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F Filloux

Publications and source records attributed to F Filloux.

27 records · Page 2Linked to original sources
PubMed1988

Selective cortical infarction reduces [3H]sulpiride binding in rat caudate-putamen: autoradiographic evidence for presynaptic D2 receptors on corticostriate terminals.

Although the existence of presynaptic D2 dopamine receptors on corticostriate terminals has been supported by numerous receptor-binding studies, recent autoradiographic data has failed to demonstrate loss of striatal D2 receptors following cortical lesions. In the present study, Long-Evans rats were subjected to unilateral middle cerebral artery (MCA) infarction in order to produce reproducible lesions of the neocortex without damaging subcortical structures. Animals were sacrificed 2 and 4 wk following lesion and brains were prepared for receptor autoradiography. D2 receptors were studied using the selective ligand [3H]sulpiride, while D1 dopamine receptors were examined using [3H]SCH 23390. Sodium-dependent, high-affinity choline uptake sites were labeled with [3H]hemicholinium-3, thereby providing a quantitative measure of cholinergic neuronal integrity. Unilateral cortical infarction resulted in approximately a 20% reduction in [3H]sulpiride binding in several discrete regions of the ipsilateral caudate-putamen (CPu), but not in the nucleus accumbens. D2 receptor binding was also reduced significantly in some areas of the contralateral CPu when compared with [3H]sulpiride binding in sham-operated, control animals. In contrast, D1 receptors (as identified by [3H]SCH 23390 and high-affinity choline uptake sites (labeled with [3H]-HC-3) were not affected by the cortical lesion. The results provide autoradiographic confirmation of the existence of presynaptic D2 receptors on corticostriate terminals.

Animals↗
PubMed1988

Localization of nigrostriatal dopamine receptor subtypes and adenylate cyclase.

Quantitative autoradiography using [3H]-SCH 23390, [3H]-sulpiride and [3H]-forskolin was used to assess the effects of single and combined neurotoxin lesions of the nigrostriatal pathway in the rat brain on dopamine (DA) receptor subtypes and adenylate cyclase (AC), respectively. Ibotenic acid (IA) lesions of the caudate-putamen (CPu) resulted in near total loss of both [3H]-SCH 23390 and of [3H]-forskolin binding in the ipsilateral CPu and substantia nigra reticulata (SNR). [3H]-sulpiride binding in the CPu was only partially removed by this same lesion, and nigral [3H]-sulpiride binding was virtually unchanged. 6-Hydroxydopamine (6-OHDA) and IA lesions of the substantia nigra compacta (SNC) did not affect [3H]-SCH 23390 or [3H]-forskolin binding, but largely removed [3H]-sulpiride binding in the SNC. A 6-OHDA lesion of the nigrostriatal pathway followed by an ipsilateral IA injection of the CPu failed to further reduce [3H]-sulpiride binding in the CPu. These results demonstrate that postsynaptic DA receptors in the CPu are of both the D1 and D2 variety; however, a portion of D2 receptors in the CPu may be presynaptic on afferent nerve terminals to this structure. D1 receptors in the SNR are presynaptic on striatonigral terminals, whereas the D2 receptors of the SNC are autoreceptors on nigral DA neurons. The existence of presynaptic D2 receptors on nigrostriatal DA-ergic terminals could not be confirmed by this study. Co-localization of D1 receptors and AC occurs in both the CPu and SNR.

Adenylyl Cyclases↗
PubMedDate not supplied

Selective, unilateral cortical infarction increases striatal muscarinic receptor binding: potential evidence for cortical modulation of intrastriatal cholinergic transmission.

The effects of unilateral cortical infarction on subcortical (striatal) muscarinic receptors in rat brain were studied by means of in vitro receptor autoradiography using [3H]quinuclidinyl benzylate ([3H]QNB) and [3H]pirenzepine. The cortical lesions could be produced without compromising subcortical structures. A dramatic (20 to 59 per cent) increase in striatal [3H]QNB binding was observed ipsilateral to the damaged cortex. The increase in binding was greatest in the caudate-putamen, but was also noted in the nucleus accumbens. [3H]Pirenzepine binding (labeling M1 receptors) was also increased but to a lesser degree, as was [3H]QNB binding in the presence of 100 nM (unlabeled) pirenzepine (an indirect means of labeling M2 receptors). The results show that unilateral cortical infarction results in an upregulation of striatal muscarinic receptors, and suggest that both the M1 and M2 subtypes contribute to this effect. These findings provide evidence for cortical modulation of intrastriatal cholinergic transmission.

Animals↗