Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P08908 (5-HT1A)
 5,574 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental lesions followed by binding of [3H]4-trans-2-carboxy-5,7-dichloro-4-phenylamino-carbonylamino-1,2 ,3,4- tetrahydroquinoline ([3H]L-689,560, a novel ligand that binds to the glycine modulatory site), [3H]glycine and [3H]glutamate (N-methyl-D-aspartate (NMDA) sensitive) to cryostat sections and quantitative autoradiography were used to investigate the cellular localization of the NMDA receptor complex in the neocortex of the rat. The lesions were produced by intrastriatal injections of either volkensin (2 and 6 ng) or ricin (10 ng): both are suicide transport agents but only the former is retrogradely transported in the CNS. The binding of [3H]L-689,560 was significantly reduced in rats receiving 2 or 6 ng volkensin in deep cortical layers of Fr1/Fr2 ipsilateral to the striatal lesion. Similar reductions were also seen in [3H]glycine and [3H]glutamate binding, but only in rats receiving 6 ng volkensin. Quantitative histological analysis had previously revealed a loss of large infragranular pyramidal neurones with sparing of both interneurones and supragranular pyramidal neurones. There were no significant reductions in binding of any ligand in the superficial layers. In cortical areas Par1/Par2, [3H]L-689,560 was also significantly reduced in deep layers but only in rats receiving 6 ng volkensin. Binding was also reduced in the superficial layers by contrast to Fr1/Fr2. [3H]Glycine and [3H]glutamate binding were unaffected in this area. Binding of [3H]L-689,560 was unaffected in any area following intrastriatal ricin injection. The present study indicates that the NMDA receptor complex is present on pyramidal cells forming the corticofugal pathways. This is discussed in terms of the 5-HT1A receptor which is enriched on these cells.
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PMID:NMDA receptors assessed by autoradiography with [3H]L-689,560 are present but not enriched on corticofugal-projecting pyramidal neurones. 136 17

Experimental lesions and quantitative autoradiography were used to investigate the cellular localisation of receptors. Lesions were produced by intrastriatal injections of either volkensin or ricin, only the former is retrogradely transported. Volkensin treatment caused significant losses in Fr1/Fr2 of neocortex in the number of infragranular pyramidal neurones and binding to deep cortical layers of both [3H]pirenzepine (muscarinic cholinergic m1 receptors) and [3H]kainate (kainate sensitive glutamate receptors). In common with previous findings, which also showed sparing of interneurones, supragranular pyramidal neurones were not reduced in number and the binding to deep cortical layers of [3H]8-hydroxy-2-(n-dipropylamino)tetralin (serotonin 1A receptors) was reduced. Significant increases in [3H]prazosin binding to both total alpha adrenoceptors and the alpha 1b subtype were observed in superficial layers. Adrenoceptors were not decreased in any layer. The binding of [3H] GABA to GABAA receptors was not affected at all. Muscarinic receptors and pyramidal neurones were also reduced in deep cortical layers of Par1/Par2 in common with serotonin 1A (5-HT1A) receptors and total alpha receptors were significantly decreased in the middle layers. Overall m1 and kainate receptors were less affected than 5-HT1A receptors. The results are discussed in terms of the biology of cortical pyramidal neurones, drugs for Alzheimer's disease and novel ligands for improving human brain in vivo scanning techniques.
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PMID:Localisation of muscarinic (m1) and other neurotransmitter receptors on corticofugal-projecting pyramidal neurones. 814 48

Experimental lesions and quantitative autoradiography were used to investigate the cellular distribution of neurotransmitter receptors in rats. Lesions were produced by intracortical injections of either volkensin or ricin. However, only the former is retrogradely transported and volkensin treatment causes significant loss of contralateral cortical pyramidal neurones. Binding of [3H]pirenzepine (muscarinic M1 receptors) and [3H]nicotine was reduced in contralateral cortex in volkensin compared with ricin and/or control (uninjected) animals. However, binding of [3H]8-hydroxy-2-(n-dipropylamino)tetralin (5-HT1A receptors), [3H]ketanserin (5-HT2A receptors), and [3H]1,3-dipropylcyclopentylxanthine (adenosine A1 receptors) was unchanged. The most likely explanation for these results is that M1 and nicotinic receptors are present in large numbers on those pyramidal neurones that are lost. The results are discussed in terms of the biology of cortical pyramidal neurones, drugs for Alzheimer's disease, and novel ligands for improving human brain scanning techniques.
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PMID:Selective loss of cholinergic receptors following unilateral intracortical injection of volkensin. 929 15