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. 2013 Dec 23;8(12):e82191. doi: 10.1371/journal.pone.0082191

Figure 8. Hypothetical mechanisms of DBS effects.

Figure 8

A) Simplified scheme of the neural connections presumably activated by HFS-STN in the rodent brain. Note that most of the collaterals and the entopeduncular nucleus were omitted. The subthalamic nucleus and the substantia nigra are shown enlarged. Abbreviations: GP - Globus pallidus, STN - subthalamic nucleus, SNr - Substantia nigra pars reticulata, SNc - Substantia nigra pars compacta. CM - centromedian nucleus, PPTg - Pedunculopontine tegmental nucleus. Ach - acetylcholine, DA - dopamine. For more details see [77]. The equivalents of primate and rodent structures are reviewed in [78]. B) Scheme of modifications presumably initiated by HFS-STN in the normal rodent brain. It is assumed that HFS-STN co-activates at least three types of afferents innervating the SNr: GABAergic afferents of striatal and pallidal origin and glutamatergic afferents of subthalamic origin. The latter is the core element of the presented circuit and exhibits the following four modifications: 1) Suppression of AP generation and conduction (recovery time: <100 ms, B) depletion of transmitter release (recovery time: <5 s), 3) heterosynaptic depression via presynaptic GABA(B) receptors (recovery time: <1 min), 4) depression of the recurrent pathway through the STN (recovery time: >10 min). Mechanism #1 has been studied in more detail by [35]. The present experiments focused on the mechanism #2. Details on mechanisms #3 and #4 will be published in a forthcoming paper.