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Striatal neurons, excitation

Spencer HJ (1976) Antagonism of cortical excitation of striatal neurons by glutamic acid diethyl ester evidence for glutamic acid as an excitatory transmitter in the rat striatum. Brain Res /02 91-101. [Pg.42]

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)...
Recent evidence indicates that PD might affect synaptic function adversely. In parkin-deficient mice, higher stimulation of corticostriatal afferents were required to evoke EPSPs in striatal spiny neurons suggesting that excitability of spiny neurons was reduced." Also, parkin, which is an ubiquitin ligase" has been shown to interact with and ubiquitinate synaptotagmin XI." " ... [Pg.741]

Aosaki T, Kiuchi K, Kawaguchi Y. 1998. Dopamine I), -1 ike receptor activation excites rat striatal large aspiny neurons in vitro. J Neurosci 18 5180-5190. [Pg.220]

Hernandez-Lopez S, Tkatch T, Perez-Garci E, Galarraga E, Bargas J, Hamm H, Surmeier DJ (2000) D2 dopamine receptors in striatal medium spiny neurons reduce L-type Ca2+ currents and excitability via a novel PLC[beta]l-IP3-calcineurin-signaling cascade. J Neurosci 20 8987-8995. [Pg.143]

Anaesthetics depress all excitable tissues including central neurones, cardiac muscle and smooth and striatal muscle. However, these tissues have different sensitivities to anaesthetics and the arca.s of the brain responsible for consciousness (middle. CD) arc among the most sensitive. Titus, il i.s possible to administer anaesthetic agents at concentrations that produce unconsciousness without unduly depressing the caidiova.scular and respiratory centres or the myocardium. However, for most nnaesthclias. the margin of safety is small. [Pg.52]


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