Poor correlation between delayed neuronal death induced by transient forebrain ischemia,and immunoreactivity for parvalbumin and calbindin D-28k in developing gerbil hippocampus

In the normal developing hippocampus of the gerbil, parvalbumin-immunoreactive neurons first appear in the stratum pyramidale of CA3 at postnatal day 15 (P15), and in CA2 and hilus of the dentate gyrus from P21 onwards. Immunoreactive terminals also follow the same sequence from CA3 to CA1 to reach adult patterns by the end of the 1st month. Calbindin D-28k immunoreactivity is seen in the external part of the upper blade of the dentate gyrus at P5, and progresses to the granule cell and molecular layers of the whole gyrus by P15, except for a thin band of immature cells located at the base of the granule cell layer which are calbindin negative. Calbindin immunoreactivity in mossy fibers progresses from the external to the hilar region of CA3 during the same period. A few immunoreactive cells are also found in the stratum radiatum/lacunare of the CA3, but no calbindin-immunoreactive cells are observed in the CA1 and CA2 subfields. The adult pattern of calbindin immunoreactivity is reached at P21. Vulnerability following transient forebrain ischemia for 20 min was examined in the hippocampal formation of gerbils during postnatal development. No cellular damage was seen in animals aged 7 days. Dying cells were observed at the base of the granule cell layer of the dentate gyrus in animals aged 15, 21 and 30 days. Pyramidal cells in the CA3 subfield were also sensitive to ischemia in gerbils aged 15 days, and less frequently in animals aged 21 days. The adult pattern of cellular damage, characterized by selective vulnerability of the CA1 subfield, was seen from day 30 onwards. These findings show that the pattern of selective vulnerability following transient forebrain ischemia is different in young and adult gerbils, and suggest that little, if any, correlation exists between resistance to delayed cellular damage and parvalbumin and calbindin D-28k content in the hippocampus of young gerbils.Supported in part by grant FIS 93-131 and a grant from the Fundacio Pi i Synyer (to A.T.)     

Co-expression of VRL-1 and calbindin D-28k in the rat sensory ganglia

The co-expression of vanilloid receptor 1-like receptor (VRL-1), a newly cloned capsaicin-receptor homologue, with calbindin D-28k was examined in the rat sensory ganglia. The co-expression was rare in the dorsal root, trigeminal and jugular ganglia and abundant in the petrosal and nodose ganglia. In the dorsal root ganglion, none of VRL-1-immunoreactive (ir) neuron co-expressed calbindin D-28k-immunoreactivity (ir). Of the VRL-1-ir neurons, 9 and 5% showed calbindin D-28k ir in the trigeminal and jugular ganglia, respectively. On the other hand, 35 and 63% of VRL-1-ir neurons in the petrosal and nodose ganglia, respectively, co-expressed these substances. The retrograde tracing method indicated that petrosal neurons which co-expressed VRL-1-and calbindin D-28k-ir innervated taste buds in the circumvallate papilla. The present findings may suggest that VRL-1 is associated with chemosensory functions in visceral sensory neurons.     

Calretinin and calbindin D-28k delay the onset of cell death after excitotoxic stimulation in transfected P19 cells

In some neurological diseases, injury to neurones reflects an over-stimulation of their receptors for excitatory amino acids. This response may disturb the Ca(2+)-homeostasis and lead to a pronounced and sustained increase in the intracellular concentration of this ion. On the basis of data derived from correlative studies, calcium-binding proteins have been postulated to play a protective role in these pathologies. We tested, directly, the capacity of the three calcium-binding proteins calretinin (CR), calbindin D-28k (CB) and parvalbumin (PV) to buffer [Ca(2+)], and to protect cells against excitotoxic death. We used P19 murine embryonic carcinoma cells, which can be specifically induced (by retinoic acid) to transform into nerve-like ones. The differentiated cells express functional glutamate-receptors and are susceptible to excitotoxic shock. Undifferentiated P19-cells were stably transfected with the cDNA for CR, CB or PV, induced to differentiate, and then exposed to NMDA, a glutamate-receptor agonist. The survival rates of clones expressing CR, CB or PV were compared with those of untransfected P19-cells using the lactate-dehydrogenase assay. CR- and CB-expressing cells were protected from death during the first 2 h of exposure to NMDA. This protection was, however, transient, and did not suffice to rescue P19-cells after prolonged stimulation. Two of the three PV-transfected clones raised were vulnerable to NMDA-induced excitotoxicity; the third, which expressed the lowest level of PV, was protected to a similar degree as that found for the CR- and CB-transfected clones. Our results indicate that in the P19-cell model, CR and CB can help to delay the onset of cell death after excitotoxic stimulation.     

Parvalbumin and calbindin D-28k immunoreactivity in transgenic mice with a G93A mutant SOD1 gene

Immunohistochemical study was performed to examine if calcium-binding proteins are involved in the degeneration of motor neurons in the brain stems and the spinal cords of transgenic mice carrying a G93A mutant human SOD1 gene. Specimens from age-matched non-transgenic wild-type mice served as controls. In the spinal cord of the controls, the density of parvalbumin-immunoreactive neurons was highest in the large anterior horn neurons and lower in the posterior horn neurons in the spinal cord. On the other hand, calbindin D-28k immunoreactivity was much less apparent than that observed with parvalbumin antisera. Rexed's lamina II was densely immunostained for calbindin D-28k, whereas, in the anterior horn, calbindin-D-28k-positive small neurons were barely dispersed in a scattered pattern. In transgenic mice, parvalbumin-positive anterior horn neurons were severely reduced, even at the presymptomatic stage, whereas calbindin-positive neurons were largely preserved. At the symptomatic stage, both parvalbumin and calbindin D-28k immunoreactivity markedly diminished or disappeared in the anterior horn. Immunoblotting analysis revealed a significant reduction of immunoreactivity to parvalbumin antibody in transgenic mice compared with the controls. In the brain stem, parvalbumin-positive oculomotor and abducens neurons and the calbindin D-28k-positive sixth nucleus were well-preserved in transgenic mice as well as in the controls. Thus, the diffuse and severe loss of parvalbumin immunoreactivity of large motor neurons even at early stages in SOD1-transgenic mice and the absence of calbindin D-28k immunoreactivity of normal large motor neurons suggest that these calcium-binding proteins may contribute to selective vulnerability and an early loss of function of large motor neurons in this SOD1-transgenic mouse model.     

Prenatal development of calbindin D-28K and parvalbumin immunoreactivities in the human retina

Two calcium binding proteins, calbindin D-28K (CB) and parvalbumin (PV), immunoreactivities were examined by immunocytochemistry in the retinas of human fetuses aged from 13 weeks (W) of gestation to term. CB- and PV-immunoreactive products were both detectable at 13 W and appeared in all layers in a roughly inside-out order by 24 W. PV-immunostaining occurred in virtually all ganglion cells, most horizontal cells, and a few amacrine cells. CB-immunoreactivity was found in most amacrine cells and some horizontal cells, and a subset of cells in the ganglion cell layer that were more frequent in the nasal than the temporal retina at 13–15 W. Bipolar cells were distinctly immunostained for CB by 24 W. Foveal cones showed faint CB labeling by 24 W and intense staining at 32 W. The patterns of CB- and PV-immunoreactivities by birth were similar to those at 32 W with the addition of faint CB-immunolabeling occurring beyond the fovea in the photoreceptors. A stronger expression of CB was seen in the nasal side of the optic nerve head from 13–24 W, peaking at 15 W. The results indicate that CB and PV expression in ganglion cells and inner nuclear layer neurons proceeds in parallel with their somal and process differentiation, suggesting a possible role for these proteins in neuronal maturation. The early expression of PV and CB in ganglion cell axons might be related to optic nerve outgrowth, including path-finding at the optic chiasm. CB expression in cones and other cells in the fovea may indicate that it is involved in foveal formation that occurs during the perinatal period. J Comp Neurol 377:565–576, 1997. © 1997 Wiley-Liss, Inc.     

Coexistence of calbindin D-28k and NADPH-diaphorase in vagal and glossopharyngeal sensory neurons of the rat

The presence and coexistence of calbindin D-28k-immunoreactivity (ir) and nicotinamide adenosine dinucleotide phosphate (NADPH)-diaphorase activity (a marker of neurons that are presumed to convert L-arginine to L-citrulline and nitric oxide) were examined in the glossopharyngeal and vagal sensory ganglia (jugular, petrosal and nodose ganglia) of the rat. Calbindin D-28k-ir nerve cells were found in moderate and large numbers in the petrosal and nodose ganglia, respectively. Some calbindin D-28k-ir nerve cells were also observed in the jugular ganglion. NADPH-diaphorase positive nerve cells were localized to the jugular and nodose ganglia and were rare in the petrosal ganglion. A considerable portion (33–51%) of the NADPH-diaphorase positive neurons in these ganglia colocalized calbindin D-28k-ir. The presence and colocalization of calbindin D-28k-ir and NADPH-diaphorase activity in neurotransmitter-identified subpopulations of visceral sensory neurons were also studied. In all three ganglia, calcitonin gene-related peptide (CGRP)-ir was present in many NADPH-diaphorase positive neurons, a subset of which also contained calbindin D-28k-ir. In the nodose ganglion, many (42%) of tyrosine hydroxylase (TH)-ir neurons also contained NADPH diaphorase activity but did not contain calbindin D-28k-ir. These data are consistent with a potential co-operative role for calbindin D-28k and NADPH-diaphorase in the functions of a subpopulation of vagal and glossopharyngeal sensory neurons.     

大鼠脑干内的calbindin D-28K可能参与内脏伤害性信息传递或调控的形态学研究

为研究calbindin D-28K(CB)是否与内脏伤害性信息的传递或调控有关,应用免疫组织化学双重标记技术,对给予内脏伤害性刺激后大鼠脑干内表达Fos蛋白的CB免疫阳性神经元分布进行了观察.结果显示:在孤束核(NTS)、延髓腹外侧区(VLM)、蓝斑(LC)、臂旁外侧核(LPB)、中脑导水管周围灰质腹外侧区(vlPAG)等核团内均可见Fos/CB双标记神经元.双标记神经元分别占上述核团内Fos蛋白免疫阳性神经元数量的比例为12.8%,42.7%,48.1%,14.0%和13.9%;占CB免疫标记阳性神经元数量的比例为14.3%,24.3%,38.4%,6.8%和8.9%.研究结果提示,CB可能参与脑干内内脏伤害性信息的传递或调控.     

Chronological alterations of calbindin D-28k immunoreactivity in the gerbil main olfactory bulb after ischemic insult

We investigated spatial and temporal alterations of calbindin D-28k (CB) immunoreactivity in the gerbil main olfactory bulb after transient ischemia-reperfusion. In sham-operated animals, CB-immunoreactive (IR) neurons were found in the periglomerular layer, external plexiform layer and granule cell layer. At 1-4 days after ischemic insult, the number of CB-IR neurons significantly increased. This result suggests that the increased CB may buffer the intracellular calcium at an early time point after the ischemic insult. In contrast, 10-30 days after the ischemic insult, the number of CB-IR neurons significantly decreased as compared to sham-operated animals. This result suggests that a malfunction in olfactory process may have occurred in the olfactory bulb at a later time point after the ischemic insult.     

Relationship of calbindin D-28k and cholinergic neurons in the nucleus basalis of Meynert of the monkey and the rat

Double-labeling immunocytochemistry reactions were carried out in the monkey and the rat nucleus basalis of Meynert (NBM) to determine the extent of overlap between cholinergic neurons and neurons immunoreactive for calbindin-D-28k (CaBP), a Vitamin D-dependent calcium binding protein. The results indicate that most, but not all, NBM cholinergic neurons in the monkey are immunoreactive for CaBP. On the other hand, none of the rat NBM cholinergic neurons are immunoreactive for CaBP.     

Expression of calbindin-D28k and parvalbumin during development of rat’s basolateral amygdaloid complex

Parvalbumin and calbindin-D28k are calcium-binding proteins, which are considered to be markers for certain populations of GABAergic neurons. Their correct development in the basolateral amygdaloid complex is critical for the proper emotional functioning in adult live of human and animals. Therefore, in this paper we describe the pattern of the morphological differentiation and distribution of immunoreactive elements of the parvalbumin and calbindin-D28k in this complex on the basis of immunohistochemically stained material obtained from embryonic (E20) and postnatal (P0-P90) rat brains. Calbindin-D28k appeared early in the development, already in the prenatal life. At this time immunopositive reaction was visible only in cell bodies. However, during development the population of immunopositive neurons was divided into four types: (1) polygonal; (2) piriform-like; (3) bipolar; and (4) pyramidal-like. Two weeks after birth calbindin-D28k immunoreactivity also appeared in neuropil. First, there were visible calbindin-D28k positive fibers and granules that encircled unstained cell bodies and formed basket-like structures. Subsequently, these granules appeared along proximal parts of unstained dendrites forming, so called 'cartridges'. The distribution of calbindin-D28k positive cells during postnatal life was rather homogenous throughout whole basolateral complex. Intensity of calbindin-D28k immunoreactivity reached mature level on the 21st day after birth.The maturation pattern of parvalbumin immunopositive elements followed the same sequence as calbindin-D28k, but it started much later - since the 17th day after birth and reached mature appearance on the 30th day of life. Contrary to calbindin-D28k, parvalbumin was not homogeneously distributed in the basolateral complex. Originally, parvalbumin was restricted to the magnocellular part of basolateral nucleus but it was finally expressed also in the parvicellular part of basolateral nucleus and the dorsolateral part of lateral nucleus. The differences in development of these two calcium-binding proteins indicate that parvalbumin and calbindin-D28k play diverse roles during development and maturation of the basolateral amygdala.     

Partial coexistence of neuropeptide Y and calbindin D28k in the trigeminal ganglion following peripheral axotomy of the inferior alveolar nerve in the rat

Immunohistochemistry was applied to examine the correlation between neuropeptide Y (NPY) and the two calcium binding proteins (CaBPs) parvalbumin (PV) and calbindin D28k (CB) in the trigeminal ganglion following peripheral axotomy of the inferior alveolar nerve (IAN) in the rat. Five days following transection and application of FluoroGold (FG) to the cut end of the IAN, approximately 14.8% (80/539) and 18.6% (90/483) of FG-labeled IAN neurons in the trigeminal ganglion showed PV-like immunoreactivity (-LI) and CB-LI, respectively. The mean ± S.D. area of FG-labeled PV-like immunoreactive (-IR) cells (FG/PV-IR cells) and FG/CB-IR cells were 835.9 ± 303.1 μm² and 712.7 ± 246.0 μm², respectively. FG/PV-IR cells were significantly larger than FG/CB-IR cells. Fourteen days following peripheral axotomy of the IAN, NPY-LI appeared in the medium- to large-sized cells. Double immunostaining revealed that approximately 3.3% (52/1569) of NPY-IR cells in the axotomized trigeminal ganglion displayed PV-LI, while approximately 26.7% (371/1392) of NPY-IR cells displayed CB-LI. The mean ± S.D. cross-sectional areas of PV-IR and CB-IR trigeminal ganglion cells displaying NPY-LI were 819.5 ± 265.6 μm² and 766.5 ± 279.7 μm², respectively. There were no significant differences in the cross-sectional areas either between NPY/PV-IR cells and NPY/CB-IR cells, or between FG/PV-IR cells and NPY/PV-IR cells, or between FG/CB-IR cells and NPY/CB-IR cells. The present results indicate that injury-evoked medium- to large-sized NPY neurons were a different population from large-sized PV neurons, and NPY was partly co-localized with CB.     

Distribution of parvalbumin immunoreactivity in the cat diencephalon

The distribution of parvalbumin-immunoreactive cell bodies and fibers in the cat diencephalon has been analyzed by using the avidin-biotin innmunoperoxidase technique. The thalamus showed a higher density of immunoreactive cell bodies than the hypothalamus. A. high or moderate density of perikarya and a high density of fibers containing parvalbumin was observed in the nuclei lateralis posterior, lateralis dorsalis, pulvinar, corpus geniculatum laterale, reticularis, medialis dorsalis, centrum medianum, subparafascicularis, ventralis postero-medialis, ventralis postero-lateralis, habenularis medialis, parafascicularis, corpus geniculaturn mediale, centralis lateralis, rhomboidens, reuniens, centraliis medialis, ventralis medialis, ventralis lateralis, parataenialis, anterior ventralis, anterior medialis, ventralis anterior, hypothalamus posterior, corpus mamillare, area hypothalamica dorsalis, and in the nucleus suprachiasmaticus. Moreover, a high or moderate density of immunoreactive fibers and a low density of parvalbumin-immunoreactive cell bodies was observed in the nuclei periventricularis anterior, anterior dorsalis, habenularis lateralis, corpus geniculatum laterale (pars ventralis), periventricularis hypothalami, hypothalamus lateralis, hypothalamus anterior, and in the hypothalamus dorsomedialis.     

Parvalbumin and calbindin D-28k in the entopeduncular nucleus,subthalamic nucleus,and substantia nigra of the rat as revealed by double-immunohistochemical methods

The cellular localization of calbindin D-28k (CB) and parvalbumin (PV) was analyzed by means of double-immunohistochemical techniques applied to single sections in the entopeduncular nucleus (EP), the subthalamic nucleus (STh), and the substantia nigra (SN) of the rat. In EP, PV-positive cells abounded centrally, where CB immunostaining was minimal. The medial and ventral sectors of EP were markedly enriched with CB neurophil but devoid of PV-positive cells. CB-positive neurons abounded particularly in the rostral pole of EP. In STh, PV-positive neurons and neuropil were concentrated in the lateral two thirds of this nucleus. Only a few PV-positive cells were detected in sectors of STh devoid of PV-positive neuropil. The STh was completely devoid of CB immunostaining. In the rostral two thirds of SN, PV-positive neurons were largely confined to the lateral half of the pars reticulata (SNR), and occurred more ventrally and medially in the caudal third. Intense CB-immunoreactive neuropil was found in medial and dorsal parts of rostral SNR, and CB-positive cells were observed in the SN pars compacta and the ventral tegmental area. PV and CB cells were also observed in the pars lateralis of SN. The markedly heterogeneous pattern of distribution of PV and CB in EP, STh, and SN suggests that these two calcium-binding proteins may label distinct functional domains in each of these three components of the rat basal ganglia. Synapse 25:359–367, 1997. © 1997 Wiley-Liss, Inc.     

Distribution of parvalbumin immunoreactivity in the cat brain stem

We studied the distribution of parvalbuminimmunoreactive cell bodies and fibers in the cat brain stem. A high or moderate density of perikarya containing parvalbumin was observed in the periaqueductal gray, interpeduncular nucleus, nucleus of the trapezoid body, superior and inferior colliculi, and in the substantia nigra. The nucleus ruber, cuneiform nucleus, preolivary nucleus, retrorubral nucleus, paracentral division of the tegmental reticular nucleus, central and lateral tegmental fields, and the pericentral division of the dorsal tegmental nucleus had the lowest density of immunoreactive cell bodies. Moreover, a high or moderate density of parvalbumin immunoreactive processes was visualized in the nucleus ruber, substantia nigra, superior and inferior colliculi, periaqueductal gray, nucleus sagulum, cuneiform nucleus, Kölliker-Fuse nucleus, nucleus of the trapezoid body, vestibular nuclei, dorsal motor nucleus of the vagus, and in the lateral reticular nucleus. Finally, a few immunoreactive fibers were observed in the pontine gray, nucleus coeruleus, marginal nucleus of the brachium conjunctivum, nucleus of the solitary tract, inferior olive, and in the tegmental fields.     

Distribution of neurons immunoreactive for calcium-binding proteins varies across areas of cat primary somatosensory cortex

The primary somatosensory (SI) cortex in the cat contains four cytoarchitectonic areas that appear to contain separate body representations and have different functions. We tested whether functional differences among these areas are reflected in the densities of neurons containing each of three calcium-binding proteins: parvalbumin (PV), calbindin (CB), and calretinin (CR). Colocalization experiments revealed that CR was localized in a population of neurons distinct from those containing PV or CB. The general laminar distributions of the three calcium-binding proteins were similar to those described in other species and cortical areas, but there were significant density differences in layers II and III across SI. The density of PV-immunoreactive neurons was higher in areas 3b and 1 than in areas 3a and 2. CB-immunoreactive neurons were found in higher densities in anterior SI than in posterior SI, and the pattern of CR-immunoreactive neurons was reciprocal to that of CB, with significantly higher densities in posterior regions of SI. Since the firing characteristics of nonpyramidal neurons appear to be related to their calcium-binding protein content, differences in regional distributions of these neurons in layers II and III may contribute to functional differences between the cytoarchitectonic areas of SI cortex.     

Postnatal development of parvalbumin and calbindin D-28k immunoreactivities in the canine anterior cingulate cortex: transient expression in layer V pyramidal cells

We have examined the ontogeny of parvalbumin (PV) and calbindin D-28k (CB) immunoreactivities in the canine anterior cingulate cortex (ACC) from the day of birth (P0) through P180. At P7, PV immunoreactivity first appeared in layer VI multipolar cells. The PV immunoreactivity in GABAergic nonpyramidal cells appeared to follow an inside-out gradient of radial emergence. Although immunoreaction was limited mainly to the developing nonpyramidal cells, pyramid-like PV immunoreactive cells were transitorily observed in layer V from P14 to P90. The developmental pattern of CB immunoreactivity differed from that of PV immunoreactivity. CB immunoreactivity first developed in layer V pyramidal cells from P0, which continued through P90. CB immunoreactive nonpyramidal cells were located in the infragranular layers and white matter at P0 and maturated in both the supragranular and infragranular layers without clear inside-out gradient.This developmental study revealed the comparable belated expression of PV immunoreactivity and the transient expression of both calcium-binding proteins in layer V pyramidal cells. These results suggest that the transient expression of calcium-binding proteins in layer V pyramidal cells might be related to the critical period of early postnatal development.     

Parvalbumin and calbindin D-28k in the human motor system and in motor neuron disease

Calbindin D-28k and parvalbumin are neuronal calcium binding proteins of interest in relation to neurodegenerative diseases. Expression of calbindin and parvalbumin may be one of the determinants of selective vulnerability in these disorders. The distribution of these proteins was surveyed in the normal human motor system and in motor neuron disease (MND) using immunocytochemistry in formalin fixed post-mortem tissues. CNS tissues from 14 MND patients (mean age 61.2 years, mean post-mortem delay 24.6 h) and seven controls (mean age 62.6 years, mean post-mortem delay 25.3 h) were studied. Preliminary studies on the effects of fixation were performed. In normal cases upper and lower motor neurons showed absent expression of both proteins.
Several neuronal groups characteristically spared in MND showed varying patterns of immunoreactivity: oculomotor neurons showed parvalbumin staining of the perikaryon; the thoracic preganglionic sympathetic neurons showed calbindin staining in perikarya, Onuf's nucleus showed calbindin staining in the neuropil only. In motor neuron disease a loss of ventral horn interneurons and calbindin immunoreactive processes was observed with no other disease related changes in the spinal cord, brainstem, or motor cortex. These findings are consistent with the hypothesis that the distribution of these proteins is one determinant of selective vulnerability to the neurodegenerative processes in MND acting via disturbance of neuronal calcium homeostasis.     

Colocalization of calbindin D-28k,calretinin, and GABA immunoreactivities in neurons of the human temporal cortex

The calcium-binding proteins calbindin D-28k (CalB) and calretinin (CalR) have been shown to be useful markers of neuronal subpopulations located mainly in layers II–III of the neocortex of a variety of species, including human. Double labeling immunocytochemical studies of CalB, CalR, and GABA in experimental animals have shown that CalB and CalR are present in separate subpopulations of neurons. However, there are no studies of colocalization of these calcium-binding proteins and GABA in the human neocortex. The principal goal of the present work was to investigate the degree of colocalization of these substances in layers II–III of the human temporal neocortex, using a postembedding immunocytochemical method. The patterns of staining for CalB, CalR, and GABA in the human cortex were similar to those found in monkey neocortex. However, the degree of colocalization for certain combinations was different from that reported in the monkey and other experimental animals. A relatively large proportion of CalB- and CalR-immunoreactive cells (approximately 71% and 74%, respectively) were found to be immunoreactive for GABA. However, the degree of colocalization of CalB with CalR was low (between 4% and 6%). Thus, our quantitative and qualitative data suggest that these calcium-binding proteins are present in similar cortical circuits in all primates, but that in the human neocortex, there might be additional GABAergic and perhaps also non-GABAergic interneurons with unique chemical characteristics. © 1996 Wiley-Liss, Inc.     

Parvalbumin and calbindin D-28 k immunoreactivity in dorsal root ganglia in acquired immunodeficiency syndrome

Various degrees of neuronal degeneration have been found in lumbosacral dorsal root ganglia of patients with acquired immunodeficiency syndrome (AIDS). To characterize the subpopulations of primary sensory neurons affected in AIDS. we immunostained dorsal root ganglion tissues from 11 AIDS patients and six controls using antibodies to the calcium binding proteins, parvalbumin and calbindin D-28 k. In controls, the proportion of neurons containing parvalbumin and calbindin was 18.0% and 22.4%, respectively. The majority of parvalbumin-positive neurons, which are thought to be proprioceptive neurons, were of medium to large size, while calbindin was found in both large- and small-sized neurons. The density of parvalbumin-immunoreactive neurons was reduced by 7.3% in AIDS patients, but the density of calbindin-immunoreactive neurons was preserved. Furthermore, in AIDS cases, the number of parvalbumin-positive neurons was reduced more in dorsal root ganglia in which human immunodeficiency virus (HIV) antigen was detected than in HIV-negative ganglia. These results suggest that specific subpopulations of sensory neurons positive for parvalbumin may be differentially affected over the course of AIDS, and that this could be related to peripheral neuropathy which frequently occurs in the late stages of AIDS.     

Two populations of calbindin D28k-immunoreactive neurones in the striatum of the rat

In order to examine the localisation of calbindin D28k in the normal striatum of the rat, immunocytochemistry using monoclonal antibodies was carried out at both the light and electron microscopic levels. As has previously been shown, many striatal spiny neurones were immunopositive, however, a small population of neurones with smooth dendrites and indented nuclei were also identified. At least some of these cells also displayed NADPH-diaphorase activity. These findings indicate that, in common with the primate striatum and grafted striatal tissue in the rat, the normal rat striatum contains at least two populations of neurones that express calbindin D28k.