scholarly journals Functional changes in piriform cortex pyramidal neurons in the chronic methamphetamine-treated rat

2015 ◽  
Vol 34 (01) ◽  
pp. 5-12 ◽  
Author(s):  
Nobuaki Hori ◽  
Tomoko Kadota ◽  
Norio Akaike
Keyword(s):  
Pyramidal Neurons ◽  
Piriform Cortex ◽  
Functional Changes

scholarly journals Disruption of Circadian Rhythms by Ambient Light during Neurodevelopment Leads to Autistic-like Molecular and Behavioral Alterations in Adult Mice

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3314
Author(s):  
Kun Fang ◽  
Dong Liu ◽  
Salil S. Pathak ◽  
Bowen Yang ◽  
Jin Li ◽  
...  
Keyword(s):  
Circadian Rhythms ◽  
Translational Control ◽  
Pyramidal Neurons ◽  
Critical Role ◽  
Mapk Signaling ◽  
Repetitive Behaviors ◽  
Behavioral Changes ◽  
Circadian Disruption ◽  
Electrophysiological Recording ◽  
Functional Changes

Although circadian rhythms are thought to be essential for maintaining body health, the effects of chronic circadian disruption during neurodevelopment remain elusive. Here, using the “Short Day” (SD) mouse model, in which an 8 h/8 h light/dark (LD) cycle was applied from embryonic day 1 to postnatal day 42, we investigated the molecular and behavioral changes after circadian disruption in mice. Adult SD mice fully entrained to the 8 h/8 h LD cycle, and the circadian oscillations of the clock proteins, PERIOD1 and PERIOD2, were disrupted in the suprachiasmatic nucleus and the hippocampus of these mice. By RNA-seq widespread changes were identified in the hippocampal transcriptome, which are functionally associated with neurodevelopment, translational control, and autism. By western blotting and immunostaining hyperactivation of the mTOR and MAPK signaling pathways and enhanced global protein synthesis were found in the hippocampi of SD mice. Electrophysiological recording uncovered enhanced excitatory, but attenuated inhibitory, synaptic transmission in the hippocampal CA1 pyramidal neurons. These functional changes at synapses were corroborated by the immature morphology of the dendritic spines in these neurons. Lastly, autistic-like animal behavioral changes, including impaired social interaction and communication, increased repetitive behaviors, and impaired novel object recognition and location memory, were found in SD mice. Together, these results demonstrate molecular, cellular, and behavioral changes in SD mice, all of which resemble autistic-like phenotypes caused by circadian rhythm disruption. The findings highlight a critical role for circadian rhythms in neurodevelopment.

scholarly journals Heterogeneous CaMKII-dependent synaptic compensations in CA1 pyramidal neurons from acute slices with dissected CA3

2021 ◽  
Author(s):  
Pablo Vergara ◽  
Gabriela Pino ◽  
Jorge Vera ◽  
Magdalena Sanhueza
Keyword(s):  
Pyramidal Neurons ◽  
Sensory Deprivation ◽  
Hippocampal Slices ◽  
Suitable Model ◽  
Functional Changes ◽  
Genetic Manipulations ◽  
Ca1 Pyramidal Neurons ◽  
Specific Frequency ◽  
Acute Hippocampal Slices ◽  
Underlying Mechanisms

Prolonged changes in neural activity trigger homeostatic synaptic plasticity (HSP) allowing neuronal networks to operate in functional ranges. Cell-wide or input-specific adaptations can be induced by pharmacological or genetic manipulations of activity, and by sensory deprivation. Reactive functional changes caused by deafferentation may partially share mechanisms with HSP. Acute hippocampal slices constitute a suitable model to investigate relatively rapid (hours) pathway-specific modifications occurring after denervation and explore the underlying mechanisms. As Schaffer collaterals constitute a major glutamatergic input to CA1 pyramidal neurons, we conducted whole-cell recordings of miniature excitatory postsynaptic currents (mEPSCs) to evaluate changes over 12 hours after slice preparation and CA3 dissection. We observed an increment in mEPSCs amplitude and a decrease in decay time, suggesting synaptic AMPA receptor upregulation and subunit content modifications. Sorting mEPSC by rise time, a correlate of synapse location along dendrites, revealed amplitude raises at two separate domains. A specific frequency increase was observed in the same domains and was accompanied by a global, unspecific raise. Amplitude and frequency increments were lower at sites initially more active, consistent with local compensatory processes. Transient preincubation with a specific Ca2+/calmodulin-dependent kinase II (CaMKII) inhibitor either blocked or occluded amplitude and frequency upregulation in different synapse populations. Results are consistent with the concurrent development of different known CaMKII-dependent HSP processes. Our observations support that deafferentation causes rapid and diverse compensations resembling classical slow forms of adaptation to inactivity. These results may contribute to understand fast-developing homeostatic or pathological events after brain injury.

Learning-Induced Reversal of the Effect of Noradrenalin on the Postburst AHP

2006 ◽  
Vol 96 (4) ◽  
pp. 1728-1733 ◽  
Author(s):  
Inbar Brosh ◽  
Kobi Rosenblum ◽  
Edi Barkai
Keyword(s):  
Potassium Current ◽  
Neuronal Excitability ◽  
Pyramidal Neurons ◽  
Piriform Cortex ◽  
Sk Channels ◽  
Similar Extent ◽  
Protein Expression Level ◽  
Calcium Dependent ◽  
The Difference ◽  
Small Conductance

Pyramidal neurons in the piriform cortex from olfactory-discrimination–trained rats have reduced postburst afterhyperpolarization (AHP), for 3 days after learning, and are thus more excitable during this period. Such AHP reduction is caused by decreased conductance of one or more of the calcium-dependent potassium currents, IAHP and s IAHP, that mediate the medium and slow AHPs. In this study, we examined which potassium current is reduced by learning and how the effect of noradrenalin (NE) on neuronal excitability is modified by such reduction. The small conductance (SK) channels inhibitor, apamin, that selectively blocks IAHP, reduced the AHP in neurons from trained, naïve, and pseudotrained rats to a similar extent, thus maintaining the difference in AHP amplitude between neurons from trained rats and controls. In addition, the protein expression level of the SK1, SK2, and SK3 channels was also similar in all groups. NE, which was shown to enhance IAHP while suppressing S IAHP, reduced the AHP in neurons from controls but enhanced the AHP in neurons from trained rats. Our data show that learning-induced enhancement of neuronal excitability is not the result of reduction in the IAHP current. Thus it is probably mediated by reduction in conductance of the other calcium-dependent potassium current, s IAHP. Consequently, the effect of NE on neuronal excitability is reversed. We propose that the change in the effect of NE after learning may act to counterbalance learning-induced hyperexcitability and preserve the piriform cortex ability to subserve olfactory learning.

Cell assembly formation and structure in a piriform cortex model

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Roger D. Traub ◽  
Yuhai Tu ◽  
Miles A. Whittington
Keyword(s):  
Action Potentials ◽  
Pyramidal Neurons ◽  
Piriform Cortex ◽  
Lateral Olfactory Tract ◽  
Firing Patterns ◽  
Anterior Piriform Cortex ◽  
Recurrent Excitation ◽  
Cortical Responses ◽  
Spike Patterns ◽  
Cell Networks

Abstract The piriform cortex is rich in recurrent excitatory synaptic connections between pyramidal neurons. We asked how such connections could shape cortical responses to olfactory lateral olfactory tract (LOT) inputs. For this, we constructed a computational network model of anterior piriform cortex with 2000 multicompartment, multiconductance neurons (500 semilunar, 1000 layer 2 and 500 layer 3 pyramids; 200 superficial interneurons of two types; 500 deep interneurons of three types; 500 LOT afferents), incorporating published and unpublished data. With a given distribution of LOT firing patterns, and increasing the strength of recurrent excitation, a small number of firing patterns were observed in pyramidal cell networks: first, sparse firings; then temporally and spatially concentrated epochs of action potentials, wherein each neuron fires one or two spikes; then more synchronized events, associated with bursts of action potentials in some pyramidal neurons. We suggest that one function of anterior piriform cortex is to transform ongoing streams of input spikes into temporally focused spike patterns, called here “cell assemblies”, that are salient for downstream projection areas.

scholarly journals Nucleolar PARP-1 Expression Is Decreased in Alzheimer’s Disease: Consequences for Epigenetic Regulation of rDNA and Cognition

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Jianying Zeng ◽  
Jenny Libien ◽  
Fatima Shaik ◽  
Jason Wolk ◽  
A. Iván Hernández
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Pyramidal Neurons ◽  
Pyramidal Cells ◽  
Hippocampal Pyramidal Neurons ◽  
Functional Changes ◽  
Epigenetic Regulator ◽  
Parp 1 ◽  
Sensitive Marker ◽  
Hippocampal Pyramidal Cells

Synaptic dysfunction is thought to play a major role in memory impairment in Alzheimer’s disease (AD). PARP-1 has been identified as an epigenetic regulator of plasticity and memory. Thus, we hypothesize that PARP-1 may be altered in postmortem hippocampus of individuals with AD compared to age-matched controls without neurologic disease. We found a reduced level of PARP-1 nucleolar immunohistochemical staining in hippocampal pyramidal cells in AD. Nucleolar PARP-1 staining ranged from dispersed and less intense to entirely absent in AD compared to the distinct nucleolar localization in hippocampal pyramidal neurons in controls. In cases of AD, the percentage of hippocampal pyramidal cells with nucleoli that were positive for both PARP-1 and the nucleolar marker fibrillarin was significantly lower than in controls. PARP-1 nucleolar expression emerges as a sensitive marker of functional changes in AD and suggests a novel role for PARP-1 dysregulation in AD pathology.

Specific expression of the chicken δ-crystallin gene in the lens and the pyramidal neurons of the piriform cortex in transgenic mice

1987 ◽  
Vol 120 (1) ◽  
pp. 177-185 ◽  
Author(s):  
Hisato Kondoh ◽  
Kazuto Katoh ◽  
Yoshiko Takahashi ◽  
Hajime Fujisawa ◽  
Minesuke Yokoyama ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Pyramidal Neurons ◽  
Piriform Cortex ◽  
Specific Expression

scholarly journals DM1 Transgenic Mice Exhibit Abnormal Neurotransmitter Homeostasis and Synaptic Plasticity in Association with RNA Foci and Mis-Splicing in the Hippocampus

2022 ◽  
Vol 23 (2) ◽  
pp. 592
Author(s):  
Brigitte Potier ◽  
Louison Lallemant ◽  
Sandrine Parrot ◽  
Aline Huguet-Lachon ◽  
Geneviève Gourdon ◽  
...  
Keyword(s):  
Time Course ◽  
Pyramidal Neurons ◽  
Granule Cells ◽  
Glutamate Uptake ◽  
Hippocampal Slices ◽  
Synaptic Cleft ◽  
Synaptic Dysfunction ◽  
Functional Changes ◽  
Rna Foci ◽  
The Impact

Myotonic dystrophy type 1 (DM1) is a severe neuromuscular disease mediated by a toxic gain of function of mutant RNAs. The neuropsychological manifestations affect multiple domains of cognition and behavior, but their etiology remains elusive. Transgenic DMSXL mice carry the DM1 mutation, show behavioral abnormalities, and express low levels of GLT1, a critical regulator of glutamate concentration in the synaptic cleft. However, the impact of glutamate homeostasis on neurotransmission in DM1 remains unknown. We confirmed reduced glutamate uptake in the DMSXL hippocampus. Patch clamp recordings in hippocampal slices revealed increased amplitude of tonic glutamate currents in DMSXL CA1 pyramidal neurons and DG granule cells, likely mediated by higher levels of ambient glutamate. Unexpectedly, extracellular GABA levels and tonic current were also elevated in DMSXL mice. Finally, we found evidence of synaptic dysfunction in DMSXL mice, suggestive of abnormal short-term plasticity, illustrated by an altered LTP time course in DG and in CA1. Synaptic dysfunction was accompanied by RNA foci accumulation in localized areas of the hippocampus and by the mis-splicing of candidate genes with relevant functions in neurotransmission. Molecular and functional changes triggered by toxic RNA may induce synaptic abnormalities in restricted brain areas that favor neuronal dysfunction.

scholarly journals Transient developmental increase of prefrontal activity alters network maturation and causes cognitive dysfunction in adult mice

2019 ◽  
Author(s):  
Sebastian H. Bitzenhofer ◽  
Jastyn A. Pöpplau ◽  
Mattia Chini ◽  
Annette Marquardt ◽  
Ileana L. Hanganu-Opatz
Keyword(s):  
Early Development ◽  
Pyramidal Neurons ◽  
Synapse Formation ◽  
Functional Changes ◽  
Gamma Frequency ◽  
Adult Mice ◽  
Neuropsychiatric Diseases ◽  
Social Abilities ◽  
Inhibitory Feedback ◽  
And Behavior

AbstractDisturbed neuronal activity in neuropsychiatric pathologies emerges during development and might cause multifold neuronal dysfunction by interfering with apoptosis, dendritic growth and synapse formation. However, how altered electrical activity early in life impacts neuronal function and behavior of adults is unknown. Here, we address this question by transiently increasing the coordinated activity of layer 2/3 pyramidal neurons in the medial prefrontal cortex of neonatal mice and monitoring long-term functional and behavioral consequences. We show that increased activity during early development causes premature maturation of pyramidal neurons and alters interneuron density. Consequently, reduced inhibitory feedback by fast-spiking interneurons and excitation/inhibition imbalance in prefrontal circuits of young adults result in weaker evoked synchronization in gamma frequency. These structural and functional changes ultimately lead to poorer mnemonic and social abilities. Thus, prefrontal activity during early development actively controls the cognitive performance of adults and might be critical for cognitive symptoms of neuropsychiatric diseases.

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