scholarly journals ASD-Associated De Novo Mutations in Five Actin Regulators Show Both Shared and Distinct Defects in Dendritic Spines and Inhibitory Synapses in Cultured Hippocampal Neurons

2018 ◽  
Vol 12 ◽  
Author(s):  
Iryna Hlushchenko ◽  
Pushpa Khanal ◽  
Amr Abouelezz ◽  
Ville O. Paavilainen ◽  
Pirta Hotulainen
Keyword(s):  
Dendritic Spines ◽  
Hippocampal Neurons ◽  
De Novo ◽  
Inhibitory Synapses ◽  
De Novo Mutations ◽  
Cultured Hippocampal Neurons

scholarly journals Mechanical tension can specify axonal fate in hippocampal neurons

2002 ◽  
Vol 159 (3) ◽  
pp. 499-508 ◽  
Author(s):  
Phillip Lamoureux ◽  
Gordon Ruthel ◽  
Robert E. Buxbaum ◽  
Steven R. Heidemann
Keyword(s):  
Growth Cone ◽  
Hippocampal Neurons ◽  
De Novo ◽  
High Rate ◽  
Neurite Length ◽  
Mechanical Tension ◽  
Spontaneous Growth ◽  
Developmental Course ◽  
Cultured Hippocampal Neurons

Here we asked whether applied mechanical tension would stimulate undifferentiated minor processes of cultured hippocampal neurons to become axons and whether tension could induce a second axon in an already polarized neuron. Experimental tension applied to minor processes produced extensions that demonstrated axonal character, regardless of the presence of an existing axon. Towed neurites showed a high rate of spontaneous growth cone advance and could continue to grow out for 1–3 d after towing. The developmental course of experimental neurites was found to be similar to that of unmanipulated spontaneous axons. Furthermore, the experimentally elongated neurites showed compartmentation of the axonal markers dephospho-tau and L-1 in towed outgrowth after 24 h. Extension of a second axon from an already polarized neuron does not lead to the loss of the spontaneous axon either immediately or after longer term growth. In addition, we were able to initiate neurites de novo that subsequently acquired axonal character even though spontaneous growth cone advance began while the towed neurite was still no longer than its sibling processes. This suggests that tension rather than the achievement of a critical neurite length determined axonal specification.

scholarly journals Neuroligins/LRRTMs prevent activity- and Ca2+/calmodulin-dependent synapse elimination in cultured neurons

2011 ◽  
Vol 194 (2) ◽  
pp. 323-334 ◽  
Author(s):  
Jaewon Ko ◽  
Gilberto J. Soler-Llavina ◽  
Marc V. Fuccillo ◽  
Robert C. Malenka ◽  
Thomas C. Südhof
Keyword(s):  
Hippocampal Neurons ◽  
Transmembrane Proteins ◽  
Synaptic Activity ◽  
Inhibitory Synapses ◽  
Excitatory Synapses ◽  
Synapse Elimination ◽  
Synapse Loss ◽  
A Cell ◽  
Dependent Signaling Pathway ◽  
Cultured Hippocampal Neurons

Neuroligins (NLs) and leucine-rich repeat transmembrane proteins (LRRTMs) are postsynaptic cell adhesion molecules that bind to presynaptic neurexins. In this paper, we show that short hairpin ribonucleic acid–mediated knockdowns (KDs) of LRRTM1, LRRTM2, and/or NL-3, alone or together as double or triple KDs (TKDs) in cultured hippocampal neurons, did not decrease synapse numbers. In neurons cultured from NL-1 knockout mice, however, TKD of LRRTMs and NL-3 induced an ∼40% loss of excitatory but not inhibitory synapses. Strikingly, synapse loss triggered by the LRRTM/NL deficiency was abrogated by chronic blockade of synaptic activity as well as by chronic inhibition of Ca2+ influx or Ca2+/calmodulin (CaM) kinases. Furthermore, postsynaptic KD of CaM prevented synapse loss in a cell-autonomous manner, an effect that was reversed by CaM rescue. Our results suggest that two neurexin ligands, LRRTMs and NLs, act redundantly to maintain excitatory synapses and that synapse elimination caused by the absence of NLs and LRRTMs is promoted by synaptic activity and mediated by a postsynaptic Ca2+/CaM-dependent signaling pathway.

Change in the shape and density of dendritic spines caused by overexpression of acidic calponin in cultured hippocampal neurons

Hippocampus ◽  
2006 ◽  
Vol 16 (2) ◽  
pp. 183-197 ◽  
Author(s):  
Guillaume Rami ◽  
Olivier Caillard ◽  
Igor Medina ◽  
Christophe Pellegrino ◽  
Abdellatif Fattoum ◽  
...  
Keyword(s):  
Dendritic Spines ◽  
Hippocampal Neurons ◽  
Cultured Hippocampal Neurons

scholarly journals Overexpression of Tropomyosin Isoform Tpm3.1 Does Not Alter Synaptic Function in Hippocampal Neurons

2021 ◽  
Vol 22 (17) ◽  
pp. 9303
Author(s):  
Chanchanok Chaichim ◽  
Tamara Tomanic ◽  
Holly Stefen ◽  
Esmeralda Paric ◽  
Lucy Gamaroff ◽  
...  
Keyword(s):  
Dendritic Spines ◽  
Hippocampal Neurons ◽  
Brain Slices ◽  
Structure And Function ◽  
Spine Morphology ◽  
Dendritic Spine Morphology ◽  
And Function ◽  
Cultured Hippocampal Neurons

Tropomyosin (Tpm) has been regarded as the master regulator of actin dynamics. Tpms regulate the binding of the various proteins involved in restructuring actin. The actin cytoskeleton is the predominant cytoskeletal structure in dendritic spines. Its regulation is critical for spine formation and long-term activity-dependent changes in synaptic strength. The Tpm isoform Tpm3.1 is enriched in dendritic spines, but its role in regulating the synapse structure and function is not known. To determine the role of Tpm3.1, we studied the synapse structure and function of cultured hippocampal neurons from transgenic mice overexpressing Tpm3.1. We recorded hippocampal field excitatory postsynaptic potentials (fEPSPs) from brain slices to examine if Tpm3.1 overexpression alters long-term synaptic plasticity. Tpm3.1-overexpressing cultured neurons did not show a significantly altered dendritic spine morphology or synaptic activity. Similarly, we did not observe altered synaptic transmission or plasticity in brain slices. Furthermore, expression of Tpm3.1 at the postsynaptic compartment does not increase the local F-actin levels. The results suggest that although Tpm3.1 localises to dendritic spines in cultured hippocampal neurons, it does not have any apparent impact on dendritic spine morphology or function. This is contrary to the functional role of Tpm3.1 previously observed at the tip of growing neurites, where it increases the F-actin levels and impacts growth cone dynamics.

Fast imaging of [Ca]i reveals presence of voltage-gated calcium channels in dendritic spines of cultured hippocampal neurons

1995 ◽  
Vol 74 (1) ◽  
pp. 484-488 ◽  
Author(s):  
M. Segal
Keyword(s):  
Calcium Channels ◽  
Dendritic Spines ◽  
Hippocampal Neurons ◽  
Numerical Aperture ◽  
Ccd Camera ◽  
Charge Coupled Device ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Calcium Indicator ◽  
Cultured Hippocampal Neurons

1. Cultured hippocampal neurons were recorded with a patch pipette containing 100 microM of the calcium indicator Fluo-3, and one of their dendrites, carrying dendritic spines, was visualized with a x100, 1.3-numerical aperture oil objective. Calcium spikes evoked by depolarizing the somata and changes in free dendrite and spine calcium concentrations ([Ca]d and [Ca]s, respectively) were monitored with a cooled charge-coupled device (CCD) camera, acquiring images at a rate of 17-20 ms per frame. In the majority of spine-dendrite pairs, [Ca]s rose faster and to a higher level than the adjacent [Ca]d. Likewise, topical application of glutamate evoked a faster and larger change in [Ca]s than in [Ca]d. The rise of intracellular calcium concentration in response to a depolarizing current pulse, but not in response to glutamate, was reduced in the presence of the calcium antagonist verapamil in both dendrites and spines. It is suggested that dendritic spines possess voltage-gated calcium channels.

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