Quantitative analysis of dendritic spines of pyramidal neurons in layer V of the sensomotor cortex of rats exposed on the ?Kosmos-1667? biosatellite

1988 ◽  
Vol 105 (6) ◽  
pp. 876-878 ◽  
Author(s):  
P. V. Belichenko
Keyword(s):  
Quantitative Analysis ◽  
Dendritic Spines ◽  
Pyramidal Neurons ◽  
Sensomotor Cortex ◽  
Layer V

Plastic changes to dendritic spines on layer V pyramidal neurons are involved in the rectifying role of the prefrontal cortex during the fast period of motor learning

2016 ◽  
Vol 298 ◽  
pp. 261-267 ◽  
Author(s):  
David González-Tapia ◽  
Nestor I. Martínez-Torres ◽  
Marisela Hernández-González ◽  
Miguel Angel Guevara ◽  
Ignacio González-Burgos
Keyword(s):  
Prefrontal Cortex ◽  
Motor Learning ◽  
Dendritic Spines ◽  
Pyramidal Neurons ◽  
Plastic Changes ◽  
Layer V

scholarly journals Fear extinction reverses dendritic spine formation induced by fear conditioning in the mouse auditory cortex

2018 ◽  
Vol 115 (37) ◽  
pp. 9306-9311 ◽  
Author(s):  
Cora Sau Wan Lai ◽  
Avital Adler ◽  
Wen-Biao Gan
Keyword(s):  
Auditory Cortex ◽  
Fear Conditioning ◽  
Dendritic Spines ◽  
Dendritic Spine ◽  
Pyramidal Neurons ◽  
Fear Extinction ◽  
Spine Formation ◽  
Synaptic Circuits ◽  
Auditory Cue ◽  
Layer V

Fear conditioning-induced behavioral responses can be extinguished after fear extinction. While fear extinction is generally thought to be a form of new learning, several lines of evidence suggest that neuronal changes associated with fear conditioning could be reversed after fear extinction. To better understand how fear conditioning and extinction modify synaptic circuits, we examined changes of postsynaptic dendritic spines of layer V pyramidal neurons in the mouse auditory cortex over time using transcranial two-photon microscopy. We found that auditory-cued fear conditioning induced the formation of new dendritic spines within 2 days. The survived new spines induced by fear conditioning with one auditory cue were clustered within dendritic branch segments and spatially segregated from new spines induced by fear conditioning with a different auditory cue. Importantly, fear extinction preferentially caused the elimination of newly formed spines induced by fear conditioning in an auditory cue-specific manner. Furthermore, after fear extinction, fear reconditioning induced reformation of new dendritic spines in close proximity to the sites of new spine formation induced by previous fear conditioning. These results show that fear conditioning, extinction, and reconditioning induce cue- and location-specific dendritic spine remodeling in the auditory cortex. They also suggest that changes of synaptic connections induced by fear conditioning are reversed after fear extinction.

Nicotinic activity depresses synaptic potentiation in layer V pyramidal neurons of mouse insular cortex

Neuroscience ◽  
2017 ◽  
Vol 358 ◽  
pp. 13-27 ◽  
Author(s):  
Hajime Sato ◽  
Tsutomu Kawano ◽  
Dong Xu Yin ◽  
Takafumi Kato ◽  
Hiroki Toyoda
Keyword(s):  
Pyramidal Neurons ◽  
Insular Cortex ◽  
Synaptic Potentiation ◽  
Layer V

Dendritic changes of the pyramidal neurons in layer V of sensory-motor cortex of the rat brain during the postresuscitation period

Resuscitation ◽  
1997 ◽  
Vol 35 (2) ◽  
pp. 157-164 ◽  
Author(s):  
Victor A Akulinin ◽  
Sergey S Stepanov ◽  
Valeriy V Semchenko ◽  
Pavel V Belichenko
Keyword(s):  
Motor Cortex ◽  
Rat Brain ◽  
Pyramidal Neurons ◽  
Postresuscitation Period ◽  
Sensory Motor ◽  
Layer V

scholarly journals Sex-dependent role for EPHB2 in brain development and autism-associated behavior

2021 ◽  
Author(s):  
Ahlem Assali ◽  
Jennifer Y. Cho ◽  
Evgeny Tsvetkov ◽  
Abha R. Gupta ◽  
Christopher W. Cowan
Keyword(s):  
Pyramidal Neurons ◽  
De Novo ◽  
Repetitive Behavior ◽  
Autism Spectrum ◽  
Repetitive Behaviors ◽  
Male Mice ◽  
Sensory Sensitivity ◽  
Hyperactivity Disorder ◽  
Specific Effects ◽  
Layer V

AbstractAutism spectrum disorder (ASD) is characterized by impairments in social communication and interaction and restricted, repetitive behaviors. It is frequently associated with comorbidities, such as attention-deficit hyperactivity disorder, altered sensory sensitivity, and intellectual disability. A de novo nonsense mutation in EPHB2 (Q857X) was discovered in a female patient with ASD [13], revealing EPHB2 as a candidate ASD risk gene. EPHB2 is a receptor tyrosine kinase implicated in axon guidance, synaptogenesis, and synaptic plasticity, positioning it as a plausible contributor to the pathophysiology of ASD and related disorders. In this study, we show that the Q857X mutation produced a truncated protein lacking forward signaling and that global disruption of one EphB2 allele (EphB2+/−) in mice produced several behavioral phenotypes reminiscent of ASD and common associated symptoms. EphB2+/− female, but not male, mice displayed increased repetitive behavior, motor hyperactivity, and learning and memory deficits, revealing sex-specific effects of EPHB2 hypofunction. Moreover, we observed a significant increase in the intrinsic excitability, but not excitatory/inhibitory ratio, of motor cortex layer V pyramidal neurons in EphB2+/− female, but not male, mice, suggesting a possible mechanism by which EPHB2 hypofunction may contribute to sex-specific motor-related phenotypes. Together, our findings suggest that EPHB2 hypofunction, particularly in females, is sufficient to produce ASD-associated behaviors and altered cortical functions in mice.

Stimulation of 5-HT2 Receptors in Prefrontal Pyramidal Neurons Inhibits Cav1.2 L-Type Ca2+Currents Via a PLCβ/IP3/Calcineurin Signaling Cascade

2002 ◽  
Vol 87 (5) ◽  
pp. 2490-2504 ◽  
Author(s):  
Michelle Day ◽  
Patricia A. Olson ◽  
Josef Platzer ◽  
Joerg Striessnig ◽  
D. James Surmeier
Keyword(s):  
Pyramidal Neurons ◽  
Inositol Trisphosphate ◽  
Cell Voltage ◽  
Signaling Cascade ◽  
Channel Modulation ◽  
Receptor Modulation ◽  
Bath Application ◽  
Voltage Dependent ◽  
Intracellular Ca ◽  
Layer V

There is growing evidence linking alterations in serotonergic signaling in the prefrontal cortex to the etiology of schizophrenia. Prefrontal pyramidal neurons are richly innervated by serotonergic fibers and express high levels of serotonergic 5-HT2-class receptors. It is unclear, however, how activation of these receptors modulates cellular activity. To help fill this gap, whole cell voltage-clamp and single-cell RT-PCR studies of acutely isolated layer V–VI prefrontal pyramidal neurons were undertaken. The vast majority (>80%) of these neurons had detectable levels of 5-HT2A or 5-HT2C receptor mRNA. Bath application of 5-HT2 agonists inhibited voltage-dependent Ca2+ channel currents. L-type Ca2+ channels were a particularly prominent target of this signaling pathway. The L-type channel modulation was blocked by disruption of Gαq signaling or by inhibition of phospholipase Cβ. Antagonism of intracellular inositol trisphosphate signaling, chelation of intracellular Ca2+, or depletion of intracellular Ca2+ stores also blocked this modulation. Inhibition of the Ca2+-dependent phosphatase calcineurin prevented receptor-mediated modulation of L-type currents. Last, the 5-HT2 receptor modulation was robustly expressed in neurons from Cav1.3 knockout mice. These findings argue that 5-HT2receptors couple through Gαq proteins to trigger a phospholipase Cβ/inositol trisphosphate signaling cascade resulting in the mobilization of intracellular Ca2+, activation of calcineurin, and inhibition of Cav1.2 L-type Ca2+currents. This modulation and its blockade by atypical neuroleptics could have wide-ranging effects on synaptic integration and long-term gene expression in deep-layer prefrontal pyramidal neurons.

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