scholarly journals A single episode of early-life status epilepticus impacts neonatal ultrasonic vocalization behavior in the Fmr1 knockout mouse

2020 ◽  
Vol 111 ◽  
pp. 107279
Author(s):  
Jessica L. Huebschman ◽  
Samantha L. Hodges ◽  
Conner D. Reynolds ◽  
Suzanne O. Nolan ◽  
Joaquin N. Lugo
2019 ◽  
Vol 157 ◽  
pp. 106193 ◽  
Author(s):  
Samantha L. Hodges ◽  
Conner D. Reynolds ◽  
Suzanne O. Nolan ◽  
Jessica L. Huebschman ◽  
James T. Okoh ◽  
...  

Epilepsia ◽  
2004 ◽  
Vol 45 (1) ◽  
pp. 13-19 ◽  
Author(s):  
Brenda E. Porter ◽  
Margaret Maronski ◽  
Amy R. Brooks-Kayal

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Anish K. Simhal ◽  
Yi Zuo ◽  
Marc M. Perez ◽  
Daniel V. Madison ◽  
Guillermo Sapiro ◽  
...  

Abstract Fragile X Syndrome (FXS), a common inheritable form of intellectual disability, is known to alter neocortical circuits. However, its impact on the diverse synapse types comprising these circuits, or on the involvement of astrocytes, is not well known. We used immunofluorescent array tomography to quantify different synaptic populations and their association with astrocytes in layers 1 through 4 of the adult somatosensory cortex of a FXS mouse model, the FMR1 knockout mouse. The collected multi-channel data contained approximately 1.6 million synapses which were analyzed using a probabilistic synapse detector. Our study reveals complex, synapse-type and layer specific changes in the neocortical circuitry of FMR1 knockout mice. We report an increase of small glutamatergic VGluT1 synapses in layer 4 accompanied by a decrease in large VGluT1 synapses in layers 1 and 4. VGluT2 synapses show a rather consistent decrease in density in layers 1 and 2/3. In all layers, we observe the loss of large inhibitory synapses. Lastly, astrocytic association of excitatory synapses decreases. The ability to dissect the circuit deficits by synapse type and astrocytic involvement will be crucial for understanding how these changes affect circuit function, and ultimately defining targets for therapeutic intervention.


2003 ◽  
Vol 145 (2) ◽  
pp. 213-218 ◽  
Author(s):  
Li-Tung Huang ◽  
Ming-Chi Lai ◽  
Chih-Lu Wang ◽  
Chien-An Wang ◽  
Chin-Hwa Yang ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Emilie Sheppard ◽  
Sarah Lippé

Epileptic encephalopathy encompasses conditions in which cognitive, motor, or sensory deficits result as a consequence of epileptic activity defining certain syndromes. It therefore represents a more severe subset of epilepsy, which can be generally characterized as frequent or severe seizures leading to cerebral dysfunction. This disturbance in cerebral functioning can in turn hinder, somewhat dramatically, cognitive development and further impact the future lives of patients. In this paper, we describe the cognitive consequences of status epilepticus in children and in adults in the context of plasticity theories. Recent studies maintain that consequences of SE may be severe cognitive sequelae, especially in early life. Since the residual consequences of SE in adulthood seem less detrimental and long-lasting, we argue that early life insults, such as those created by SE, during a rapid period of development and functional specialization, result in specific cognitive deficits dependent on the sensitive period at which SE occurred.


2011 ◽  
Vol 1369 ◽  
pp. 167-172 ◽  
Author(s):  
Diogo Losch de Oliveira ◽  
Caren Bavaresco ◽  
Ben Hur Mussulini ◽  
Alice Fischer ◽  
Diogo Onofre Souza ◽  
...  

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