scholarly journals Mapping Function Onto Neuronal Morphology

2007 ◽  
Vol 98 (1) ◽  
pp. 513-526 ◽  
Author(s):  
Klaus M. Stiefel ◽  
Terrence J. Sejnowski
Keyword(s):  
Pyramidal Neurons ◽  
Morphological Structure ◽  
Mapping Function ◽  
Optimization Procedure ◽  
Neuronal Morphology ◽  
Neuronal Function ◽  
Automated Mapping ◽  
Wide Range ◽  
Cortical Pyramidal Neurons ◽  
Apical Dendrites

Neurons have a wide range of dendritic morphologies the functions of which are largely unknown. We used an optimization procedure to find neuronal morphological structures for two computational tasks: first, neuronal morphologies were selected for linearly summing excitatory synaptic potentials (EPSPs); second, structures were selected that distinguished the temporal order of EPSPs. The solutions resembled the morphology of real neurons. In particular the neurons optimized for linear summation electrotonically separated their synapses, as found in avian nucleus laminaris neurons, and neurons optimized for spike-order detection had primary dendrites of significantly different diameter, as found in the basal and apical dendrites of cortical pyramidal neurons. This similarity makes an experimentally testable prediction of our theoretical approach, which is that pyramidal neurons can act as spike-order detectors for basal and apical inputs. The automated mapping between neuronal function and structure introduced here could allow a large catalog of computational functions to be built indexed by morphological structure.

Mechanisms Underlying Burst and Regular Spiking Evoked by Dendritic Depolarization in Layer 5 Cortical Pyramidal Neurons

1999 ◽  
Vol 81 (3) ◽  
pp. 1341-1354 ◽  
Author(s):  
Peter Schwindt ◽  
Wayne Crill
Keyword(s):  
Action Potentials ◽  
Pyramidal Neurons ◽  
Critical Level ◽  
Pyramidal Cells ◽  
Burst Firing ◽  
Action Current ◽  
Constant Frequency ◽  
Functional Implications ◽  
Cortical Pyramidal Neurons ◽  
Apical Dendrites

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.

Glutamate Receptors Form Hot Spots on Apical Dendrites of Neocortical Pyramidal Neurons

2001 ◽  
Vol 86 (3) ◽  
pp. 1412-1421 ◽  
Author(s):  
A. Frick ◽  
W. Zieglgänsberger ◽  
H.-U. Dodt
Keyword(s):  
Glutamate Receptors ◽  
Hot Spots ◽  
Pyramidal Neurons ◽  
Flash Photolysis ◽  
Apical Dendrite ◽  
Brain Regions ◽  
Branch Points ◽  
Cortical Pyramidal Neurons ◽  
Layer V ◽  
Apical Dendrites

Apical dendrites of layer V cortical pyramidal neurons are a major target for glutamatergic synaptic inputs from cortical and subcortical brain regions. Because innervation from these regions is somewhat laminar along the dendrites, knowing the distribution of glutamate receptors on the apical dendrites is of prime importance for understanding the function of neural circuits in the neocortex. To examine this issue, we used infrared-guided laser stimulation combined with whole cell recordings to quantify the spatial distribution of glutamate receptors along the apical dendrites of layer V pyramidal neurons. Focally applied (<10 μm) flash photolysis of caged glutamate on the soma and along the apical dendrite revealed a highly nonuniform distribution of glutamate responsivity. Up to four membrane areas (extent 22 μm) of enhanced glutamate responsivity (hot spots) were detected on the dendrites with the amplitude and integral of glutamate-evoked responses at hot spots being three times larger than responses evoked at neighboring sites. We found no association of these physiological hot spots with dendritic branch points. It appeared that the larger responses evoked at hot spots resulted from an increase in activation of both α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-d-aspartate (NMDA) receptors and not a recruitment of voltage-activated sodium or calcium conductances. Stimulation of hot spots did, however, facilitate the triggering of both Na+ spikes and Ca2+ spikes, suggesting that hot spots may serve as dendritic initiation zones for regenerative spikes.

Differential Cholinergic Modulation of Ca2+ Transients Evoked by Backpropagating Action Potentials in Apical and Basal Dendrites of Cortical Pyramidal Neurons

2008 ◽  
Vol 99 (6) ◽  
pp. 2833-2843 ◽  
Author(s):  
Kwang-Hyun Cho ◽  
Hyun-Jong Jang ◽  
Eun-Hui Lee ◽  
Shin Hee Yoon ◽  
Sang June Hahn ◽  
...  
Keyword(s):  
High Frequency ◽  
Action Potentials ◽  
Pyramidal Neurons ◽  
Channel Blocker ◽  
Dependent Manner ◽  
Type K ◽  
Basal Dendrites ◽  
Cortical Pyramidal Neurons ◽  
Apical Dendrites ◽  
Whole Cell Recordings

The effect of the cholinergic agonist carbachol (CCh) on backpropagating action potential (bAP)–evoked Ca2+ transients in distal apical and basal dendrites of layer 2/3 pyramidal neurons in the primary visual cortex of rats was studied using whole cell recordings and confocal Ca2+ imaging. In the presence of CCh (20 μM), initial bAP-evoked Ca2+ transients were followed by large propagating secondary Ca2+ transients that were restricted to proximal apical dendrites ≤40 μm from the soma. In middle apical dendrites (41–100 μm from the soma), Ca2+ transients evoked by AP bursts at 20 Hz, but not by single APs, were increased by CCh without secondary transients. CCh failed to increase the bAP-evoked Ca2+ transients in distal apical dendrites (101–270 μm from the soma). In contrast, in basal dendrites, CCh increased Ca2+ transients evoked by AP bursts, but not by single APs, and these transients were relatively constant over the entire length of the dendrites. CCh further increased the enhanced bAP-evoked Ca2+ transients in the presence of 4-aminopyridine (200 μM), an A-type K+ channel blocker, in basal and apical dendrites, except in distal apical dendrites. CCh increased large Ca2+ transients evoked by high-frequency AP bursts in basal dendrites, but not in distal apical dendrites. CCh-induced increase in Ca2+ transients was mediated by InsP3-dependent Ca2+-induced Ca2+-release. These results suggest that cholinergic stimulation differentially increases the bAP-evoked increase in [Ca2+]i in apical and basal dendrites, which may modulate synaptic activities in a location-dependent manner.

scholarly journals Branch specific and spike-order specific action potential invasion in basal, oblique, and apical dendrites of cortical pyramidal neurons

2014 ◽  
Vol 2 (2) ◽  
pp. 021006 ◽  
Author(s):  
Wen-Liang Zhou ◽  
Shaina M. Short ◽  
Matthew T. Rich ◽  
Katerina D. Oikonomou ◽  
Mandakini B. Singh ◽  
...  
Keyword(s):  
Action Potential ◽  
Pyramidal Neurons ◽  
Cortical Pyramidal Neurons ◽  
Apical Dendrites

scholarly journals Reversal of dendritic phenotypes in 16p11.2 microduplication mouse model neurons by pharmacological targeting of a network hub

2016 ◽  
Vol 113 (30) ◽  
pp. 8520-8525 ◽  
Author(s):  
Katherine D. Blizinsky ◽  
Blanca Diaz-Castro ◽  
Marc P. Forrest ◽  
Britta Schürmann ◽  
Anthony P. Bach ◽  
...  
Keyword(s):  
Mental Disorders ◽  
Mouse Model ◽  
Gene Networks ◽  
Pyramidal Neurons ◽  
Genetic Alterations ◽  
Copy Number Variations ◽  
Driver Gene ◽  
Wide Range ◽  
Cortical Pyramidal Neurons ◽  
Cellular Phenotypes

The architecture of dendritic arbors contributes to neuronal connectivity in the brain. Conversely, abnormalities in dendrites have been reported in multiple mental disorders and are thought to contribute to pathogenesis. Rare copy number variations (CNVs) are genetic alterations that are associated with a wide range of mental disorders and are highly penetrant. The 16p11.2 microduplication is one of the CNVs most strongly associated with schizophrenia and autism, spanning multiple genes possibly involved in synaptic neurotransmission. However, disease-relevant cellular phenotypes of 16p11.2 microduplication and the driver gene(s) remain to be identified. We found increased dendritic arborization in isolated cortical pyramidal neurons from a mouse model of 16p11.2 duplication (dp/+). Network analysis identified MAPK3, which encodes ERK1 MAP kinase, as the most topologically important hub in protein–protein interaction networks within the 16p11.2 region and broader gene networks of schizophrenia-associated CNVs. Pharmacological targeting of ERK reversed dendritic alterations associated with dp/+ neurons, outlining a strategy for the analysis and reversal of cellular phenotypes in CNV-related psychiatric disorders.

scholarly journals The use of viral gene transfer in studies of brainstem noradrenergic and serotonergic neurons

2009 ◽  
Vol 364 (1529) ◽  
pp. 2565-2576 ◽  
Author(s):  
S. Kasparov ◽  
A. G. Teschemacher
Keyword(s):  
Viral Vectors ◽  
Pyramidal Neurons ◽  
Viral Gene ◽  
Volume Transmission ◽  
Neuronal Populations ◽  
Central Neurons ◽  
Wide Range ◽  
Cortical Pyramidal Neurons ◽  
The Brain

In contrast to some other neuronal populations, for example hippocampal or cortical pyramidal neurons, mechanisms of synaptic integration and transmitter release in central neurons that contain noradrenaline (NA) and serotonin (5HT) are not well understood. These cells, crucial for a wide range of autonomic and behavioural processes, have long un-myelinated axons with hundreds of varicosities where transmitters are synthesized and released. Both seem to signal mostly in ‘volume transmission’ mode. Very little is known about the rules that apply to this type of transmission in the brain and the factors that regulate the release of NA and 5HT. We discuss some of our published studies and more recent experiments in which viral vectors were used to investigate the physiology of these neuronal populations. We also focus on currently unresolved issues concerning the mechanism of volume transmission by NA and 5HT in the brain. We suggest that clarifying the role of astroglia in this process could be essential for our understanding of central noradrenergic and 5HT signalling.

scholarly journals Implantable microcoils for intracortical magnetic stimulation

2016 ◽  
Vol 2 (12) ◽  
pp. e1600889 ◽  
Author(s):  
Seung Woo Lee ◽  
Florian Fallegger ◽  
Bernard D. F. Casse ◽  
Shelley I. Fried
Keyword(s):  
Cortical Neurons ◽  
Magnetic Stimulation ◽  
Pyramidal Neurons ◽  
Brain Slices ◽  
Behavioral Responses ◽  
Wide Range ◽  
Cortical Pyramidal Neurons ◽  
Over Time

Neural prostheses that stimulate the neocortex have the potential to treat a wide range of neurological disorders. However, the efficacy of electrode-based implants remains limited, with persistent challenges that include an inability to create precise patterns of neural activity as well as difficulties in maintaining response consistency over time. These problems arise from fundamental limitations of electrodes as well as their susceptibility to implantation and have proven difficult to overcome. Magnetic stimulation can address many of these limitations, but coils small enough to be implanted into the cortex were not thought strong enough to activate neurons. We describe a new microcoil design and demonstrate its effectiveness for both activating cortical neurons and driving behavioral responses. The stimulation of cortical pyramidal neurons in brain slices in vitro was reliable and could be confined to spatially narrow regions (<60 μm). The spatially asymmetric fields arising from the coil helped to avoid the simultaneous activation of passing axons. In vivo implantation was safe and resulted in consistent and predictable behavioral responses. The high permeability of magnetic fields to biological substances may yield another important advantage because it suggests that encapsulation and other adverse effects of implantation will not diminish coil performance over time, as happens to electrodes. These findings suggest that a coil-based implant might be a useful alternative to existing electrode-based devices. The enhanced selectivity of microcoil-based magnetic stimulation will be especially useful for visual prostheses as well as for many brain-computer interface applications that require precise activation of the cortex.

Ectopic HCN4 expression drives mTOR-dependent epilepsy in mice

2020 ◽  
Vol 12 (570) ◽  
pp. eabc1492
Author(s):  
Lawrence S. Hsieh ◽  
John H. Wen ◽  
Lena H. Nguyen ◽  
Longbo Zhang ◽  
Stephanie A. Getz ◽  
...  
Keyword(s):  
Mouse Model ◽  
Pyramidal Neurons ◽  
Focal Cortical Dysplasia ◽  
Repetitive Firing ◽  
Intracellular Camp ◽  
Main Role ◽  
Channel Activity ◽  
Mechanistic Target Of Rapamycin ◽  
Cortical Pyramidal Neurons ◽  
Causative Link

The causative link between focal cortical malformations (FCMs) and epilepsy is well accepted, especially among patients with focal cortical dysplasia type II (FCDII) and tuberous sclerosis complex (TSC). However, the mechanisms underlying seizures remain unclear. Using a mouse model of TSC- and FCDII-associated FCM, we showed that FCM neurons were responsible for seizure activity via their unexpected abnormal expression of the hyperpolarization-activated cyclic nucleotide–gated potassium channel isoform 4 (HCN4), which is normally not present in cortical pyramidal neurons after birth. Increasing intracellular cAMP concentrations, which preferentially affects HCN4 gating relative to the other isoforms, drove repetitive firing of FCM neurons but not control pyramidal neurons. Ectopic HCN4 expression was dependent on the mechanistic target of rapamycin (mTOR), preceded the onset of seizures, and was also found in diseased neurons in tissue resected from patients with TSC and FCDII. Last, blocking HCN4 channel activity in FCM neurons prevented epilepsy in the mouse model. These findings suggest that HCN4 play a main role in seizure and identify a cAMP-dependent seizure mechanism in TSC and FCDII. Furthermore, the unique expression of HCN4 exclusively in FCM neurons suggests that gene therapy targeting HCN4 might be effective in reducing seizures in FCDII or TSC.

scholarly journals Gonadal Hormones Modulate the Dendritic Spine Densities of Primary Cortical Pyramidal Neurons in Adult Female Rat

2009 ◽  
Vol 19 (11) ◽  
pp. 2719-2727 ◽  
Author(s):  
J.-R. Chen ◽  
Y.-T. Yan ◽  
T.-J. Wang ◽  
L.-J. Chen ◽  
Y.-J. Wang ◽  
...  
Keyword(s):  
Adult Female ◽  
Dendritic Spine ◽  
Pyramidal Neurons ◽  
Gonadal Hormones ◽  
Female Rat ◽  
Cortical Pyramidal Neurons
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