Relevant bibliographies by topics / AIA interneurons

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  2. Dissertations / Theses

Academic literature on the topic 'AIA interneurons'

Author: Grafiati
Published: 4 June 2021
Last updated: 5 February 2022

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Journal articles on the topic "AIA interneurons"

1

Shinkai, Y., Y. Yamamoto, M. Fujiwara, et al. "Behavioral Choice between Conflicting Alternatives Is Regulated by a Receptor Guanylyl Cyclase, GCY-28, and a Receptor Tyrosine Kinase, SCD-2, in AIA Interneurons of Caenorhabditis elegans." Journal of Neuroscience 31, no. 8 (2011): 3007–15. http://dx.doi.org/10.1523/jneurosci.4691-10.2011.

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D’Angelo, Vincenza, Mauro Giorgi, Emanuela Paldino, et al. "A2A Receptor Dysregulation in Dystonia DYT1 Knock-Out Mice." International Journal of Molecular Sciences 22, no. 5 (2021): 2691. http://dx.doi.org/10.3390/ijms22052691.

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We aimed to investigate A2A receptors in the basal ganglia of a DYT1 mouse model of dystonia. A2A was studied in control Tor1a+/+ and Tor1a+/− knock-out mice. A2A expression was assessed by anti-A2A antibody immunofluorescence and Western blotting. The co-localization of A2A was studied in striatal cholinergic interneurons identified by anti-choline-acetyltransferase (ChAT) antibody. A2A mRNA and cyclic adenosine monophosphate (cAMP) contents were also assessed. In Tor1a+/+, Western blotting detected an A2A 45 kDa band, which was stronger in the striatum and the globus pallidus than in the entopeduncular nucleus. Moreover, in Tor1a+/+, immunofluorescence showed A2A roundish aggregates, 0.3–0.4 μm in diameter, denser in the neuropil of the striatum and the globus pallidus than in the entopeduncular nucleus. In Tor1a+/−, A2A Western blotting expression and immunofluorescence aggregates appeared either increased in the striatum and the globus pallidus, or reduced in the entopeduncular nucleus. Moreover, in Tor1a+/−, A2A aggregates appeared increased in number on ChAT positive interneurons compared to Tor1a+/+. Finally, in Tor1a+/−, an increased content of cAMP signal was detected in the striatum, while significant levels of A2A mRNA were neo-expressed in the globus pallidus. In Tor1a+/−, opposite changes of A2A receptors’ expression in the striatal-pallidal complex and the entopeduncular nucleus suggest that the pathophysiology of dystonia is critically dependent on a composite functional imbalance of the indirect over the direct pathway in basal ganglia.
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3

Song, Wen-Jie, Tatiana Tkatch, and D. James Surmeier. "Adenosine Receptor Expression and Modulation of Ca2+Channels in Rat Striatal Cholinergic Interneurons." Journal of Neurophysiology 83, no. 1 (2000): 322–32. http://dx.doi.org/10.1152/jn.2000.83.1.322.

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Adenosine is a potent regulator of acetylcholine release in the striatum, yet the mechanisms mediating this regulation are largely undefined. To begin to fill this gap, adenosine receptor expression and coupling to voltage-dependent Ca2+ channels were studied in cholinergic interneurons by combined whole cell voltage-clamp recording and single-cell reverse transcription–polymerase chain reaction. Cholinergic interneurons were identified by the presence of choline acetyltransferase mRNA. Nearly all of these interneurons (90%, n = 28) expressed detectable levels of A1 adenosine receptor mRNA. A2a and A2b receptor mRNAs were less frequently detected. A3 receptor mRNA was undetectable. Adenosine rapidly and reversibly reduced N-type Ca2+ currents in cholinergic interneurons. The A1 receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine completely blocked the effect of adenosine. The IC50 of the A1 receptor selective agonist 2-chloro-N6-cyclopentyladenosine was 45 nM, whereas it was near 30 μM for the A2a receptor agonist CGS-21680. Dialysis with GDPβS or brief exposure to the G protein (Gi/o) alkylating agent N-ethylmaleimide also blocked the adenosine modulation. The reduction in N-type currents was partially reversed by depolarizing prepulses. A membrane-delimited pathway mediated the modulation, because it was not seen in cell-attached patches when agonist was applied to the bath. Activation of protein kinase C attenuated the adenosine modulation. Taken together, our results argue that activation of A1 adenosine receptors in cholinergic interneurons reduces N-type Ca2+currents via a membrane-delimited, Gi/o class G-protein pathway that is regulated by protein kinase C. These observations establish a cellular mechanism by which adenosine may serve to reduce acetylcholine release.
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4

Freund, T. F., and G. Buzsáki. "Interneurons of the hippocampus." Hippocampus 6, no. 4 (1998): 347–470. http://dx.doi.org/10.1002/(sici)1098-1063(1996)6:4<347::aid-hipo1>3.0.co;2-i.

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5

Kharazia, V. N., R. J. Wenthold, and R. J. Weinberg. "GluR1-immunopositive interneurons in rat neocortex." Journal of Comparative Neurology 368, no. 3 (1996): 399–412. http://dx.doi.org/10.1002/(sici)1096-9861(19960506)368:3<399::aid-cne6>3.0.co;2-0.

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6

Arcangeli, Sara, Alessandro Tozzi, Michela Tantucci, et al. "Ischemic-LTP in Striatal Spiny Neurons of both Direct and Indirect Pathway Requires the Activation of D1-Like Receptors and NO/Soluble Guanylate Cyclase/cGMP Transmission." Journal of Cerebral Blood Flow & Metabolism 33, no. 2 (2012): 278–86. http://dx.doi.org/10.1038/jcbfm.2012.167.

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Striatal medium-sized spiny neurons (MSNs) are highly vulnerable to ischemia. A brief ischemic insult, produced by oxygen and glucose deprivation (OGD), can induce ischemic long-term potentiation (i-LTP) of corticostriatal excitatory postsynaptic response. Since nitric oxide (NO) is involved in the pathophysiology of brain ischemia and the dopamine D1/D5-receptors (D1-like-R) are expressed in striatal NOS-positive interneurons, we hypothesized a relation between NOS-positive interneurons and striatal i-LTP, involving D1R activation and NO production. We investigated the mechanisms involved in i-LTP induced by OGD in corticostriatal slices and found that the D1-like-R antagonist SCH-23390 prevented i-LTP in all recorded MSNs. Immunofluorescence analysis confirmed the induction of i-LTP in both substance P-positive, (putative D1R-expressing) and adenosine A2A-receptor-positive (putative D2R-expressing) MSNs. Furthermore, i-LTP was dependent on a NOS/cGMP pathway since pharmacological blockade of NOS, guanylate-cyclase, or PKG prevented i-LTP. However, these compounds failed to prevent i-LTP in the presence of a NO donor or cGMP analog, respectively. Interestingly, the D1-like-R antagonism failed to prevent i-LTP when intracellular cGMP was pharmacologically increased. We propose that NO, produced by striatal NOS-positive interneurons via the stimulation of D1-like-R located on these cells, is critical for i-LTP induction in the entire population of MSNs involving a cGMP-dependent pathway.
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7

Buckmaster, Paul S., and Ivan Soltesz. "Neurobiology of hippocampal interneurons: A workshop review." Hippocampus 6, no. 3 (1996): 330–39. http://dx.doi.org/10.1002/(sici)1098-1063(1996)6:3<330::aid-hipo9>3.0.co;2-q.

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8

Maxwell, D. J., R. Kerr, E. Jankowska, and J. S. Riddell. "Synaptic connections of dorsal horn group II spinal interneurons: Synapses formed with the interneurons and by their axon collaterals." Journal of Comparative Neurology 380, no. 1 (1997): 51–69. http://dx.doi.org/10.1002/(sici)1096-9861(19970331)380:1<51::aid-cne4>3.0.co;2-s.

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9

Cicchetti, Francesca, Thomas G. Beach, and Andr� Parent. "Chemical phenotype of calretinin interneurons in the human striatum." Synapse 30, no. 3 (1998): 284–97. http://dx.doi.org/10.1002/(sici)1098-2396(199811)30:3<284::aid-syn6>3.0.co;2-7.

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10

Ratt�, St�phanie, and Ronald Chase. "Morphology of interneurons in the procerebrum of the snailHelix aspersa." Journal of Comparative Neurology 384, no. 3 (1997): 359–72. http://dx.doi.org/10.1002/(sici)1096-9861(19970804)384:3<359::aid-cne4>3.0.co;2-2.

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Dissertations / Theses on the topic "AIA interneurons"

1

Layne, Robert Michael. "The AIB interneurons are modulated by excitatory and inhibitory signaling pathways to shape aversive behaviors in response to 1-octanol." University of Toledo / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1445452178.

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