Afferent specific localization of muscarinic acetylcholine receptors in cingulate cortex

Vogt, BA

doi:10.1523/jneurosci.04-09-02191.1984

Cited by 28 publications

(17 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Second, does transneuronal degeneration account for alterations subsequent to deafferentation lesions (Hattori and Fibiger, 1982)? As noted previously (Vogt, 1984), 2 peaks in PrBCM binding in cingulate cortex were reduced by 40-50% following ATN or undercut lesions, and they remained after ibotenic acid lesions. We have explored ibotenic acid-ablated cortex electron microscopically and found that, although neurons are virtually nonexistent, axon terminals did remain (unpublished observations).…”

Section: Methodssupporting

confidence: 81%

“…Peak layer Ia binding was usually reduced by 40-50% for the former ligands. Although incomplete ATN lesions could account for some variation, complete undercut lesions also failed to abolish the layer Ia peak in PrBCM binding (Vogt, 1984). In addition, ibotenic acid lesions always reduced peak binding of PrBCM and OXO/PZ in layers Ia and IV by about 50%.…”

Section: Localization Of Dendritic M Receptorsmentioning

confidence: 91%

“…Thus, the 2 peaks in PrBCM/ PZ and OXO/PZ binding in laminae Ia and IV remain after ATN lesions, PrBCM peak binding persists after undercut lesions (Vogt, 1984), and cortical ibotenic acid lesions reduce, but do not abolish, peaks in PrBCM and OXO/PZ binding, although binding in all layers is reduced by all lesions except the undercut procedure. A combination of cortical and thalamic lesions abolishes the 2 peaks, indicating that both cortical neurons and afferents contribute to the M, component of classical antagonist binding.…”

Section: Localization Of Dendritic M and M2 Sitesmentioning

confidence: 91%

“…Thalamic and cortical ablations were made as previously reported (Vogt, 1984) in 96 hooded, Long-Evans male rats (300-350 gm). Laminar lesions were made by either injecting small amounts of ibotenic acid into deep cortical layers with a 5 ~1 Hamilton syringe (0.05 ~1 injections of 10 rg ibotenic acid dissolved in 1 pl of physiological saline) or by making very large injections in one hemisphere (3 injections of 0.3 ~1 each) and analyzing receptor binding in the contralateral hemisphere.…”

Section: Methodsmentioning

confidence: 99%

See 3 more Smart Citations

Experimental localization of muscarinic receptor subtypes to cingulate cortical afferents and neurons

Vogt

1988

J. Neurosci.

Self Cite

View full text Add to dashboard Cite

A technique was developed to evaluate the potency of ligand binding at M2 ACh receptors and to experimentally localize the M1 and M2 subtypes to specific neuronal processes. Normal and experimental material was prepared with tritiated ligand binding to cryostat-sectioned area 29c of posterior cingulate cortex in rat, coverslip autoradiography, and single-grain-counting techniques. Three fundamental issues were addressed. 1. A morphological criterion termed an index of heterogeneity was developed by which the specificity of M2 binding by different ligands could be assessed. The index was calculated by first determining the laminar distribution of pirenzepine (PZ) binding sites and then summing absolute laminar variations from this distribution for each ligand. According to this measure the most efficient protocol for assaying M2 sites was tritiated oxotremorine-M (OXO) coincubated in unlabeled PZ (5 x 10(-8) M). The classical muscarinic antagonist propylbenzilylcholine mustard (Pr-BCM), however, when coincubated in PZ, was almost as efficient as PZ-blocked OXO binding. 2. Terminal axons of neurons in the anterior thalamic nuclei (ATN) have M2 receptors based on the following observations. First, specific binding of the M1 ligand PZ was unaffected by ATN lesions. Second, tritiated OXO and PrBCM binding blocked with unlabeled PZ, conditions favoring M2 receptor binding, showed significant reductions in binding in layers la, lb, and IV following ATN ablations. Third, IC50 values as determined by competition of PZ for PrBCM binding sites were shifted to lower concentrations in superficial layers by ATN lesions but not in deep layers where the thalamus does not terminate. Finally, in contrast to PZ-blocked OXO and PrBCM binding, binding of PZ-blocked 3H- quinuclidinyl benzilate (QNB) was reduced to homogeneity following ATN lesions. 3. Cortical pyramidal neurons have dendritic receptors that are primarily of the M1 subtype but may also include M2 sites. Thus, full depth ibotenic acid lesions reduced PZ binding by almost 70%. Neurotoxin lesions of neurons in layers II-IV or Vb-VI were followed by degeneration of the apical dendrites of pyramids in layer I and 78 and 15% reductions, respectively, in PZ binding. Also, full-depth neurotoxin lesions combined with ATN ablations completely abolished heterogeneities in PrBCM and PZ-blocked OXO binding. These data demonstrate that experimental techniques can be used in conjunction with normal material to make morphological assessments of the efficiency of binding of putative M2 ligands.

show abstract

Section: Methodssupporting

confidence: 81%

Section: Localization Of Dendritic M Receptorsmentioning

confidence: 91%

Section: Localization Of Dendritic M and M2 Sitesmentioning

confidence: 91%

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Experimental localization of muscarinic receptor subtypes to cingulate cortical afferents and neurons

Vogt

1988

J. Neurosci.

Self Cite

View full text Add to dashboard Cite

show abstract

“…Figure 13 shows high expression of AChE in layer Ia where AV axons terminate and greater than 50% loss of this activity following thalamic lesions (right side of Fig. 13 "Ablation"; Vogt, 1984).…”

Section: Thalamic Afferentsmentioning

confidence: 99%

Cingulate Cortex and Pain Architecture

Vogt

2015

The Rat Nervous System

View full text Add to dashboard Cite

Afferent connections of anterior thalamus in rats: Sources and association with muscarinic acetylcholine receptors

Sikes

Vogt

1987

J of Comparative Neurology

View full text Add to dashboard Cite

Afferent connections of the anterior thalamic nuclei (ATN) are classically thought to originate in the mammillary body and limbic cortex. This study explores nonlimbic sources of ATN afferents by using retrograde transport of horseradish peroxidase (HRP) to ascertain the relative contribution of these connections. Spread of HRP into adjacent regions was prevented either by removing the overlying cortex or by injecting through permanently implanted cannulas. The main sources of nonlimbic ATN afferents are the pretectum and central gray. Pretectal neurons were HRP-labeled primarily in the contralateral medial pretectal nucleus with a smaller number in the ipsilateral posterior pretectal nucleus. In the central gray, labeled cells were concentrated ipsilaterally in the laterodorsal tegmental nucleus. Additional projections to ATN originate in the reticular and ventral lateral geniculate nuclei of the thalamus, raphe nuclei, peripontine tegmental nucleus, and locus coeruleus. The association of ATN afferents with muscarinic receptors was also explored by means of in vitro receptor autoradiography with the muscarinic ligands propylbenzilylcholine mustard (PrBCM) and pirenzepine (PZ) in normal rats and rats with ablations. Ibotenic acid injections into ATN were used to destroy intrinsic neurons while leaving afferent fibers intact. Whereas such ablations produced statistically significant decreases in PrBCM binding in the anterior dorsal (AD, -45%) and anterior ventral, magnocellular part (AVm, -51%) nuclei, binding in the anterior ventral, parvicellular part (AVp) and anterior medial (AM) nuclei was not significantly decreased. Furthermore, PZ binding in normal rat ATN was significantly less (-72%) than PrBCM binding. These results suggest that a major proportion of muscarinic binding is associated with presynaptic elements. Ibotenic acid ablations of the mammillary body reduced PrBCM binding in ATN whereas lesions in cingulate cortex and laterodorsal tegmental nucleus had no effect. Compared to sham lesion controls, mammillary body lesions resulted in statistically significant decreases in binding bilaterally in AD (-15%), AVm (-19%), and AM (-20%). In conclusion, ATN receive afferents from several nonlimbic regions. Of these inputs, the pretectum may be the primary route through which sensory information reaches ATN. In addition, cholinergic input may modulate activity in projections from the mammillary body to ATN through presynaptic muscarinic receptors.

show abstract

Afferent specific localization of muscarinic acetylcholine receptors in cingulate cortex

Abstract: The laminar distribution of acetylcholine receptors in rat cingulate cortex and their localization to axons of neurons in the anterior thalamic nuclei (ATN) were evaluated with the muscarinic antagonist[3H]propylbenzilylcholine mustard (PrBCM) in vitro.

Cited by 28 publications

References 42 publications

Experimental localization of muscarinic receptor subtypes to cingulate cortical afferents and neurons

Experimental localization of muscarinic receptor subtypes to cingulate cortical afferents and neurons

Cingulate Cortex and Pain Architecture

Afferent connections of anterior thalamus in rats: Sources and association with muscarinic acetylcholine receptors

Contact Info

Product

Resources

About