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also found that the same number of stimulations were required whether they were spaced by
24 hours or 7 days.
Brain slice models of epilepsy
In addition to studies involving synaptic plasticity and LTP, the brain slice preparation
has served as an important model of epilepsy providing investigators a wealth of information
on seizure-like activity associated with epilepsy [15]. Past investigators, and our lab as well,
have successfully used in vitro hippocampal and neocortical preparations in conjunction with
a variety of recording buffer recipes or convulsant agents for inducing and modeling seizure-
like events [44]. In this paradigm, the epileptiform activity observed in hippocampal slices
has been compared to the interictal spike discharge seen in EEG recordings of epilepsy
patients [45]. In our laboratory, we routinely use the so-called low magnesium model of
epilepsy in rodent hippocampal brain slices where MgCl 2 is removed from our recording
buffer, which results in the appearance of multiple spikes. Our current research also involves
the recording of in vitro spontaneous epileptform events from human neocortical brain tissue
obtained from living epileptic patients during surgery. Animal models in concert with viable
human tissue create a powerful approach for recording electrical events during seizure
activity.
In one application of the brain slice model, in vivo kindling stimulation was first induced
and then followed by an in vitro assessment of excitability in the brain slice in an attempt to
understand mechanisms responsible for kindling [46]. In this experiment, slices from the
amygdala-piriform-perirhinal cortex were created after daily 60 Hz stimulation (2 secs) in the
dorsal hippocampus. It was found that dorsal hippocampal kindling resulted in changes in the
origin of the spontaneous discharges similar to past studies involving amygdala kindling,
however, the observed changes in this case were shown in both hemispheres, thus showing a
potential seizure recruitment process in this model.
The influence of in vivo kindling on in vitro LTP has also been examined in hippocampal
brain slices [13]. Field potential recordings were made in brain slices obtained from kindled
rats one day after the last kindling where it was found that kindling impaired primed-burst
induced LTP in CA1 hippocampus. However, in some rat slices the GABA B antagonist
CGP35348 was applied, suggesting that LTP is suppressed by downregulation of GABA B
autoreceptors.
Collectively these studies illustrate that the analysis of epileptiform activity and events
involving synaptic plasticity can be evaluated in brain slices models. This is due to the fact
that the brain slice preparation retains enough intrinsic complexity to be able to manifest
events such as synchronized bursts, seizure-like activity, and LTP. However, the model is
simpler than in vivo models since some axons and afferents are lost upon slicing with in vitro
preparations. Nevertheless, the analysis of the interictal spike in the brain slice preparation
remains a powerful tool and provides great insight into epileptic mechanisms.
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