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Subthalamic nucleus

Figure 15.2(a) A schematic presentation of possible normal basal ganglia circuitry. Activity in the cortico-thalamic pathway is modulated by striatal control of the globus pallidus (pallidum) through two pathways, the indirect pathway (Ind Path) to the external pallidum/globus pallidus (GPext) and the subthalamic nucleus (SThN) and the direct pathway (Dir Path) to GPint. Scheme... [Pg.301]

The indirect pathway (Ind Path) which also influences GPint and SN but only after going through the external (lateral) GPext and the subthalamic nucleus (SThN). [Pg.302]

Figure 15.9 Peptide modulation of striatal input to the globus pollidus. Enkephalin released from axon terminals of neurons of the indirect pathway (see Fig. 15.2 for details) is thought to inhibit GABA release from the same terminals so that feedback (auto) inhibition is reduced. This will free the neurons to inhibit the subthalamic nucleus (SThN) and its drive to GPint and SNr which in turn will have less inhibitory effect on cortico-thalamic traffic and possibly reduce akinesia. Dynorphin released from terminals of neurons of the direct pathway may also reduce glutamate release and excitation in the internal globus pallidus and further depress its inhibition of the cortico-thalamic pathway. High concentrations of these peptides may, however, result in dyskinesias. (See Henry and Brotchie 1996 and Maneuf et al. 1995)... Figure 15.9 Peptide modulation of striatal input to the globus pollidus. Enkephalin released from axon terminals of neurons of the indirect pathway (see Fig. 15.2 for details) is thought to inhibit GABA release from the same terminals so that feedback (auto) inhibition is reduced. This will free the neurons to inhibit the subthalamic nucleus (SThN) and its drive to GPint and SNr which in turn will have less inhibitory effect on cortico-thalamic traffic and possibly reduce akinesia. Dynorphin released from terminals of neurons of the direct pathway may also reduce glutamate release and excitation in the internal globus pallidus and further depress its inhibition of the cortico-thalamic pathway. High concentrations of these peptides may, however, result in dyskinesias. (See Henry and Brotchie 1996 and Maneuf et al. 1995)...
Urbain N., Gervasoni D., Souliere F. et al. (2000). Unrelated course of subthalamic nucleus of globus pallidus neuronal activities across vigilance states in the rat. Eur. ]. Neurosci. 12, 3361-74. [Pg.222]

Bergman, H., Wichmann, T. and DeLong, M. R. Reversal of experimental parkinsonism by lesions of the subthalamic nucleus. Science 249 1436-1438,1990. [Pg.778]

The diencephalon is composed of several nuclei that are grossly grouped into the thalamus, hypothalamus, epithalamus, and subthalamic nucleus. The thalamus serves as a sensory relay, receiving projections from all of... [Pg.62]

Also included are the epithalamus and subthalamic nucleus. The epithalamus is a collective term for the pineal gland, habenular nucleus, stria medullaris, and tenia thalami. The subthalamic nucleus is interconnected with the basal ganglia and plays a role in motor regulation. [Pg.63]

Other symptomatic therapeutic interventions are surgical procedures and deep brain simulation with three targets ventral intermediate nucleus of thalamus, the internal segment of the globus pallidus and the subthalamic nucleus. [Pg.691]

Wichmann, T., Bergman, H., and DeLong, M.R. (1994) The primate subthalamic nucleus. III. Changes in motor behavior and neuronal activity in the internal pallidum induced by subthalamic inactivation in the MPTP model of parkinsonism. / Neurophysiol 72 521-530. [Pg.163]

Functional circuitry between the cortex, basal ganglia, and thalamus. The major neurotransmitters are indicated. In Parkinson s disease, there is degeneration of the pars compacta of the substantia nigra, leading to overactivity in the indirect pathway (red) and increased glutamatergic activity by the subthalamic nucleus. [Pg.601]

Stimulation of the subthalamic nucleus or globus pallidus by an implanted electrode and stimulator has yielded good results for the management of the clinical fluctuations occurring in advanced parkinsonism. The anatomic substrate for such therapy is indicated in Figure 28-1. Such procedures are contraindicated in patients with secondary or atypical parkinsonism, dementia, or failure to respond to dopaminergic medication. [Pg.612]

Ashkan K, Wallace B, Bell BA, Benabid AL. Deep brain stimulation of the subthalamic nucleus in Parkinson s disease 1993-2003 where are we 10 years on Br J Neurosurg. 2004 18 19-34. [Pg.132]

Butson C.R., Cooper S.E., McIntyre C.C. Deep brain stimulation of the subthalamic nucleus Patient specific analysis of the volume of tissue activated. 10th Annual Conference of the International FES Society, July 2005, Montreal, Canada. [Pg.369]

Fraix v., Houeto J.L., Lagrange C., Le Pen C. et al. Clinical and economic results of bilateral subthalamic nucleus stimulation in Parkinson s disease. / Neurol Neurosurg Psychiatry, 2006, 77,443-449. [Pg.369]

Kita H., Tachibana Y., Nambu A., Chiken S. Balance of monosynaptic excitatory and disynaptic inhibitory responses of the globus pallidus induced after stimulation of the subthalamic nucleus in the monkey. J Neurosci, 2005, 25(38), 8611-8619. [Pg.370]


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Globus pallidus, external segment subthalamic nucleus

Spiny projection neuron subthalamic nucleus

Subthalamic nucleus globus pallidus input

Subthalamic nucleus lesions

Subthalamic nucleus neurons (glutamatergic

Subthalamic nucleus output

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