Muscarinic antagonists microinjected into the subthalamic nucleus decrease muscular rigidity in reserpinized rats

Hernández‐López, Salvador; Flores, Gonzalo; Rosales, Manuel G.; Sierra, Arturo; Martínez‐Fong, Daniel; Aceves, Jorge

doi:10.1016/0304-3940(96)12872-x

Cited by 8 publications

(2 citation statements)

References 15 publications

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“…, 2004), probably through a combination of pre‐ and postsynaptic effects (e.g., Bevan & Bolam, 1995), which may involve M3‐muscarine type and other cholinergic receptors (at least in rodents; see Flores et al. , 1996; Hernandez‐Lopez et al. , 1996; Shen & Johnson, 2000).…”

Section: Methodsmentioning

confidence: 99%

Neuronal activity in the subthalamic nucleus modulates the release of dopamine in the monkey striatum

Shimo

Wichmann

2008

Eur J of Neuroscience

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The primate subthalamic nucleus (STN) is commonly seen as a relay nucleus between the external and internal pallidal segments, and as an input station for cortical and thalamic information into the basal ganglia. In rodents, STN activity is also known to influence neuronal activity in the dopaminergic substantia nigra pars compacta (SNc) through inhibitory and excitatory mono- and polysynaptic pathways. Although the anatomical connections between STN and SNc are not entirely the same in primates as in rodents, the electrophysiologic and microdialysis experiments presented here show directly that this functional interaction can also be demonstrated in primates. In three Rhesus monkeys, extracellular recordings from SNc during microinjections into the STN revealed that transient pharmacologic activation of the subthalamic nucleus by the acetylcholine-receptor agonist carbachol substantially increased burst firing of single nigral neurons. Transient inactivation of the STN with microinjections of the GABA-A-receptor agonist muscimol had the opposite effect. While the firing rates of individual SNc neurons changed in response to the activation or inactivation of the STN, these changes were not consistent across the entire population of SNc cells. Permanent lesions of the STN, produced in two animals with the fiber-sparing neurotoxin ibotenic acid, reduced burst firing and firing rates of SNc neurons, and substantially decreased dopamine levels in the primary recipient area of SNc projections, the striatum, as measured with microdialysis. These results suggest that activity in the primate SNc is prominently influenced by neuronal discharge in the STN, which may thus alter dopamine release in the striatum.

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Section: Methodsmentioning

confidence: 99%

Neuronal activity in the subthalamic nucleus modulates the release of dopamine in the monkey striatum

Shimo

Wichmann

2008

Eur J of Neuroscience

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“…The SNc, via dopaminergic terminals and external globus pallidus through GABAergic terminals, inhibit this activity (Bevan and Bolam, ; Campbell et al, ; Flores et al, ; Ohye et al, ; Rouzaire‐Dubois et al, ; Tsubokawa and Sutin, ). However, serotonergic input from raphe nuclei (mainly from dorsal raphe nuclei), and the pedunculopontine tegmental nucleus (via cholinergic projection) may enhance it (Dray, ; Feger et al, ; Flores et al, , 1999; Hernández et al, ). Cerebral cortex, via the neurotransmitter glutamate and the locus coeruleus through the noradrenergic terminals, may also regulate the subthalamic neuronal activity (Arcos et al, ; Feger et al, ; Kita and Kitai, ; Rosales et al, ; Rouzaire‐Dubois and Scarnati, ).…”

Section: Introductionmentioning

confidence: 99%

Rearrangement of the dendritic morphology of the neurons from prefrontal cortex and hippocampus after subthalamic lesion in Sprague–Dawley rats

Camacho-Ábrego

Tellez-Merlo

Melo

et al. 2013

Synapse

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Several studies in rodents have suggested the inactivation of the subthalamic nucleus (STN) as an alternative strategy to Parkinson's disease (PD) treatment. The STN is part of the basal ganglia and plays an important role in the motor function; however, recent data suggest that this structure has a critical role in the cognitive function of the limbic system. The STN receives direct projection from the prefrontal cortex (PFC), structure interconnected with the hippocampus and both structures send excitatory projections to the nucleus accumbens (NAcc). Here, we determined whether and which changes occurred 4 weeks after a STN lesion in the dendritic morphology of pyramidal neurons of the layers 3 and 5 of the PFC and basolateral amygdala, neurons of the ventral hippocampus, and the medium spiny neurons of the NAcc and caudate-putamen. Dendritic morphology was measured using the Golgi-Cox procedure followed by Sholl analysis. We also evaluated the effects of STN lesion on locomotor behavior assessed by an open field test, social interaction, acoustic startle response, prepulse inhibition, and locomotor activity induced by a novel environment and amphetamine. We found that STN damage induced a deficit in locomotion measured by open field test with neuronal hypertrophy in PFC (layer 5) and reduced spinogenesis in CA1 ventral hippocampus and PFC (layer 3). Taken together, these data suggest that the behavioral and morphological effects of STN lesion are, at least partially, mediated by limbic subregions with possible consequences for cognitive-related behaviors observed in PD treatment.

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Non‐Dopaminergic Approaches to the Treatment of Parkinson's Disease

Fox

Brotchie

2011

Parkinson's Disease

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Muscarinic antagonists microinjected into the subthalamic nucleus decrease muscular rigidity in reserpinized rats

Cited by 8 publications

References 15 publications

Neuronal activity in the subthalamic nucleus modulates the release of dopamine in the monkey striatum

Neuronal activity in the subthalamic nucleus modulates the release of dopamine in the monkey striatum

Rearrangement of the dendritic morphology of the neurons from prefrontal cortex and hippocampus after subthalamic lesion in Sprague–Dawley rats

Non‐Dopaminergic Approaches to the Treatment of Parkinson's Disease

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