Febrile seizures – Semiology in humans and animal models: Evidence of focality and heterogeneity

2010 ◽  
Vol 32 (1) ◽  
pp. 33-36 ◽  
Author(s):  
Brian G.R. Neville ◽  
Diane Gindner
Author(s):  
Aylin Y. Reid ◽  
Michael A. Galic ◽  
G. Campbell Teskey ◽  
Quentin J. Pittman

Febrile seizures (FSs) are seizures that occur during fever, usually at the time of a cold or flu, and represent the most common cause of seizures in the pediatric population. Up to 5% of children between the ages of six months and five years-of-age will experience a FS. Clinically these seizures are categorized as benign events with little impact on the growth and development of the child. However, studies have linked the occurrence of FSs to an increased risk of developing adult epileptic disorders. There are many unanswered questions about FSs, such as the mechanism of their generation, the long-term effects of these seizures, and their role in epileptogenesis. Answers are beginning to emerge based on results from animal studies. This review summarizes the current literature on animal models of FSs, mechanisms underlying the seizures, and functional, structural, and molecular changes that may result from them.


2019 ◽  
Vol 42 ◽  
Author(s):  
Nicole M. Baran

AbstractReductionist thinking in neuroscience is manifest in the widespread use of animal models of neuropsychiatric disorders. Broader investigations of diverse behaviors in non-model organisms and longer-term study of the mechanisms of plasticity will yield fundamental insights into the neurobiological, developmental, genetic, and environmental factors contributing to the “massively multifactorial system networks” which go awry in mental disorders.


2015 ◽  
Vol 223 (3) ◽  
pp. 157-164 ◽  
Author(s):  
Georg Juckel

Abstract. Inflammational-immunological processes within the pathophysiology of schizophrenia seem to play an important role. Early signals of neurobiological changes in the embryonal phase of brain in later patients with schizophrenia might lead to activation of the immunological system, for example, of cytokines and microglial cells. Microglia then induces – via the neurotoxic activities of these cells as an overreaction – a rarification of synaptic connections in frontal and temporal brain regions, that is, reduction of the neuropil. Promising inflammational animal models for schizophrenia with high validity can be used today to mimic behavioral as well as neurobiological findings in patients, for example, the well-known neurochemical alterations of dopaminergic, glutamatergic, serotonergic, and other neurotransmitter systems. Also the microglial activation can be modeled well within one of this models, that is, the inflammational PolyI:C animal model of schizophrenia, showing a time peak in late adolescence/early adulthood. The exact mechanism, by which activated microglia cells then triggers further neurodegeneration, must now be investigated in broader detail. Thus, these animal models can be used to understand the pathophysiology of schizophrenia better especially concerning the interaction of immune activation, inflammation, and neurodegeneration. This could also lead to the development of anti-inflammational treatment options and of preventive interventions.


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