Diffuse transmission by acetylcholine in the CNS

Descarries, Laurent; Gisiger, Victor; Steriade, Mircea

doi:10.1016/s0301-0082(97)00050-6

Cited by 379 publications

(307 citation statements)

References 238 publications

Supporting

Mentioning

287

Contrasting

Unclassified

Order By: Relevance

“…Scale bar: 5 m. figured in conventional PSDs but rather are more distributed and respond to agonist supplied more diffusely. This would be consistent with suggestions that cholinergic innervation in the CNS, such as that provided by the septal input to the hippocampus, may be diffuse, delivering ACh at a distance for "volume transmission" (McKinney et al, 1983;Frotscher and Leranth, 1985;Descarries et al, 1997;Descarries, 1998;Zoli et al, 1999; but see Turrini et al, 2001). Because ␣7-nAChRs can also respond to choline as an agonist (Papke et al, 1996;Alkondon et al, 1997b), hydrolysis of ACh by extracellular acetylcholinesterase need not prevent distally released agonist from affecting the receptors.…”

Section: Postsynaptic/perisynaptic Sitessupporting

confidence: 82%

Nicotinic α7 receptors: Synaptic options and downstream signaling in neurons

2002

View full text Add to dashboard Cite

Nicotinic receptors are cation-ion selective ligand-gated ion channels that are expressed throughout the nervous system. Most have significant calcium permeabilities, enabling them to regulate calcium-dependent events. One of the most abundant is a species composed of the ␣7 gene product and having a relative calcium permeability equivalent to that of NMDA receptors. The ␣7-containing receptors can be found presynaptically where they modulate transmitter release, and postsynaptically where they generate excitatory responses. They can also be found in perisynaptic locations where they modulate other inputs to the neuron and can activate a variety of downstream signaling pathways. The effects the receptors produce depend critically on the sites at which they are clustered. Instructive preparations for examining ␣7-containing receptors are the rat hippocampus, where they are thought to play a modulatory role, and the chick ciliary ganglion, where they participate in throughput transmission as well as regulatory signaling. Relatively high levels of ␣7-containing receptors are found in the two preparations, and the receptors display a variety of synaptic options and functions in the two cases. Progress is starting to be made in understanding the mechanisms responsible for localizing the receptors at specific sites and in identifying components tethered in the vicinity of the receptors that may facilitate signal transduction and downstream signaling.

show abstract

Section: Postsynaptic/perisynaptic Sitessupporting

confidence: 82%

Nicotinic α7 receptors: Synaptic options and downstream signaling in neurons

2002

View full text Add to dashboard Cite

show abstract

“…They have extensive axonal arborization and many of their terminals form synapses (largely excitatory via M1 muscarinic receptors) on the dendrites-and cell bodies of the medium spiny g-aminobutyric acidcontaining output neurons (Phelps and Vaughn, 1986). These cholinergic interneurons also form an extensive network of extrasynaptic varicosities (denser than elsewhere in the brain) through which the ACh they release may influence glutamateric and dopaminergic inputs and g-aminobutyric acidergic output of the accumbens by 'volume' transmission (Descarries et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Fluoxetine Alleviates Behavioral Depression while Decreasing Acetylcholine Release in the Nucleus Accumbens Shell

Chau

Rada

Kim

et al. 2011

Neuropsychopharmacol

View full text Add to dashboard Cite

Selective serotonin reuptake inhibitors, such as fluoxetine, have demonstrated the ability to alleviate behavioral depression in the forced swim test; however, the sites and mechanisms of their actions remain to be further elucidated. Previous studies have suggested that behavioral depression in the swim test is mediated in part by acetylcholine (ACh) stimulating the cholinergic M1 receptors in the nucleus accumbens (NAc) shell. The current study tested whether acute, local, and chronic, subcutaneous fluoxetine treatments increase escape motivation during the swim test while simultaneously lowering extracellular ACh in the NAc shell. Experiment 1: Fluoxetine (1.0 mM) infused unilaterally in the NAc shell for 40 min reduced extracellular ACh while simultaneously increasing swimming time. Experiment 2: Fluoxetine (0.2, 0.5, and 0.75 mM) infused bilaterally in the NAc shell on day 3 dose-dependently decreased immobility and increased the total escape attempts (swimming and climbing) compared with Ringer given on day 2. Experiment 3: Fluoxetine (0.5 mM) infused bilaterally in the NAc for 40 min did not affect activities in an open field. Experiment 4: Chronic systemic fluoxetine treatment decreased immobility scores and increased total escape attempt scores compared with control saline treatment. In all, 14 days after the initial swim test, basal extracellular ACh in the shell was still elevated in the saline-treated group, but not in the fluoxetine-treated group. In summary, these data suggest that one of the potential mechanisms by which fluoxetine alleviates behavioral depression in the forced swim test may be to suppress cholinergic activities in the NAc shell.

show abstract

“…Cholinergic interneurons in the striatum establish intricate axonal projections that represent a widespread neurotransmission system [116][117][118]. Mechanistic studies revealed local regulation of dopamine release by acetylcholine as well as by proteins known to be disrupted in Parkinson's disease and other movement disorders [2,119].…”

Section: (A) Mechanisms Linking No With Cox2 Expressionmentioning

confidence: 99%

Are cyclooxygenase-2 and nitric oxide involved in the dyskinesia of Parkinson's disease induced byl-DOPA?

Bortolanza

Padovan-Neto

Cavalcanti-Kiwiatkoski

et al. 2015

Phil. Trans. R. Soc. B

View full text Add to dashboard Cite

Inflammatory mechanisms are proposed to play a role in l -DOPA-induced dyskinesia. Cyclooxygenase-2 (COX2) contributes to inflammation pathways in the periphery and is constitutively expressed in the central nervous system. Considering that inhibition of nitric oxide (NO) formation attenuates l -DOPA-induced dyskinesia, this study aimed at investigating if a NO synthase (NOS) inhibitor would change COX2 brain expression in animals with l -DOPA-induced dyskinesia. To this aim, male Wistar rats received unilateral 6-hydroxydopamine microinjection into the medial forebrain bundle were treated daily with l -DOPA (21 days) combined with 7-nitroindazole or vehicle. All hemi-Parkinsonian rats receiving l -DOPA showed dyskinesia. They also presented increased neuronal COX2 immunoreactivity in the dopamine-depleted dorsal striatum that was directly correlated with dyskinesia severity. Striatal COX2 co-localized with choline-acetyltransferase, calbindin and DARPP-32 (dopamine-cAMP-regulated phosphoprotein-32), neuronal markers of GABAergic neurons. NOS inhibition prevented l -DOPA-induced dyskinesia and COX2 increased expression in the dorsal striatum. These results suggest that increased COX2 expression after l -DOPA long-term treatment in Parkinsonian-like rats could contribute to the development of dyskinesia.

show abstract

Diffuse transmission by acetylcholine in the CNS

Cited by 379 publications

References 238 publications

Nicotinic α7 receptors: Synaptic options and downstream signaling in neurons

Nicotinic α7 receptors: Synaptic options and downstream signaling in neurons

Fluoxetine Alleviates Behavioral Depression while Decreasing Acetylcholine Release in the Nucleus Accumbens Shell

Are cyclooxygenase-2 and nitric oxide involved in the dyskinesia of Parkinson's disease induced byl-DOPA?

Contact Info

Product

Resources

About