Abstract
The absence epilepsy typical electroencephalographic pattern of sharp spikes and slow waves (SWDs) is considered to be due to an interaction of an initiation site in the cortex and a resonant circuit in the thalamus. The hyperpolarization-activated cyclic nucleotide-gated cationic I h pacemaker channels (HCN) play an important role in the enhanced cortical excitability. The role of thalamic HCN in SWD occurrence is less clear. Absence epilepsy in the WAG/Rij strain is accompanied by deficiency of the activity of dopaminergic system, which weakens the formation of an emotional positive state, causes depression-like symptoms, and counteracts learning and memory processes. It also enhances GABAA receptor activity in the striatum, globus pallidus, and reticular thalamic nucleus, causing a rise of SWD activity in the cortico-thalamo-cortical networks. One of the reasons for the occurrence of absences is that several genes coding of GABAA receptors are mutated. The question arises: what the role of DA receptors is. Two mechanisms that cause an infringement of the function of DA receptors in this genetic absence epilepsy model are proposed.
Highlights
Absence seizures, typical for many different patients with absence epilepsy, principally differ from convulsive seizures
Our hypothesis that burst firing in TC neurons is caused by hyperpolarization-activated Ih channel and hyperpolarization-activated (ICa,T) channel and that burst firing of at least some TC cells plays a role in spikewave discharges (SWDs) occurrence, is supported by pharmacological studies indicating that increased GABAergic inhibition in the ventral basal (VB) complex of the thalamus, as induced by local injections of GABA-agonists, enhances SWDs
Bilateral injections of R-baclofen into the specific relay nuclei of nonepileptic rats induced synchronized rhythmic oscillations on the cortical EEG. These results suggest that GABAB receptors in the ventrolateral thalamus and in the reticular thalamic nucleus (RTN) are involved in an oscillatory activity which underlies SWDs [132]
Summary
Typical for many different patients with absence epilepsy, principally differ from convulsive seizures. SWDs, as can be found in WAG/Rij rats, have a local cortical origin in the perioral region of the somatosensory cortex [6,7,8,9,10,11,12], which is confirmed in GAERS [13, 14], another well validated and often used strain of rats with absence epilepsy [15, 16]. We assume that the Ih pacemaker channels localized in the somatosensory cortex contribute to the initiation of the occurrence of SWDs and that a second set of pacemaker channels can be found in the thalamus The latter is responsible for the occurrence of thalamic delta activity and sleep spindles, as can be assumed from the classical studies of the firing pattern in thalamic relay cells, tonic and burst firing modes [53, 54]. The RTN and its widespread connections to other thalamic nuclei form a pathway in the propagation of cortically triggered SWDs and sustain oscillations
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