Sun, 20 Jul 2008 21:30:54 BST CiteULike: nelmor Bolam http://www.citeulike.org/user/nelmor/author/Bolam CiteULike.org en-gb Copyright © 2004-2008 citeulike.org http://www.citeulike.org/user/nelmor/article/2744750 <i>J. Neurosci., Vol. 28, No. 18. (30 April 2008), pp. 4795-4806.</i><br /><br />In the subthalamic nucleus (STN) of Parkinson's disease (PD) patients, a pronounced synchronization of oscillatory activity at beta frequencies (15-30 Hz) accompanies movement difficulties. Abnormal beta oscillations and motor symptoms are concomitantly and acutely suppressed by dopaminergic therapies, suggesting that these inappropriate rhythms might also emerge acutely from disrupted dopamine transmission. The neural basis of these abnormal beta oscillations is unclear, and how they might compromise information processing, or how they arise, is unknown. Using a 6-hydroxydopamine-lesioned rodent model of PD, we demonstrate that beta oscillations are inappropriately exaggerated, compared with controls, in a brain-state-dependent manner after chronic dopamine loss. Exaggerated beta oscillations are expressed at the levels of single neurons and small neuronal ensembles, and are focally present and spatially distributed within STN. They are also expressed in synchronous population activities, as evinced by oscillatory local field potentials, in STN and cortex. Excessively synchronized beta oscillations reduce the information coding capacity of STN neuronal ensembles, which may contribute to parkinsonian motor impairment. Acute disruption of dopamine transmission in control animals with antagonists of D1/D2 receptors did not exaggerate STN or cortical beta oscillations. Moreover, beta oscillations were not exaggerated until several days after 6-hydroxydopamine injections. Thus, contrary to predictions, abnormally amplified beta oscillations in cortico-STN circuits do not result simply from an acute absence of dopamine receptor stimulation, but are instead delayed sequelae of chronic dopamine depletion. Targeting the plastic processes underlying the delayed emergence of pathological beta oscillations after continuing dopaminergic dysfunction may offer considerable therapeutic promise. 10.1523/JNEUROSCI.0123-08.2008 Disrupted Dopamine Transmission and the Emergence of Exaggerated Beta Oscillations in Subthalamic Nucleus and Cerebral Cortex Nicolas Mallet Alek Pogosyan Andrew Sharott Jozsef Csicsvari Paul Bolam Peter Brown Peter Magill doi:10.1523/JNEUROSCI.0123-08.2008 J. Neurosci., Vol. 28, No. 18. (30 April 2008), pp. 4795-4806. 2008-05-02T08:52:58-00:00 2008 J. Neurosci. 28 18 4795 4806 dopamine oscillations parkinson plasticity stn synchronization http://www.citeulike.org/user/nelmor/article/591986 <i>Science, Vol. 303, No. 5666. (26 March 2004), pp. 2040-2042.</i><br /><br />Dopamine neurons play a key role in reward-related behaviors. Reward coding theories predict that dopamine neurons will be inhibited by or will not respond to aversive stimuli. Paradoxically, between 3 and 49% of presumed dopamine neurons are excited by aversive stimuli. We found that, in the ventral tegmental area of anesthetized rats, the population of presumed dopamine neurons that are excited by aversive stimuli is actually not dopaminergic. The identified dopamine neurons were inhibited by the aversive stimulus. These findings suggest that dopamine neurons are specifically excited by reward and that a population of nondopamine neurons is excited by aversive stimuli. Uniform inhibition of dopamine neurons in the ventral tegmental area by aversive stimuli. MA Ungless PJ Magill JP Bolam doi:10.1126/science.1093360 Science, Vol. 303, No. 5666. (26 March 2004), pp. 2040-2042. 2006-04-20T15:07:05-00:00 2004 Science 1095-9203 303 5666 2040 2042 aversive dopamine