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SUMMARYInterest in temporal lobe seizure pathways has a long history based initially on the human condition of temporal lobe epilepsy (TLE). This interest in TLE has extended more recently into explorations of experimental models. In this review, the network structures in the temporal lobe that are recruited in animal models during various forms of limbic seizures and status epilepticus are described. Common to all of the various models is recruitment of the parahippocampal cortices, including the piriform, perirhinal, and entorhinal areas. This cortical involvement is seen in in vitro and in vivo electrophysiological recordings throughout the network, in trans-synaptic neuroplastic changes in associ- In this review, we present evidence that the parahippocampal structures of the temporal lobe are perhaps critical to the expression of convulsive seizures in animal models of temporal lobe epilepsy (TLE), and by analogy, the clinical expression of TLE in humans. The experimental evidence describing the seizure pathways associated with TLE comes from a variety of sources, including (1) electrophysiological studies employing both in vitro and in vivo recordings, (2) trans-synaptic neuroplastic changes in the network as a consequence of activation in the kindling model, (3) metabolic changes in the pathway, including mRNAs and protein expression, (4) pathway energy utilization realized in 14C 2-deoxyglucose (2-DG) uptake, and (5) network lesions and their impact on the expression of secondarily generalized seizures from focal onset in the temporal lobe. These various observations on pathway activation should be viewed against the backdrop of the common clinical assumption made by neurologists doing deep recordings in humans from various temporal lobe structures that focal seizures restricted to the hippocampus are without clinical symptoms, and that it is only when

Autism spectrum disorder (ASD) patients commonly exhibit a variety of comorbid traits including seizures, anxiety, aggressive behavior, gastrointestinal problems, motor deficits, abnormal sensory processing, and sleep disturbances for which the cause is unknown. These features impact negatively on daily life and can exaggerate the effects of the core diagnostic traits (social communication deficits and repetitive behaviors). Studying endophenotypes relevant to both core and comorbid features of ASD in rodent models can provide insight into biological mechanisms underlying these disorders. Here we review the characterization of endophenotypes in a selection of environmental, genetic, and behavioral rodent models of ASD. In addition to exhibiting core ASD-like behaviors, each of these animal models display one or more endophenotypes relevant to comorbid features including altered sensory processing, seizure susceptibility, anxiety-like behavior, and disturbed motor functions, suggesting that these traits are indicators of altered biological pathways in ASD. However, the study of behaviors paralleling comorbid traits in animal models of ASD is an emerging field and further research is needed to assess altered gastrointestinal function, aggression, and disorders of sleep onset across models. Future studies should include investigation of these endophenotypes in order to advance our understanding of the etiology of this complex disorder.

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Adult Fast (seizure-prone) and Slow (seizure-resistant) kindling rat strains exhibit divergent behaviors in paradigms relevant to attention-deficit/hyperactivity disorder (ADHD) in humans. Similar dissociations in rodent behavior have been linked to disparities in early life experience, suggesting that differential maternal care or postnatal interactions may underlie these behaviors. Consequently, the authors compared maternal behavior and preweaning pup weights in these 2 strains under control and cross-fostered conditions and examined its effects on subsequent adult offspring behavior. Ultimately, several distinct maternal behaviors were apparent between the 2 strains under control conditions, and some of those behaviors were then malleable by pup condition. Yet, in spite of the resultant complex maternal patterns across groups, all offspring showed behavioral phenotypes akin to their genetic strain. Thus, a specific postnatal environment is unlikely to underwrite ADHD-like behaviors in the seizure-prone Fast rats, which implicates a genetic or prenatal origin for the ADHD phenotype.

SUMMARYIt was questioned whether amygdala kindling, a model of temporal lobe epilepsy, is under genetic control, and is associated with comorbid behavioral features. Initially, rats were selectively bred for speed of amygdala kindling, and, in subsequent generations, were assessed in behavioral paradigms to measure activity, emotionality, impulsivity, and learning. Clearly kindling was under genetic control, as two strains were developed to be either Fast or Slow to kindle, and each was associated with different neurological, electrophysiological and behavioral features. Behaviorally, the Fast rats appear much like humans with attention deficit hyperactivity disorder (ADHD), showing easy distraction, hyperactivity and impulsivity, compared to Slow rats. KEY WORDS: Kindling, Genetics, Selective breeding, ADHD.It was initially questioned whether amygdala kindling, a common model of human temporal lobe epilepsy (TLE), was under genetic control. If kindling was genetically sensitive, it implied that TLE also might be under considerable genetic control. During the selective breeding of rats for their rate of amygdala kindling, two strains were developed from an original parent population of a Long Evans Hooded and Wistar cross. One was Fast kindling and one was Slow. The latter profile was deemed important, as the forces that oppose kindling we believed to be no less interesting than the forces that promote it. After six generations of selection, the two new strains were nonoverlapping in their kindling rates (Racine et al., 1999). Following the 11th generation, the selection procedure was relaxed, and all subsequent generations have arisen from second cousin pairings . Presently the rats are in their 62nd generation. The selection was truly for the rate of kindling, and not other notable features, like focal amygdala after-discharge (AD) thresholds (ADT), which were similar between the two strains. However, the focal AD durations were longer in the Fast rats from the beginning, suggesting that local recruitment and seizure-offset mechanisms were different between the