EEG Radiotelemetry in Small Laboratory Rodents: A Powerful State-of-the Art Approach in Neuropsychiatric, Neurodegenerative, and Epilepsy Research

Figure 6

Pharmacological induction of epileptic discharges. (a) Surface EEG recording displaying ictal discharges after i.p. administration of 4-aminopyridine (4 AP, 10 mg/kg). Sporadic spikes (T) evolve into a transitory episode of continuous spiking (1), resulting in an EEG depression (decreased amplitude, 2-3). Shortly after this period a second spike-train concomitant to the development of a generalized tonic-clonic seizure with wild running and jumping becomes apparent which finally results in a tonic extension of the hindlimbs (4) and death. The remaining tiny signal following brain death represents an ECG (R-spike) contamination. (b) After i.p. administration of bicuculline methobromide (BMB, 10 mg/kg) mice show trains of characteristic spikes and spike waves. (c) Administration of baclofen (20 mg/kg) resulting in sporadic occurrence of spiking activity. (d) Intrahippocampal electroencephalographic (EEG) recordings following i.p. administration of KA (30 mg/kg). (I): deep CA1 recording from a C57Bl/6J mouse for 2 h immediately after KA administration. At 30 mg/kg KA contiguous hippocampal seizure activity is observed occasionally interrupted by postictal depression (arrows). Ictal discharges are characterized by spike and/or spike-wave activity (see insets) in the delta- and theta-wave range (4–8 Hz). (II–IV) At days 1, 3, and 5 after injection 1 h CA1 EEG recordings illustrate declining but still continuous ictal discharges related to neuronal excitotoxic degeneration (with permission from [96, 97]).

(a) 4-Aminopyridine

(b) Bicuculline methobromide

(c) R/S-Baclofen

(d)