Experimental epilepsy: developmental aspects

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EPIDEMIOLOGIC studies indicate that in humans, seizures occur more frequently early in life.1,2 During the first few years some of the seizure types are age-specific3,4 and difficult to control with conventional therapies.5 The high incidence of seizures cannot be attributed only to the greater number of insults that may occur during the newborn period and early infancy. Experimental evidence suggests that the immature central nervous system (CNS) is more susceptible to seizures than its mature counterpart,6–14 at least during a specific stage of development. Ontogenetic seizure studies have demonstrated that 15-to-18-day-old rat pups are more prone to the development of bilateral, asynchronous convulsions and status epilepticus than adult rats regardless of the seizure model used to induce the seizures.6–10 These behavioral observations parallel the human epidemiologic and behavioral data concerning the expression of seizures as a function of age.3,4 Ongoing studies suggest that some of the age-related differences in seizure susceptibility may be due to a functional immaturity of the substantia nigra (SN).15–19


The SN is considered to be a critical site involved in the expression of generalized seizures in adult animals.15,20,21 It has been repeatedly demonstrated that electrographic seizure activity propagates in the SN.22–23 Autoradiographic studies of 2-deoxyglucose (DG) indicate that during a seizure there is an increase in DG uptake in the SN.15,24–27 Furthermore, information has accumulated suggesting that in adult rats, the gamma-aminobutyric-acid (GABA)-sensitive substantia nigra pars reticulata (SNR) neurons may be responsible,. . .



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