Photochemical and pharmacological evaluation of 7-nitroindolinyl-and 4-methoxy-7-nitroindolinyl-amino acids as novel, fast caged neurotransmitters

Canepari, Marco; Nelson, Lawrence J.; Papageorgiou, George; Corrie, John E. T.; Ogden, David

doi:10.1016/s0165-0270(01)00451-4

Cited by 200 publications

(173 citation statements)

References 20 publications

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“…LSPS was performed as described by . Recirculating ACSF solution contained the following (in mM): 0.37 NI (nitroindolinyl)-caged glutamate (Canepari et al, 2001) (Sigma/RBI, Natick, MA), 0.005 CPP [(Ϯ)-3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid], 4 CaCl 2 , and 4 MgCl 2 . Once whole-cell recording was established, focal photolysis of caged glutamate was accomplished with a 1 ms pulse of a pulsed UV laser (wavelength, 355 nm; repetition rate, 100 kHz; DPSS Lasers, San Jose, CA) consisting of 100 pulses.…”

Section: Methodsmentioning

confidence: 99%

Circuit and Plasticity Defects in the Developing Somatosensory Cortex ofFmr1Knock-Out Mice

Bureau¹,

Shepherd²,

Svoboda³

2008

J. Neurosci.

183

202

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Silencing of the Fmr1 gene causes fragile X syndrome. Although defects in synaptic plasticity in the cerebral cortex have been linked to cognitive impairments in Fmr1 knock-out (ko) mice, the specific cortical circuits affected in the syndrome are unknown. Here, we investigated the development of excitatory projections in the barrel cortex of Fmr1 ko mice. In 2-week-old Fmr1 ko mice, a major ascending projection connecting layer 4 (L4) to L3 (L43 L3), was defective in multiple and independent ways: its strength was reduced, caused by a lower connection probability; the axonal arbors of L4 cells were spatially diffuse in L2/3; the L43 L3 projection did not show experience-dependent plasticity. By 3 weeks, the strength of the L43 L3 projection was similar to that of wild type. Our data indicate that Fmr1 shapes sensory cortical circuits during a developmental critical period.

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Section: Methodsmentioning

confidence: 99%

Circuit and Plasticity Defects in the Developing Somatosensory Cortex ofFmr1Knock-Out Mice

Bureau¹,

Shepherd²,

Svoboda³

2008

J. Neurosci.

183

202

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“…Nitroindolinyl (NI)-caged glutamate (Canepari et al, 2001) (Sigma-RBI, St. Louis, MO) stock solution was prepared by dissolving 50 mg of NI-glutamate in distilled water and stored in 0.1 ml aliquots at Ϫ20°C for up to several weeks. An aliquot was added to the recirculating ACSF for a concentration of 0.37 mM.…”

Section: Methodsmentioning

confidence: 99%

Laminar and Columnar Organization of Ascending Excitatory Projections to Layer 2/3 Pyramidal Neurons in Rat Barrel Cortex

Shepherd

Svoboda

2005

Journal of Neuroscience

215

269

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Excitatory synaptic projections to layer 2/3 (L2/3) pyramidal neurons in brain slices from the rat barrel cortex were measured using quantitative laser-scanning photostimulation (LSPS) mapping. In the barrel cortex, cytoarchitectonic "barrels" and "septa" in L4 define a stereotypical array of landmarks, allowing alignment and averaging of LSPS maps from multiple cells in different slices. We distinguished inputs to L2 and L3 neurons above barrels and septa. Average input maps revealed that barrel-related ascending projections (L432/3 barrel ) interdigitated with a novel septum-related projection (L5A32 septum ). We also explored the functional organization of these projections by comparing the input maps of multiple cells in individual slices. L2/3 cells sharing the same barrel-related column showed strong correlations in their input maps, independent of their precise locations within the column; otherwise, correlations fell rapidly as a function of intersomatic separation. Our data indicate that barrel-related and septum-related columns are associated with distinct functional circuits. These projections are likely to mediate parallel processing of somatosensory signals within the barrel cortex, with L432/3 barrel and L5A32 septum representing the intracortical continuations of, respectively, the subcortical lemniscal and paralemniscal systems conveying somatosensory information to the barrel cortex.

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“…Both compounds are suitable for studies on NMDA receptors (16,17), with MNI-caged amino acids being characterized by higher photorelease efficiency compared with the NI-based precursors (18). MNI-caged glutamate, therefore, was used preferentially with low affinity mutant receptors.…”

Section: Methodsmentioning

confidence: 99%

Disruption of Interdomain Interactions in the Glutamate Binding Pocket Affects Differentially Agonist Affinity and Efficacy of N-methyl-d-aspartate Receptor Activation

Maier

Schemm

Grewer

et al. 2007

Journal of Biological Chemistry

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Ionotropic glutamate receptors (iGluRs)4 are the major mediators of excitatory neurotransmission in the brain and play important roles both in neuronal development and synaptic function (1). They are tetrameric protein complexes (2, 3) in which each subunit is composed of (i) an extracellular aminoterminal domain, (ii) a ligand binding domain (LBD), sharing sequence homology to bacterial periplasmic binding proteins, (iii) a membrane-associated domain with the transmembrane helices M1-M4 that forms the ion pore, and (iv) an intracellular carboxyl-terminal domain (4).The family of iGluRs is divided into the subclasses of AMPA, kainate, and NMDA receptors that differ, among other things, in their ligand specificities (1). Despite the pharmacological differences, crystal structures have been obtained for LBDs of subunits from all three subclasses of iGluRs (5-9) and have revealed a conserved clam shell-like architecture of two lobes (D1 and D2) around a central cleft that harbors the ligand binding site. Lobe D1 is formed from residues preceding the first transmembrane domain (M1) and the C-terminal residues of the extracellular loop between transmembrane domains 3 and 4, whereas the N-terminal part of this loop forms lobe D2.LBD structures in complex with different ligands (10 -12) have shed light on the molecular mechanism of ligand binding and, in the absence of structural information on the transmembrane domain, have led to the formulation of hypotheses on how agonist binding may be coupled to channel gating. Agonists differ from antagonists in that they promote closure of the LBD clam shell through rotation of lobe D2 toward D1. In a largely mechanical model of receptor activation (11), this motion is thought to generate conformational strain within the tetrameric receptor complex that transduces to the membrane regions and, eventually, causes channel opening. Several studies in AMPA and kainate iGluRs (6, 7, 11) relating structure to agonist efficacy show that the degree of domain closure induced by different agonists correlates with their functional activity. Interestingly, there is evidence that the glycine binding domain of the NR1 subunit of the NMDA receptor does not exhibit a similar correlation between domain closure and agonist efficacy (8,12). Recent structure-function data show that engineering sterical restrictions within the glutamate-binding pocket of the NR2B subunit of the NMDA receptor is correlated to the degree of agonist efficacy (13), implicating that the action of glutamate and glycine on the NR2 and NR1 subunits, respectively, may induce different structural mechanisms underlying agonist efficacy.However, although crystallographic data have uncovered the difference between agonist-and antagonist-bound LBD struc-

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Photochemical and pharmacological evaluation of 7-nitroindolinyl-and 4-methoxy-7-nitroindolinyl-amino acids as novel, fast caged neurotransmitters

Cited by 200 publications

References 20 publications

Circuit and Plasticity Defects in the Developing Somatosensory Cortex ofFmr1Knock-Out Mice

Circuit and Plasticity Defects in the Developing Somatosensory Cortex ofFmr1Knock-Out Mice

Laminar and Columnar Organization of Ascending Excitatory Projections to Layer 2/3 Pyramidal Neurons in Rat Barrel Cortex

Disruption of Interdomain Interactions in the Glutamate Binding Pocket Affects Differentially Agonist Affinity and Efficacy of N-methyl-d-aspartate Receptor Activation

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