft diameter and negatively with spine length. This seriously restricts the usefulness of comparisons of spine density between dendrites, or even between segments of the same dendrite. In the present report, a geometrically based method is presented whereby total dendritic spine numbers can be estimated with reasonable accuracy, taking into account factors such as dendrite diameter and spine length. The technique entails the following principal steps: a determination, for a given length of dendrite over which spines are to be enumerated, of the volume of the flanking zones in which spines are visible and can be counted; a determination of the volume of the entire zone which encircles the dendritic shaft and which contains all spines, both visible and not visible; and a proportional extrapolation from the number of visible spines to obtain an estimate of the true total spine number. Tests of the predictive accuracy of the technique using dendrites of known total spine number suggest that estimates which deviate from true total spine numbers by less than 10% can be achieved.

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PubMed1981

White-matter dendrites in the upper cervical spinal cord of the adult cat: a light and electron microscopic study.

The organization and structure of dendrites penetrating into the white matter of upper cervical spinal segments have been examined by means of Golgi staining techniques, intracellular horseradish peroxidase (HRP) injections, and ultrastructural studies. The Golgi studies established that several groups of neurons located in intermediate and ventral laminae of the upper cervical spinal cord have a substantial part of their dendritic tree extending into adjacent ventral and lateral funiculi. Most dendrites in white matter showed irregular varicosities along their length. They were devoid of spines and followed relatively direct paths. In contrast, grey matter dendrites were occasionally observed with spines and complex appendages frequently followed tortuous paths. The size and location of some Golgi stained neurons suggested that white matter dendrites might originate from neck muscle motoneurons. This possibility was confirmed using intracellular HRP injections. These studies also showed that the distribution of white matter dendrites of neck muscle motoneurons depended on the location of the motoneuron soma. White matter dendrites of neck muscle motoneurons located deep in the ventral horn projected into all regions of white matter surrounding the ventral horn. Other neck muscle motoneurons, located in the spinal accessory nucleus, had white matter dendrites largely confined to the lateral funiculus. White matter dendrites of motoneurons in the commissural nucleus were found to project across the ventral commissure into the contralateral spinal cord. Light microscopic studies of semi-thin sections stained with toluidine blue and electron microscopic studies of thin sections revealed that white matter dendrites were confined to special regions of the white matter. These regions resembled the grey matter neuropil and contained dendrites and unmyelinated and small diameter myelinated axons. Axon terminals were also found in white matter. These terminals contained either flattened or spherical vesicles and formed synaptic contacts on white matter dendrites. White matter dendrites, by virtue of their frequency of occurrence, distribution, and type of synaptic contacts may represent a means by which descending or ascending spinal systems can influence spinal neurons without recourse to axon collaterals which terminate in grey matter.

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