High Resolution Electroencephalography in Freely Moving Mice

Choi, Jee Hyun; Koch, Klaus Peter; Poppendieck, Wigand; Lee, Mina; Shin, Hee‐Sup

doi:10.1152/jn.00188.2010

Cited by 64 publications

(69 citation statements)

References 45 publications

(43 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In particular, in GAERS and WAG/Rij 83,84, as well as in humans 18,19, there is evidence of a cortical initiation site. Whether this is the case in the GHB model remains to be ascertained, although there is some evidence that, within the cortex, seizures are initiated in the primary somatosensory cortex 143. In addition, in GAERS, intracellular or extracellular recordings from thalamic and cortical neurons have provided a clear view of their firing dynamics during ASs, in vivo 83,144,145, whereas a similar description is not available for GHB-elicited ASs.…”

Section: Mechanism Of Ghb-induced Ass In the Ratmentioning

confidence: 99%

A Critical Evaluation of the Gamma‐Hydroxybutyrate (GHB) Model of Absence Seizures

2014

View full text Add to dashboard Cite

Typical absence seizures (ASs) are nonconvulsive epileptic events which are commonly observed in pediatric and juvenile epilepsies and may be present in adults suffering from other idiopathic generalized epilepsies. Our understanding of the pathophysiological mechanisms of ASs has been greatly advanced by the availability of genetic and pharmacological models, in particular the γ-hydroxybutyrate (GHB) model which, in recent years, has been extensively used in studies in transgenic mice. GHB is an endogenous brain molecule that upon administration to various species, including humans, induces not only ASs but also a state of sedation/hypnosis. Analysis of the available data clearly indicates that only in the rat does there exist a set of GHB-elicited behavioral and EEG events that can be confidently classified as ASs. Other GHB activities, particularly in mice, appear to be mostly of a sedative/hypnotic nature: thus, their relevance to ASs requires further investigation. At the molecular level, GHB acts as a weak GABA-B agonist, while the existence of a GHB receptor remains elusive. The pre- and postsynaptic actions underlying GHB-elicited ASs have been thoroughly elucidated in thalamus, but little is known about the cellular/network effects of GHB in neocortex, the other brain region involved in the generation of ASs.

show abstract

Section: Mechanism Of Ghb-induced Ass In the Ratmentioning

confidence: 99%

A Critical Evaluation of the Gamma‐Hydroxybutyrate (GHB) Model of Absence Seizures

2014

View full text Add to dashboard Cite

show abstract

“…Pharmacologically-evoked absence seizures in mice have been produced through the systemic administration of GABA A R antagonists and GABA B R agonists. None of the experiments that used these drugs suggested a sex-dependent phenotype; the studies were either reported without specifying mouse sex or were performed using only males or females without a stated rationale (Aizawa et al, 1997; IIshige et al, 1996; Weiergraber et al, 2008; Zaman et al, 2011; Choi et al, 2010). …”

Section: Sex Differences In Mouse Models Of Typical and Atypical Absementioning

confidence: 99%

Animal models of absence epilepsies: What do they model and do sex and sex hormones matter?

Luijtelaar

Onat

Gallagher

2014

Neurobiology of Disease

View full text Add to dashboard Cite

While epidemiological data suggest a female prevalence in human childhood- and adolescence-onset typical absence epilepsy syndromes, the sex difference is less clear in adult-onset syndromes. In addition, although there are more females than males diagnosed with typical absence epilepsy syndromes, there is a paucity of studies on sex differences in seizure frequency and semiology in patients diagnosed with any absence epilepsy syndrome. Moreover, it is unknown if there are sex differences in the prevalence or expression of atypical absence epilepsy syndromes. Surprisingly, most studies of animal models of absence epilepsy either did not investigate sex differences, or failed to find sex-dependent effects. However, various rodent models for atypical syndromes such as the AY9944 model (prepubertal females show a higher incidence than prepubertal males), BN model also with a higher prevalence in males and the Gabra1 deletion mouse in the C57BL/6J strain offer unique possibilities for the investigation of the mechanisms involved in sex differences. Although the mechanistic bases for the sex differences in humans or these three models are not yet known, studies of the effects of sex hormones on seizures have offered some possibilities. The sex hormones progesterone, estradiol and testosterone exert diametrically opposite effects in genetic absence epilepsy and pharmacologically-evoked convulsive types of epilepsy models. In addition, acute pharmacological effects of progesterone on absence seizures during proestrus are opposite to those seen during pregnancy. 17β-Estradiol has anti-absence seizure effects, but it is only active in atypical absence models. It is speculated that the pro-absence action of progesterone, and perhaps also the delayed pro-absence action of testosterone, are mediated through the neurosteroid allopregnanolone and its structural and functional homolog, androstanediol. These two steroids increase extrasynaptic thalamic tonic GABAergic inhibition by selectively targeting neurosteroid-selective subunits of GABAA receptors (GABAARs). Neurosteroids also modulate the expression of GABAAR containing the γ2, α4, and δ subunits. It is hypothesized that differences in subunit expression during pregnancy and ovarian cycle contribute to the opposite effects of progesterone in these two hormonal states.

show abstract

“…Patterns of brain responses triggered by stimuli called event related potentials (ERPs) can be measured on the scalp electroencephalogram in both humans and mice and serve as a neurophysiological outcome measure for abnormal information processing (Choi et al , 2010; He et al , 2001; Olichney et al , 2010). Direct in vivo neurophysiolgoical recording has become more readily accessible in mice to evaluate the firing patterns of cells across brain regions during task performance ( cf.…”

Section: Behavioral Phenotyping Strategiesmentioning

confidence: 99%

Comprehensive neurocognitive endophenotyping strategies for mouse models of genetic disorders

Hunsaker

2012

Progress in Neurobiology

View full text Add to dashboard Cite

There is a need for refinement of the current behavioral phenotyping methods for mouse models of genetic disorders. The current approach is to perform a behavioral screen using standardized tasks to define a broad phenotype of the model. This phenotype is then compared to what is known concerning the disorder being modeled. The weakness inherent in this approach is twofold: First, the tasks that make up these standard behavioral screens do not model specific behaviors associated with a given genetic mutation but rather phenotypes affected in various genetic disorders; secondly, these behavioral tasks are insufficiently sensitive to identify subtle phenotypes. An alternate phenotyping strategy is to determine the core behavioral phenotypes of the genetic disorder being studied and develop behavioral tasks to evaluate specific hypotheses concerning the behavioral consequences of the genetic mutation. This approach emphasizes direct comparisons between the mouse and human that facilitate the development of neurobehavioral biomarkers or quantitative outcome measures for studies of genetic disorders across species.

show abstract

High Resolution Electroencephalography in Freely Moving Mice

Cited by 64 publications

References 45 publications

A Critical Evaluation of the Gamma‐Hydroxybutyrate (GHB) Model of Absence Seizures

A Critical Evaluation of the Gamma‐Hydroxybutyrate (GHB) Model of Absence Seizures

Animal models of absence epilepsies: What do they model and do sex and sex hormones matter?

Comprehensive neurocognitive endophenotyping strategies for mouse models of genetic disorders

Contact Info

Product

Resources

About