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The COVID-19 pandemic dramatically affected the operations of New York City hospitals during March and April of 2020. This article describes the transformation of a neurology division at a 450-bed tertiary care hospital in a multi-ethnic community in Brooklyn during this initial wave of COVID-19. In lieu of a mass redeployment of staff to internal medicine teams, we report a novel method for a neurology division to participate in a hospital's expansion of care for patients with COVID-19 while maintaining existing team structures and their inherent supervisory and interpersonal support mechanisms., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Calbindin D(28K) (CB) expression was analyzed in the rat hippocampus following 10-min-cardiac arrest-induced ischemia within a year after reperfusion. In rats examined 3 days after ischemia, CB immunoreactivity disappeared completely from CA1 pyramidal neurons and from most CA2 pyramids. In the stratum granulosum of the dentate gyrus, mossy fibers, and hippocampal interneurons, CB immunoreactivity was preserved, although staining was somewhat paler than that in control rats. A similar pattern of CB immunoreactivity was found in rats sacrificed 14 days and 1 month after cardiac arrest. From the 14th postischemic day, neuronal loss in the stratum pyramidale of CA1 but not in that of CA2 became apparent. The reappearance of CB immunoreactivity in CA1 and CA2 pyramidal neurons was noticed 6 months after ischemia, and the pattern was identical to that observed in animals sacrificed 12 months after the ictus. The prolonged loss and delayed reappearance of CB immunoreactivity in the hippocampus demonstrate that ischemia may induce long-term disturbances of protein expression, which may in turn result in impairment of hippocampal functioning.

The pattern of neuronal loss in the rat hippocampus following 10-min-long cardiac arrest-induced global ischemia was analyzed using the unbiased, dissector morphometric technique and hierarchical sampling. On the third day after ischemia, the pyramidal layer of sector CA1 demonstrated significant (27%) neuronal loss (P<0.05). At this time, no neuronal loss was observed in other cornu Ammonis sectors or the granular layer of the dentate gyrus. On the 14th postischemic day, further neuronal loss in the sector CA1 pyramidal layer was noticed. At this time, this sector contained 31% fewer pyramidal neurons than on the third day (P<0.05) and 58% fewer than in the control group (P<0.01). On the 14th day, neuronal loss in other hippocampal subdivisions also was observed. The pyramidal layer of sector CA3 contained 36% fewer neurons than in the control group (P<0.05), whereas the granular layer of the dentate gyrus contained 40% fewer (P<0.05). The total number of pyramidal neurons in sector CA2 remained unchanged. After the 14th day, no significant alterations in the total number of neurons were observed in any subdivision of the hippocampus until the 12th month of observation. Unbiased morphometric analysis emphasizes the exceptional susceptibility of sector CA1 pyramidal neurons to hypoxia/ischemia but also demonstrates significant neuronal loss in sector CA3 and the dentate granular layer, previously considered 'relatively resistant'. The different timing of neuronal dropout in sectors CA1 and CA3 and the dentate gyrus may implicate the existence of region-related properties, which determine earlier or later reactions to ischemia. However, the hippocampus has a unique, unidirectional system of intrinsic connections, whereby the majority of dentate granular neuron projections target the sector CA3 pyramidal neurons, which in turn project mostly to sector CA1. As a result, the early neuronal dropout in sector CA1 may result in retrograde transynaptic degeneration of neurons in other areas. The lack of neuronal loss in sector CA2 can be explained by the resistance of this sector to ischemia/hypoxia and the fact that this sector is not included in the major chain of intrahippocampal connections and hence is not affected by retrograde changes.

The retrograde axonal transport method was used to compare the topography and organization of the visual zone of the claustrum in rat, guinea pig, rabbit and cat. First, massive Fluoro-Gold injections were placed into the primary visual cortex and the secondary areas. Experiments showed differences in the location of the visual zone among the animals under study. In rat, the visual zone occupied the posteroventral part of the claustrum and spread to its anterior pole. In guinea pig, neurons projecting to the visual cortex were located dorsally in the posterior half of the claustrum. In rabbit, similarly to the rat, they were localized in the posteroventral part; however, they did not reach the anterior pole. In cat, neurons that project to the visual cortex were concentrated dorsally in the posterior fourth of the claustrum. In double-injection experiments, Fast Blue and Diamidino Yellow were placed into the primary and secondary visual areas in various combinations. The experiments showed that in the rat and the rabbit claustral neurons project to primary visual cortex (area 17) as well as to both secondary visual areas (areas 18a and b). Populations of neurons sending axons to the primary and secondary areas showed full overlap. The presence of double-labeled neurons indicates that some claustral neurons project both to the primary and secondary fields. In cat, neurons that project to the primary visual cortex appear to be clearly separated from those connected with the secondary visual area, as no double-labeled neurons were found. In all studied species, the double injections placed into the visual and primary somatosensory cortex did not result in any double-labeling neurons. Our results indicate that the location of the visual zone in the posterior part of the claustrum is a phylogenetically stable feature, whereas its dorsoventral shift as well as the extent toward the anterior pole is related to the particular species. The overlap of neurons projecting to the primary and secondary visual areas in the rat and rabbit as well as the separation of both projections in cat appear to reflect the higher degree of complexity of the visual system in the latter.

A characteristic feature of the parvopyramidal layer of the presubiculum of 6 individuals with Alzheimer disease (AD) was the presence of large, evenly distributed amyloid-beta (A beta) deposits, which in the end stage of the disease occupy 80.9 +/- 12.2% of the parvopyramidal layer. The strong reaction of A beta deposits with antibodies 4G8 (17-24 amino acids, aa), 6E10 (1-17 aa), and R165 (32-42 aa), and their weak reaction with antibody R162 (32-40 aa) indicate that potentially highly fibrillogenic A beta1-42 is a major constituent of presubicular amyloid. However, A beta deposits in the presubiculum are thioflavin-S- and Congo red-negative--and thus, nonfibrillar--even after 11 to 19 years of AD. The unique properties of presubicular amyloid appear to be related to their origin; amyloid-associated proteins such as apolipoproteins E, and AI, alpha1-antichymotrypsin, and heparan sulfate proteoglycan, which are promoters of fibrillization or stabilizers of A beta in neuritic plaques, are absent; activated astrocytes, which are the source of these proteins, are also absent. The unchanged number and distribution and the resting appearance of microglial cells revealed with RCA-I histochemistry suggest that they do not respond to diffuse A beta deposits. The source of nonfibrillar presubicular A beta is probably local neurons or neuronal projections to the parvocellular layer of the presubiculum. Neuronal, lake-like A beta deposition appears to be characteristic of AD pathology. The presubiculum is most likely the model brain structure for the study of amyloid of exclusively neuronal origin. The parvopyramidal layer of the presubiculum reveals only a small population of the neurons (2.5 +/- 2%) affected by neurofibrillary pathology.

Methods of retrograde axonal transport were employed to evaluate the topography and overlap of claustroneocortical connections in the rat. Fluorescent tracers Fast Blue (FB) and Diamidino Yellow (DY) were injected simultaneously in various combinations into the motor, somatosensory, auditory and visual cortical areas. Experiments showed that claustroneocortical projections are organized in two main cortico-related zones: sensorimotor and visuoauditory. The sensorimotor zone occupies the anterodorsal part whereas the visuoauditory occupies the posteroventral part of the claustrum. Between these two main zones only a scanty overlap was observed. In the sensorimotor zone a large overlap between neurons projecting to the motor and somatosensory cortical areas exists. The visuoauditory zone is characterized by a full overlap of neuronal populations projecting to the visual and auditory areas.

The morphology of claustral neurons projecting to the motor, somatosensory, auditory and visual cortical areas in the rat was analyzed by means of combination of axonal retrograde transport and morphometric analysis. Fluoro-Gold (FG) injections placed into various cortical fields resulted in labeling in the claustrum four neuronal types: pyramidal with thick main dendrite, oval with a few thin dendrites spreading out in various directions, fusiform possessing two main dendrites arising from opposite poles of the cell body and polygonal. Pyramidal neurons prevailed in populations of neurons projecting to the motor cortex of the contralateral hemisphere. Oval neurons outnumbered other types in populations projecting to the somatosensory, auditory and visual cortical fields. The number of fusiform and polygonal neurons did not exceed at 12.5% together in any populations. Neurons projecting to the contralateral hemisphere were the largest claustral neurons (mean cross-section are 167.19 +/- 2.9 micron 2) whereas neurons projecting to the motor cortex where the largest claustral neurons projecting ipsilaterally (141.89 +/- 2.22 micron 2). There was no significant difference between neurons projecting to the somatosensory (113.46 +/- 1.9 micron 2) cortex and to the visual (111.8 +/- 1.4 micron 2) cortex whereas neurons related to the auditory are (95.98 +/- 1.75 micron 2) were the smallest claustral neurons. These observations pointed out that the morphology of claustral neurons is closely related to a cortical area to which they send axons.