Localization of α-bungarotoxin binding sites in mouse brain by light and electron microscopic autoradiography

Arimatsu, Yasuyoshi; Seto, Akiko; Amano, Takehiko

doi:10.1016/0006-8993(78)90782-5

Cited by 70 publications

(11 citation statements)

References 14 publications

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“…(Arimatsu et al 1978), did not reduce the response of i.p.n. neurones to carbachol nor did the drug produce a sustained block of the response to f.r.m.…”

Section: Effects Of Drug Administrationmentioning

confidence: 73%

“…(Arimatsu et al 1978), ac-bungarotoxin itself was ineffective as a blocker of responses to cholinomimetic agonists. The distinction between binding and blocking actions of a-bungarotoxin is reminiscent of its action on the ganglionic nicotinic receptor (Brown & Fumagalli, 1977;Brown, 1979).…”

Section: Discussionmentioning

confidence: 89%

“…a-Bungarotoxin (0-1-1 /M, n = 4), which has been used as a specific ligand for nicotinic receptors in the mammalian C.N.S. (Arimatsu et al 1978), did not reduce the response of i.p.n. neurones to carbachol nor did the drug produce a sustained block of the response to f.r.m.…”

Section: Transmission In the Interpeduncular Nucleusmentioning

confidence: 98%

“…Also, the i.p.n. has been shown to contain a high concentration of binding sites for the nicotinic receptor marker az-bungarotoxin (Arimatsu, Seto & Amano, 1978) and fewer (Kobayashi, Palkovits, Hruska, Rosthchild & Yamamura, 1978;Kuhar et al 1975), but intensely localized (Rotter, Birdsall, Field & Raisman, 1979), muscarinic binding sites. F.r.m.…”

Section: Introductionmentioning

confidence: 99%

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Chemical transmission in the rat interpeduncular nucleus in vitro.

Brown¹,

Docherty²,

Halliwell³

1983

The Journal of Physiology

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SUMMARY1. We have used a rat brain-slice preparation to study the effects of some cholinomimetic and amino acid agonists and antagonists on the discharge frequency of neurones in the interpeduncular nucleus (i.p.n.), and on the response of these neurones to electrical stimulation of their main excitatory input, the fasciculus retroflexus of Meynert (f.r.m.).2. A high proportion of i.p.n. neurones were excited by carbachol, acetylcholine (ACh) and muscarine, but methacholine was less effective. The amino acids L-glutamate and L-aspartate were highly effective stimulants of i.p.n. neurones.3. The responses to ACh or carbachol were greatly reduced by the nicotinic blocking agents hexamethonium, d-tubocurarine and mecamylamine but only slightly reduced by atropine. The response to muscarine was abolished by low doses of atropine. a-Bungarotoxin did not block the response of i.p.n. neurones to f.r.m. stimulation or to cholinomimetic agonists. 4. The response of i.p.n. neurones to f.r.m. stimulation was not appreciably affected by high doses of nicotinic antagonists or atropine nor was there any enhancement of the response by physostigmine.5. The amino acid antagonists y-D-glutamylglycine (yDGG) and 2-aminophosphonovalerate (2-APV) were effective blockers ofthe response to f.r.m. stimulation and preferentially reduced responses to aspartate while having little effect on responses to glutamate or cholinomimetic agonists.6. It is concluded that ACh is an unlikely candidate for transmitter in this pathway despite abundant neurochemical evidence in its favour. It is more likely that the transmitter is an excitatory amino acid, probably an aspartate-like substance.

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“…(Arimatsu et al 1978), did not reduce the response of i.p.n. neurones to carbachol nor did the drug produce a sustained block of the response to f.r.m.…”

Section: Effects Of Drug Administrationmentioning

confidence: 73%

Section: Discussionmentioning

confidence: 89%

Section: Transmission In the Interpeduncular Nucleusmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Chemical transmission in the rat interpeduncular nucleus in vitro.

Brown¹,

Docherty²,

Halliwell³

1983

The Journal of Physiology

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“…An autoradiographic approach using '%-labeled 2-deoxyglucose has been employed to determine which areas in the brain become metabolically active following parenteral administration of nicotine (Pazdemik et al, 1982;London et al, 1988). Finally, binding studies have attempted to label nicotinic receptors autoradiographically by utilizing radiolabeled analogs of the following nicotinic ligands: ACh (Rainbow et al, 1984;Clarke et al, 1985b), nicotine (Clarke et al, 1984(Clarke et al, , 1985bLondon et al, 1985) and cr-bungarotoxin ((rBT; Arimatsu et al, 1978;Hunt and Schmidt, 1978;Segal et al, 1978;Clarke et al, 1985b).…”

mentioning

confidence: 99%

Autoradiographic localization of putative nicotinic receptors in the rat brain using 125I-neuronal bungarotoxin

et al. 1991

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Neuronal bungarotoxin (NBT), a snake venom neurotoxin, selectively blocks nicotinic receptors in many peripheral and central neuronal preparations. alpha-Bungarotoxin (alpha BT), on the other hand, a second toxin isolated from the venom of the same snake, is an ineffective nicotinic antagonist in most vertebrate neuronal preparations studied thus far. To examine central nicotinic receptors recognized by NBT, we have characterized the binding of 125I-labeled NBT (125I-NBT) to rat brain membranes and have mapped the distribution of 125I-NBT binding in brain sections using quantitative light microscopic autoradiography. The binding of 125I-NBT was found to be saturable, of high affinity, and heterogeneously distributed in the brain. Pharmacological studies suggested that more than one population of sites is labeled by 125I-NBT. For example, one component of 125I-NBT binding was also recognized by alpha BT, while a second component, not recognized by alpha BT, was recognized by the nicotinic agonist nicotine. The highest densities of these alpha BT-insensitive, nicotine-sensitive sites were found in the fasciculus retroflexus, the lateral geniculate nucleus, the medial terminal nucleus of the accessory optic tract, and the olivary pretectal nucleus. alpha BT-sensitive NBT binding sites were found in highest density in the lateral geniculate nucleus, the subthalamic nucleus, the dorsal tegmental nucleus, and the medial mammillary nucleus (lateral part). The number of brain regions with a high density of 125I-NBT binding sites, blocked either by alpha BT or by nicotine, is low when compared with results obtained using other approaches to studying the central distribution of nicotinic receptors, such as labeling with 3H-nicotine or labeling with cDNA probes to mRNAs coding for putative receptor subunits. It is proposed that 125I-NBT labels a subpopulation of nicotinic receptors in the rat brain, and that, given its ability to block nicotinic receptors in a variety of neuronal preparations, NBT will be a useful probe for studying the functional properties of these sites.

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Quantitative electron microscopic evidence for reinnervation in the adult rat interpeduncular nucleus after lesions of the fasciculus retroflexus

Murray

Zimmer

Raisman

1979

J of Comparative Neurology

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The method of electron dense degeneration has been used to make a quantitative study of the projection from the habenula through the fasciculus retroflexus (FR) to the interpeduncular nucleus (IPN) in the rat. The IPN si a midline structure onto which the right and left fasciculi converge. In the rostral part of the IPN the fascicular axons from each side form synapses throughout the mediolateral extent of the ventral two-thirs of the nucleus. In the caudal part of the IPN the fascicular axons from each side terminate to an equal extent in two discrete, parasagittal zones, situated one on side in the mid-mediolateral extent of the IPN. These zones contain clusters of neurons located along the course of a characteristic row of arterioles and venules penetrating the IPN from its ventral surface. In both rostral and caudal parts of the IPN the fascicular axons form single synaptic contaerpeduncular neurons, but caudally, in the two parasagittal zones they also form crest synapses. Crest synapses are only found in this part of the IPN. In crest synapses two presynaptic terminals form markedly asymmetrical contacts with the parallel opposing sides of an attenuated dendritic appendage (the crest). After unilateral fascicular lesions only one member of a pair of axon terminals contacting a crest degenerates. After bilateral fascicular lesions, however, there are many instances in which both members of a crest pair degenerate. This indicates that the axon terminals from the right and left fasciculi are segregated at the level of the crests, in such a way that one terminal comes from the right fasciculus and one from the left. At longer survivals after unilateral or bilateral fasciculus lesions the degeneration is completely removed, but crest synapses are still present, indicating that the presence of fascicular axons is not necessary for the maintenan ce of crests in the IPN. To investigate the effects of chronic deafferentation, the left fasciculus was destroyed and, after a survival of at least six weeks (sufficient for all degeneration to be removed) the right fasciculus was destroyed one day before killing. Under these conditions there are many crests in which both axon terminals show degeneration. The proportion of such doubly degenerating crest synapses is similar to that found after acute (1 day) bilateral lesions, indicating that axons from the right fasciculus have reinnervated sites formerly occupied by the left fasciculus. We conclude that during normal development there is some constraint which prevents both sides of a crest being innervated by axons from the fasciculus of the same side of the brain, but that this constraint is not effective after unilateral fascicular lesions in the adult.

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Localization of α-bungarotoxin binding sites in mouse brain by light and electron microscopic autoradiography

Cited by 70 publications

References 14 publications

Chemical transmission in the rat interpeduncular nucleus in vitro.

Chemical transmission in the rat interpeduncular nucleus in vitro.

Autoradiographic localization of putative nicotinic receptors in the rat brain using 125I-neuronal bungarotoxin

Quantitative electron microscopic evidence for reinnervation in the adult rat interpeduncular nucleus after lesions of the fasciculus retroflexus

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