Biomedical subjects

L J Vogt

Publications and source records attributed to L J Vogt.

6 recordsLinked to original sources

PubMed1995

Human cingulate cortex: surface features, flat maps, and cytoarchitecture.

The surface morphology and cytoarchitecture of human cingulate cortex was evaluated in the brains of 27 neurologically intact individuals. Variations in surface features included a single cingulate sulcus (CS) with or without segmentation or double parallel sulci with or without segmentation. The single CS was deeper (9.7 +/- 0.81 mm) than in cases with double parallel sulci (7.5 +/- 0.48 mm). There were dimples parallel to the CS in anterior cingulate cortex (ACC) and anastomoses between the CS and the superior CS. Flat maps of the medial cortical surface were made in a two-stage reconstruction process and used to plot areas. The ACC is agranular and has a prominent layer V. Areas 33 and 25 have poor laminar differentiation, and there are three parts of area 24: area 24a adjacent to area 33 and partially within the callosal sulcus has homogeneous layers II and III, area 24b on the gyral surface has the most prominent layer Va of any cingulate area and distinct layers IIIa-b and IIIc, and area 24c in the ventral bank of the CS has thin layers II-III and no differentiation of layer V. There are four caudal divisions of area 24. Areas 24a' and 24b' have a thinner layer Va and layer III is thicker and less dense than in areas 24a and 24b. Area 24c' is caudal to area 24c and has densely packed, large pyramids throughout layer V. Area 24c' g is caudal to area 24c' and has the largest layer Vb pyramidal neurons in cingulate cortex. Area 32 is a cingulofrontal transition cortex with large layer IIIc pyramidal neurons and a dysgranular layer IV. Area 32' is caudal to area 32 and has an indistinct layer IV, larger layer IIIc pyramids, and fewer neurons in layer Va. Posterior cingulate cortex has medial and lateral parts of area 29, a dysgranular area 30, and three divisions of area 23: area 23a has a thin layer IIIc and moderate-sized pyramids in layer Va, area 23b has large and prominent pyramids in layers IIIc and Va, and area 23c has the thinnest layers V and VI in cingulate cortex. Area 31 is the cinguloparietal transition area in the parasplenial lobules and has very large layer IIIc pyramids. Finally, variations in architecture between cases were assessed in neuron perikarya counts in area 23a. There was an age-related decrease in neuron density in layer IV (r = -0.63; ages 45-102), but not in other layers.(ABSTRACT TRUNCATED AT 400 WORDS)

Brain Mapping↗

PubMed1995

AF-DX 384 binding in rabbit cingulate cortex: two site kinetics and section autoradiography.

Autoradiographic studies of muscarinic receptors are limited by the lack of selective ligands. Inasmuch as AF-DX 384 has a higher affinity for m2 than m4 receptors and pirenzepine (PZ) has a reverse affinity profile, competition between these ligands was used to label m2 receptors in homogenized and sectioned tissue. Rabbit cingulate cortex was used because m2 receptors are expressed by anterior thalamic axons in posterior cingulate cortex (PCC) and this region is easily deafferented with undercut lesions to demonstrate presynaptic binding. Saturation isotherms and Scatchard analysis of [3H]AF-DX 384 binding showed one binding site with a KD of 9 +/- 2.3 nM (mean +/- SEM) and a Bmax of 1405 +/- 146 fmol/mg protein. Competition studies with [3H]AF-DX 384 (2 nM) and 10(-10)-10(-4) M PZ were performed in anterior cingulate cortex (ACC) and PCC. In both regions, the best fit was a two site model for low (BL) and high (BH) affinity binding in which Bmax values were similar (ACC: BL = 535 +/- 62 fmol/mg, BH = 676 +/- 85; PCC: BL = 552 +/- 41; BH = 675 +/- 85). Although affinities for KH were similar in each region (ACC: KH = 4.69 +/- 1.36 nM; PCC: KH = 8.53 +/- 3.69 nM), those for KL were significantly different (ACC: 181 +/- 15.4 nM; PCC: 285 +/- 42; P = .018). Binding of [3H]AF-DX 384 with PZ (150 nM) was best fit with a single site model (KD = 6 +/- 0.01 nM; Bmax = 688 +/- 31 fmol/mg), suggesting that PZ blocks the lower affinity site. (ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Limbic thalamus in rabbit: architecture, projections to cingulate cortex and distribution of muscarinic acetylcholine, GABAA, and opioid receptors.

Nuclei of the thalamus that project to cingulate cortex have been implicated in responses to noxious stimuli, cholinergic and motor functions. The rabbit limbic thalamus may play an important role in these functions, but has not been studied extensively in terms of its cytoarchitecture, the topographical organization of its cortical projections, and differential transmitter regulation of its subnuclei. Therefore, the architecture, projections to cingulate cortex, and radioligand binding were investigated in the anterior, ventral, lateral, and midline nuclei of rabbit thalamus. The anterior nuclei are highly differentiated because both the dorsal and ventral nuclei have parvicellular and magnocellular divisions. Fluorescent dyes were injected into cingulate cortex to evaluate limbic thalamocortical connections. The anterior medial, submedial, and parafascicular nuclei project primarily to anterior cingulate cortex, while they have small or no projections to posterior areas. The ventral anterior and ventral lateral nuclei have a significant projection to dorsal cingulate cortex, including areas 24b and 29d. Projections of the anterior ventral nucleus are topographically organized, since medial parts of the parvicellular division project to rostral area 29, and lateral parts project to caudal area 29. The lateral nuclei and the parvicellular and magnocellular divisions of the anterior dorsal nucleus project with progressively higher densities in the rostrocaudal plane of area 29. Finally, the magnocellular division of the anterior ventral nucleus projects almost exclusively to caudal and ventral area 29, i.e., granular retrosplenial cortex. Ligand binding studies employed coverslip autoradiography and single grain counting techniques. Muscarinic receptor binding was moderate for both pirenzepine and oxotremorine-M in the parvicellular anterior ventral nucleus, while in other nuclei, there was an inverse relationship in the binding for these ligands. Most notably, the anterior dorsal nucleus, which receives no cholinergic input, had very high oxotremorine-M and low pirenzepine binding, while the anterior medial nucleus, which receives a moderate cholinergic input, had the highest pirenzepine binding and very low oxotremorine-M binding. Muscimol binding to GABAA receptors was highest in the anterior ventral nucleus, while it was at moderate levels in the anterior dorsal and lateral nuclei. The binding of Tyr-D-Ala-Gly-MePhe-Gly-ol to mu opioid receptors and 2-D-penicillamine-5-D-penicillamine-enkephalin to delta opioid receptors were both high in the parvicellular and low in the magnocellular divisions of the anterior dorsal nucleus. The magnocellular division of the anterior ventral, the lateral dorsal, and the parafascicular nuclei had high mu opioid binding, while the lateral dorsal and lateral magnocellular nuclei had low levels of delta opioid binding.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1991

Muscarinic receptor binding increases in anterior thalamus and cingulate cortex during discriminative avoidance learning.

Training-induced neuronal activity develops in the mammalian limbic system during discriminative avoidance conditioning. This study explores behaviorally relevant changes in muscarinic ACh receptor binding in 52 rabbits that were trained to one of five stages of conditioned response acquisition. Sixteen naive and 10 animals yoked to criterion performance served as control cases. Upon reaching a particular stage of training, the brains were removed and autoradiographically assayed for 3H-oxotremorine-M binding with 50 nM pirenzepine (OXO-M/PZ) or for 3H-pirenzepine binding in nine limbic thalamic nuclei and cingulate cortex. Specific OXO-M/PZ binding increased in the parvocellular division of the anterodorsal nucleus early in training when the animals were first exposed to pairing of the conditional and unconditional stimuli. Elevated binding in this nucleus was maintained throughout subsequent training. In the parvocellular division of the anteroventral nucleus (AVp), OXO-M/PZ binding progressively increased throughout training, reached a peak at the criterion stage of performance, and returned to control values during extinction sessions. Peak OXO-M/PZ binding in AVp was significantly elevated over that for cases yoked to criterion performance. In the magnocellular division of the anteroventral nucleus (AVm), OXO-M/PZ binding was elevated only during criterion performance of the task, and it was unaltered in any other limbic thalamic nuclei. Specific OXO-M/PZ binding was also elevated in most layers in rostral area 29c when subjects first performed a significant behavioral discrimination. Training-induced alterations in OXO-M/PZ binding in AVp and layer Ia of area 29c were similar and highly correlated.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Laminar distribution of neuron degeneration in posterior cingulate cortex in Alzheimer's disease.

The laminar distribution of neuron losses in posterior cingulate cortex were evaluated in 25 clinically and neuropathologically diagnosed cases of dementia of the Alzheimer type (DAT). The layer of maximal neuron loss in area 23a for each DAT case was determined by comparison with mean neuron densities for each layer of 17 neurologically intact control cases. The DAT cases were separated into five classes: class 1, 12% of all DAT cases, no or less than 40% neuron loss in any layer; class 2, 24%, maximal neuron losses in layers II or III; class 3, 28%, losses mainly in layer IV; class 4, 12%, losses mainly in layers V or VI; class 5, 24%, severe losses in all layers. An analysis of large and small neurons showed that in class 2 there was an equal loss of both in layer IIIa--b, in class 3 mostly small neurons were lost in layer IV, in class 4 mostly large neurons were lost in layers III, IV and V, while in class 5 there was no selectivity. The age of disease onset and length of the disease were the same for all classes, although classes 4 and 5 tended to have an earlier onset. No measures of thioflavin S-stained neuritic plaque (NP) or neurofibrillary tangle (NFT) density discriminated among these classes. In 64% of all DAT cases there was a progressive shift in NFT from ventral area 30 where most were in layer II to areas 23a--b where there was a balance between those in superficial and deep layers to dorsal area 23c where most were in layers V and VI.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMedDate not supplied

Reorganization of cingulate cortex in Alzheimer's disease: neuron loss, neuritic plaques, and muscarinic receptor binding.

Pathology related to dementia of the Alzheimer type (DAT) develops later in cingulate cortex than in medial temporal areas. Therefore, end-stage cases have earlier forms of pathology in cingulate cortex, and postmortem studies of this region may provide a window on processes that temporal cortices pass through decades before death. Five classes of DAT have been described on the basis of neuron degeneration and receptor binding in posterior cingulate cortex. The present study assessed binding of 3H-oxotremorine-M with pirenzepine (OXO-M/PZ), a protocol for presynaptic muscarinic receptors, and thioflavin S-stained neuritic plaques (NPs) in cingulate area 23a in 12 DAT cases distributed over four classes of pathology and in nine age-matched control cases. OXO-M/PZ binding was significantly elevated in layers I, II, IV, and VI of all DAT cases and was very high in layer V compared to control cases. Almost 75% of the layer Va increase was due to binding in classes 2 and 3, while classes 1 and 4 were least affected. In class 3 cases, neuron density in layer Va was inversely correlated with OXO-M/PZ binding (r = -0.98) and primitive NP densities (r = -0.93). The close association between neuron densities and presynaptic muscarinic ligand binding in some classes confirms that there are independent classes of DAT. The high and inverse correlations between cortical pathology and ligand binding in class 3 cases suggest that there is a progression in class 3 pathology. Finally, elevated OXO-M/PZ binding and a report of increased choline uptake suggest that cholinergic axons sprout in DAT, and this sprouting may be associated with a progressive loss of postsynaptic elements.

Alzheimer Disease↗