76 research outputs found

    The pedunculopontine tegmental nucleus and the nucleus basalis magnocellularis: Do both have a role in sustained attention?

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    It is well established that nucleus basalis magnocellularis (NbM) lesions impair performance on tests of sustained attention. Previous work from this laboratory has also demonstrated that pedunculopontine tegmental nucleus (PPTg) lesioned rats make more omissions on a test of sustained attention, suggesting that it might also play a role in mediating this function. However, the results of the PPTg study were open to alternative interpretation. We aimed to resolve this by conducting a detailed analysis of the effects of damage to each brain region in the same sustained attention task used in our previous work. Rats were trained in the task before surgery and post-surgical testing examined performance in response to unpredictable light signals of 1500 ms and 4000 ms duration. Data for PPTg lesioned rats were compared to control rats, and rats with 192 IgG saporin infusions centred on the NbM. In addition to operant data, video data of rats' performance during the task were also analysed

    Excitatory amino acidergic pathways and receptors in the basal ganglia

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    The striatum receives the majority of excitatory amino acidergic input to the basal ganglia from neocortical and allocortical sources. The subthalamic nucleus and the substantia nigra also receive excitatory amino acidergic inputs from neocortex. The subthalamic nucleus, which has prominent projections to the pallidum and nigra, is the only known intrinsic excitatory amino acidergic component of the basal ganglia. Possible excitatory amino acidergic inputs reach the basal ganglia from the intralaminar thalamic nuclei and the pedunculo-pontine nucleus. The striatum is richly endowed with all subtypes of excitatory amino acid receptors and these appear to be inhomogeneously distributed within the striatal complex. The non-striatal nuclei contain lesser levels of excitatory amino acid receptors and the relative proportion of these receptors varies between nuclei. The presence of high densities of excitatory amino acid receptors is a phylogenetically conserved feature of the striatum and its non-mammalian homologues. In Huntington's disease, there is substantial depletion of α -amino-3-hydroxy-5-methylisoxazole-4-propionic acid, N-methyl-D-aspartate, and kainate receptors within the striatum. In Parkinson's disease substantia nigra, there is significant loss of N-methyl-D-aspartate and α -amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptors.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/41734/1/726_2004_Article_BF00814003.pd

    Role of tonically-active neurons in the control of striatal function: cellular mechanisms and behavioral correlates

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    1. The striatum is primarily involved in motor planning and motor learning. Human diseases involving its complex circuitry lead to movement disorders such as Parkinson's disease (PD) and Huntington's disease (HD). Moreover the striatum has been involved in processes linked to reward, cognition and drug addiction. 2. The high content of acetylcholine (ACh) found in the striatum is due to the presence of cholinergic interneurons. The intrinsic electrical and synaptic properties of these interneurons have been recently characterized. However, their functional significance is far from being fully elucidated. 3. In vivo electrophysiological experiments from behaving monkeys have identified these cholinergic interneurons as "Tonically Active Neurons" (TANs). They are activated by presentation of sensory stimuli of behavioral significance or linked to reward. 4. Experimental evidence showed that integrity of the nigrostriatal dopaminergic system is essential for TANs to express learned activity. 5. PD is known to be due to the loss of the nigrostriatal dopaminergic pathway and the ensuing imbalance between the content of dopamine and acetylcholine in the striatum. This evidence supports the hypothesis that cholinergic interneurons, or TANs, play a key role in the modulation of striatal function
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