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Functional organization of the circuits connecting the cerebral cortex and the basal ganglia: implications for the role of the basal ganglia in epilepsy Volume 4, supplément 3, Supplement 3, December 2002


   
   Figure 1. Fibre connections of the basal ganglia nuclei. For clarity the cortical and thalamic connections to the STN have been omitted. Abbreviations: CG: central gray; colliculus sup, inf: superior and inferior colliculus; CM: central medial thalamic nucleus; CL: central lateral thalamic nucleus; EN: entopeduncular nucleus; GPe: external segment of the globus pallidus; GPi: internal segment of the globus pallidus; Hb: habenula; LD: lateral dorsal thalamic nucleus; MD: medial dorsal thalamic nucleus; MDl: paralamellar subdivision of the medial dorsal thalamic nucleus; MRF: mesencephalic reticular formation; Pf: parafascicular thalamic nucleus; PF: prefrontal cortex; PM: premotor cortex; PPN: pedunculo pontine nucleus; SNR: substantia nigra pars reticulata; STN: subthalamic nucleus; VA/VL: ventral anterior/Ventral lateral thalamic nuclei; VM: ventral medial thalamic nucleus; VPl: lateral ventral pallidum.



   
   Figure 2. Typical triphasic excitatory-inhibitory-excitatory responses evoked in SNR cells following cortical stimulation. The short latency excitation results from activation the fast cortico-subthalamo-nigral circuit (1), the inhibitory response results from activation of the direct cortico-striato-nigral circuit (2) and the late excitatory response results from the so-called indirect cortico-striato-pallido-subthalamonigral circuit (3).



   
   Figure 3. Schematic diagram of the afferent and efferent circuits of the shell subdivision of the nucleus accumbens. CA1: CA1 area of the hippocampus; Nacc: nucleus accumbens; PFC: prefrontal cortex; PL/MO: prelimbic/medial orbital areas of the prefrontal cortex; Thal: thalamus; VPm: medial ventral pallidum; VTA/ SNC: ventral tegmental area/substantia nigra pars compacta.



   
   Figure 4. Classical model of the intrinsic connections of the basal ganglia stressing the distinct neuronal origin of the direct and indirect trans-striatal circuits and the differential influence exerted by the dopaminergic system on these two populations of striatal output neurons.



   
   Figure 5. Cortico-striatal neurons display rhythmic synaptic depolarisations during SWDs. A Intracellular activity of a layer V cortico-striatal pyramidal neuron during a SWD, from the resting membrane potential (Vm) (middle panel) and during intracellular injection of positive (top panel) and negative (bottom panel) DC current. The intensity of the injected current (nA) and the corresponding membrane potential (mV) are indicated. In this and the subsequent figure the top trace is the ECoG and the lower trace shows the corresponding intracellular record. B Expanded traces from the intracellular records shown in A. The frequency of cellular oscillations was not significantly modified by changes in membrane potential (C; P > 0.1, one-way ANOVA). D Superimposition of single depolarisations showing their increase in amplitude as a function of the steady hyperpolarisation. A is reproduced from Charpier et al., 1999 [89].



   
   Figure 6. High-frequency synaptic depolarisations in cortical neurons and its relation to ECoG activity. A-C Simultaneous recordings of a cortical neuron's intracellular activity and of the corresponding ECoG (paired top traces). Lower traces show an expansion of the recording periods indicated by the letters. Mean frequency (± S.D.) of the neuronal activity was calculated from the cellular events indicated by the filled circles. We took into account the peak of subthreshold synaptic depolarisations, single spikes and the first spike in a burst. In A (a vs b) and C (b vs c) note the higher frequency of the membrane potential oscillations at the start of the SWD (~ 10 Hz) compared to that observed during the main body of the SWD (~ 8 Hz). B Epochs of cellular rhythmic depolarisations that are not reflected by paroxysmal activity in the ECoG. These isolated oscillations have the same frequency (~ 10 Hz) as that occurring at the start of the SWD. C Example of a SWD where prior cellular oscillations occurred with a frequency of about 12 Hz (Ca). This activity was interrupted (D), leading to a high-frequency burst of action potentials (arrow).



   
   Figure 7. Correlated oscillations in the cortex and in the related striatal sector during SWDs. A Simultaneous recording of the ECoG from the orofacial motor cortex (top trace) and the LFP from the corresponding region of the striatum (bottom trace) during a SWD. The rhythmic activity in the ECoG was reflected in the striatal oscillatory LFP. A2 and A3 Successive SWCs and the corresponding striatal LFPs, from the period indicated with an asterisk in A1, were overlaid (A2) and averaged (A3) using the peak of the spike component of the SWCs as the reference. B Relative power spectrum of the ECoG shown in A1. The SWD frequency was 7.8 Hz (arrow). C Cross-correlation between the ECoG and the striatal LFP obtained from the SWD shown in A1. The period (130 ms) was consistent with the ECoG frequency during the SWD (B).