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D A Kristt

Publications and source records attributed to D A Kristt.

At least 37 records · Page 2Linked to original sources

High density of cholinergic muscarinic receptors accompanies high intensity acetylcholinesterase-staining in layer IV of infant rat somatosensory cortex.

In this study the laminar localization of binding sites for the muscarinic radioligand [3H]3-quinuclidinylbenzilate was studied in somatosensory cortex of infant rat. Using light autoradiographic techniques, [3H]QNB was found to be concentrated in layer IV. Atropine-pretreated pups showed evenly dispersed, nonspecific binding in all layers. We conclude that cholinergic muscarinic receptors are concentrated in layer IV of infant rat somatosensory cortex. It is also in this lamina that an acetylcholinesterase-rich pathway terminates.

Acetylcholine↗

Acetylcholinesterase in the ventrobasal thalamus: transience and patterning during ontogenesis.

In this study, maturational alterations in acetylcholinesterase-dependent staining of the thalamic ventrobasal complex of rat and mouse were examined. The study was undertaken to address the question of whether this nucleus exhibits transient acetylcholinesterase positivity during its development and whether the enzyme is likely to be synthesized by its immature intrinsic neurons. Also, the patterning due to acetylcholinesterase staining of cells and fibers, and the developmental changes in these patterns, have not been described in earlier work. In contrast to surrounding thalamic nuclei, the ventrobasal complex is acetylcholinesterase-positive at birth. In rat, acetylcholinesterase staining of the ventrobasal thalamus is still more intense than in adjacent nuclei at the end of the first week postnatally. Virtually all somata in the nucleus are filled with dense reaction product at this time. Ultrastructurally, reaction product is associated with the granular endoplasmic reticulum. At this stage, there is a marked difference in intensity of staining between the medial and lateral subdivisions of the nucleus, and patterned clustering of somata within each subdivision is readily appreciated in acetylcholinesterase-stained material. In the second postnatal week, intrinsic acetylcholinesterase activity is progressively lost. By the end of the third postnatal week, the nucleus is quite pale except for one area. In the posterior portion of the lateral subdivision, adjacent to the nucleus reticularis, interconnecting bundles of acetylcholinesterase-positive fibers enter the nucleus. They course medially in the lateral subdivision and break up into a plexus of fine fibers. The development of acetylcholinesterase-dependent staining patterns in the mouse is quite similar, except that histochemically detectable levels of enzyme are substantially lower in the neonatal period. It is concluded that the ventrobasal complex can be distinguished from other thalamic nuclei in regard to earlier onset and/or transience of acetylcholinesterase staining. Ultrastructural observations suggest that virtually all immature ventrobasal neurons are synthesizing acetylcholinesterase. It is suggested that the transient staining for enzyme is due primarily to alteration in synthesis and/or turnover in neurons of the ventrobasal complex. In addition, the acetylcholinesterase staining reveals a patterning of fibers and cells that also undergoes developmental alteration. Evidence is discussed suggesting that axons in the barrels of somatosensory cortex (SmI) are derived from these transiently acetylcholinesterase-positive somata. Consequently, the loss of acetylcholinesterase fiber staining in the barrels, during the third postnatal week (noted previously), may be related to a decrease in synthesis of enzyme in the neuronal somata of the ventrobasal complex.

Acetylcholinesterase↗

A procedure for sampling specific portions of identified neurons for ultrastructural examination.

A procedure is described which facilitates the ultrastructural examination of selected regions of a neuron identified because it is Golgi-impregnated or HRP-filled. The procedure involves assigning a two-dimensional coordinate to every point on a drawing of the neuron by superimposing a grid over the drawing. A complete series of thick sections through the block containing the identified cells can then be related to each point on the drawn cell. A thick section which contains a region of interest is remounted on a plastic blank. From this new block one obtains thin sections for ultrastructural examination.

Axons↗

Developmental reorganization of acetylcholinesterase-rich inputs to somatosensory cortex of the mouse.

In this histochemical study, maturational changes in acetylcholinesterase-(AChE) staining in the barrel field of mouse somatosensory cortex were traced. Three distinct stages in the maturation of the AChE positive barrel innervation of mouse can be observed. In the first stage, individual AChE-positive fibers are initially detected in layer IV between 4-5 days postnatal (dpn). This lamina remains lightly stained for the next several days. At 11-12 dpn there is an abrupt increase in the intensity of AChE activity in the barrel hollows, that marks the beginning of the second stage. In the third stage between 17 and 21 dpn, this AChE-rich plexus of fibers is reorganized in the following manner. AChE fiber staining of the barrel hollows becomes limited to the superficial 75-100 microns of barrel depth, i.e. at the boundary between layers III and IV. At deeper levels in layer IV only the septae are AChE-positive. These observations differ from those previously reported for the rat, both in terms of the organization and development of the AChE-positive innervation to the barrels. The present work also provides the first indication that there is a stratification of inputs to the barrels.

Acetylcholinesterase↗

Horseradish peroxidase pellets implanted into infant neocortex: some technical considerations.

This study was undertaken to examine whether implanting pellets of horseradish peroxidase (HRP), rather than injecting an aqueous solution, would improve the sensitivity of the retrograde tracing method as applied to infant rat neocortex. From 1 to 10 pellets, each containing approximately 10 microgram of HRP, were implanted into somatosensory cortex of 6-day-old rats. Implantation of one pellet labeled 4 neuronal groups; 5 pellets, 37 groups. Higher doses of injected HRP (20--50 microgram and 200-400 microgram) are needed to label the same number of groups. Also, individual neurons of a group generally contain more granules/cell after pellets than following injections of much higher doses of HRP. The pellet implant technique offers a high degree of reproducibility and is technically simpler than injections. We conclude that HRP pellet implants offer advantages over injections in identifying potential afferents to immature neocortex.

Animals↗

The origin of the acetylcholinesterase-rich afferents to layer IV of infant somatosensory cortex. A histochemical analysis following lesions.

In this histochemical study, possible origins of the acetylcholinesterase-rich inputs to the barrel field of somatosensory cortex (SmI) were examined. Rats were studied between 6 and 16 days of age when acetylcholinesterase (AChE) positivity is readily detectable in the barrel centers. The experiments involved making lesions in either the ventrobasal thalamus or midbrain and noting the effects on AChE staining in SmI. Also, the results of destroying the large mystacial vibrissae at birth and 6 days of age were histochemically evaluated. Thalamic lesions eliminated most of the AChE positivity in layer IV but midbrain hemisection had no detectable effect. Destruction of the contralateral vibrissae, at birth, altered the pattern of AChE staining of the barrel field. Vibrissal damage at 6 days of age did not result in a noticeable alteration in staining of the barrel centers for AChE. We conclude that the AChE-positive barrel afferents are likely to originate from the ventrobasal complex.

Acetylcholinesterase↗

Development of neocortical circuitry: quantitative ultrastructural analysis of putative monoaminergic synapses.

The distribution, numbers and morphology of presumed monoaminergic (MA) synapses were examined in somatosensory cortex of neonatal rats and mice (newborn to 16 days of age). MA synapses were identified using an ultrastructural cytochemical marker, 5-hydroxydopamine (5-OHDA), which results in the appearance of small granular vesicles (SGV) in their presynaptic terminals. From birth to 7 days of age, 20--30% of all synapses sampled in somatosensory cortex contain SGVs. However, few SGV synapses are seen in 8-day-old cortex and by 12 days of age, SGVs are no longer detectable in cortex. A specific laminar distribution for these SGV synapses -- which is distinct from the overall synaptic distribution -- is first seen at 3 days of age and is essentially unchanged until 7 days postnatally. During this entire period, the SGV synapses predominate in the primordium of layer IV, where they account for 50--70% of all synapses. Morphometric analysis of SGV synapses indicates that there are differences in junctional symmetry, vesicle shape and configuration of the contact zone between SGV and non-SGV synapses, as well as between SGV synapses themselves in the various cortical layers. The laminar distribution and morphological characteristics of SGV synapses suggest that the MA projection to neocortex exhibits a high degree of spatial specificity during its ingrowth. Also, the relatively high proportion of SGV synapses in the first postnatal week may reflect a potent influence exerted by the MA inputs on immature neocortex. The decreased numerical density of SGV synapses after 7 days of age is probably due to the development of the blood-brain barrier to 5-OHDA.

Aging↗

Development of neocortical circuitry: histochemical localization of acetylcholinesterase in relation to the cell layers of rat somatosensory cortex.

Acetylcholinesterase (AchE) was histochemically localized in neocortex cerebri of newborn to 1-week-old rats. At birth AchE-dependent staining is limited to scattered somata (Cajal-Retzius cells) in the marginal zone and a few fibers and somata in primordial layer VI. By the end of the first week, neuronal elements are relatively well stained in particular cell laminae, giving the appearance of three horizontal AchE-rich "bands" which alternate with AchE-poor laminae. The subpial band (layer I) is a narrow tangential zone of intensely staining fibers and scattered somata. The mid-cortical band contains an AchE-positive fiber plexus (primordial layer IV) and numerous stained somata (pyramids of primordial layer V). In layer IV of the SmI region, intermittent foci of staining are noted which overlap the barrels' distribution in the barrel field. The deep cortical band (bottom of primordial layer VI) consists of numerous stained somata (Martinotti cells). It is concluded that there is a laminar pattern of acetylcholinesterase-dependent staining in postnatal rat somatosensory cortex, and that the laminar pattern bears a consistent spatial relation both to the cell layers and to the depths of high synapse density in immature cortex.

Acetylcholinesterase↗

Acetylcholinesterase-containing neurons of layer VIb in immature neocortex: possible component of an early formed intrinsic cortical circuit.

In this ontogenetic study the neurons of layer VIb of rodent somatosensory cortex have been characterized using acetylcholinesterase (AchE) histochemistry, Golgi, and electron microscopic techniques. Already, at birth, the neurons were found to be AchE-rich. They contain presumed AchE reaction product within their granular endoplasmic reticulum. These cells send fine axons upwards towards the subpial layer where they terminate in a dense, AchE-rich, fiber plexus. In chronically undercut cortex, AchE staining persists in layer VIb neurons and in the subpial fiber plexus. These observations continue to support the view that there is an intrinsic neuronal circuit connecting layer VI with I in immature neocortex. The findings also raise the possibility that the putative circuit is cholinergic.

Acetylcholinesterase↗

Somatosensory cortex: acetylcholinesterase staining of barrel neuropil in the rat.

Acetylcholinesterase (AchE) staining of layer IV of rat somatosensory (SmI) cortex was studied. In the barrel field of SmI, there are periodic, intensely AchE staining foci in the pattern and with the dimensions of barrels. The onset of this staining, at age 3 days, corresponds with the arrival of thalamocortical input to the barrels. Undercutting of SmI prevents staining in layer IV. We conclude that there are AchE-rich zones in layer IV that coincide with the specific thalamocortical projection to SmI.

Acetylcholinesterase↗

Neuronal differentiation in somatosensory cortex of the rat. I. Relationship to synaptogenesis in the first postnatal week.

Newborn (P-0 and P-1) through 6-day-old (P-6) rats were studied using light microscopic (Golgi) and ultrastructural methods. Previous studies demonstrated that early-formed synapses are concentrated at specific cortical depths, i.e. in strata. The present study shows that the synaptic stratum in the marginal zone corresponds to a dense fiber plexus and few somata (Cajal-Retzius cells). Axons in this zone almost exclusively form synapses on distal branches of dendrites originating in deeper lamina. In newborn neocortex there is a second synaptic stratum located deep to the cortical plate. It contains numerous axosomatic and axoproximal dendritic synapses as well as the most highly differentiated somata and proximal dendrites. By age P-6 there are 3 synaptic strata; one each in the marginal zone, cortical plate and 'subplate' layers. For all 3 strata a neuron's most differentiated dendrites are directed towards, traverse or run within, the nearest synaptic stratum. We conclude that, throughout the first postnatal week, the most mature dendrites of a given neuron generally occur at depths where synapse density is highest. At P-0 the most mature somata are similarly related to synaptic density.

Age Factors↗

Learned control of blood pressure in patients with high blood pressure.

UNLABELLED: Five patients with documented histories of essential hypertension of at least ten years' duration participated in a triphasic study of training to control systolic blood pressure (SBP). Phase 1 was a seven week period during which patients took their BP (systolic and diastolic) at home and mailed these data to us daily. Phase 2 was a three week period during which patients were taught to control SBP using a noninvasive technique: patients were trained to raise, to lower and to alternately lower and raise SBP. Phase 3 was a three month period during which patients again took their BP at home and mailed these data to us daily. RESULTS: (1) all patients learned SBP control: average increas 15%; average decrease 11%; (2) during SBP control heart rates, breathing rates, triceps brachii muscle tension and EEG activity did not change; (3) follow-up tests at one and three months showed evidence of retained SBP control; (4) baseline SBP fell from 153 mm Hg during laboratory training to 135 mm Hg at the three month follow-up; (5) phase 3 home BPs fell 18/8 mm Hg from phase 1 levels; (6) at home patients also were able to reduce SBP from 141 mm Hg (average) to 125 mm Hg (average) by means of the lowering technique learned in the laboratory.

Aged↗