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PubMed2002

Human cortical distal nephron: distribution of electrolyte and water transport pathways.

The exact distributions of the different salt transport systems along the human cortical distal nephron are unknown. Immunohistochemistry was performed on serial cryostat sections of healthy parts of tumor nephrectomized human kidneys to study the distributions in the distal convolution of the thiazide-sensitive Na-Cl cotransporter (NCC), the beta subunit of the amiloride-sensitive epithelial Na channel (ENaC), the vasopressin-sensitive water channel aquaporin 2 (AQP2), and aquaporin 3 (AQP3), the H(+) ATPase, the Na-Ca exchanger (NCX), plasma membrane calcium-ATPase, and calbindin-D28k (CaBP). The entire human distal convolution and the cortical collecting duct (CCD) display calbindin-D28k, although in variable amounts. Approximately 30% of the distal convolution profiles reveal NCC, characterizing the distal convoluted tubule. NCC overlaps with ENaC in a short portion at the end of the distal convoluted tubule. ENaC is displayed all along the connecting tubule (70% of the distal convolution) and the CCD. The major part of the connecting tubule and the CCD coexpress aquaporin 2 with ENaC. Intercalated cells, undetected in the first 20% of the distal convolution, were interspersed among the segment-specific cells of the remainder of the distal convolution, and of the CCD. The basolateral calcium extruding proteins, Na-Ca exchanger (NCX), and the plasma membrane Ca(2+)-ATPase were found all along the distal convolution, and, in contrast to other species, along the CCD, although in varying amounts. The knowledge regarding the precise distribution patterns of transport proteins in the human distal nephron and the knowledge regarding the differences from that in laboratory animals may be helpful for diagnostic purposes and may also help refine the therapeutic management of electrolyte disorders.

Aged↗
PubMed1994

A new histochemical double-stain method using three-dimensional analysis with confocal laser scanning microscopy.

We describe a new technique for immunohistochemical and enzyme-histochemical double staining using confocal laser scanning microscopy in the reflection mode. As an example, we investigated the immunoreactivity for Spot 35-calbindin-D28K, a vitamin D-dependent calcium binding protein, and the enzyme activity for Ca(2+)-ATPase in the rat kidney. The lead precipitation method for Ca(2+)-ATPase was initially used to process kidney slices. Each specimen was then dehydrated and embedded in a water soluble resin. Thin sections were cut from the resin block, and an indirect immunocolloidal gold method with silver enhancement for Spot 35-calbindin-D28K antigen was carried out on the glass slides. Results were then observed by confocal laser scanning microscopy in the reflection mode. The three-dimensional distribution of the reaction products was detected by serial optic slice images. Lead phosphate particles, which represented the location of Ca(2+)-ATPase, were distributed deep in the section. The most intense signals from the silver particles were detected from the surface slice of the section. A stereoscopic image generated from the serial optic slices clearly showed the differences in their distribution.

Animals↗
PubMed1999

Adult-generated neurons in the dentate gyrus send axonal projections to field CA3 and are surrounded by synaptic vesicles.

The subgranule zone of the dentate gyrus in rats has been shown to be proliferative into adulthood and senescence. However, the connectivity of newly generated, identified neurons in the adult has not been definitively described. In the present study, 9 weeks after a series of intraperitoneal injections of 5-bromo-2'-deoxyuridine (BrdU), animals received stereotaxic iontophoretic injections of Fluoro-Gold (FG) into field CA3. Three weeks after FG injections, sections were analyzed for BrdU immunoreactivity (proliferative label), FG retrograde label, and either calbindin-D28k or synaptophysin immunohistochemistry. A large proportion (up to 44%) of BrdU-labeled cells in the dentate gyrus within regions of FG retrograde label incorporated FG. All of the doubly labeled (BrdU-FG) neurons also immunolabeled with the antibody to calbindin-D28k. Many doubly labeled (BrdU-FG) cells were also surrounded in three planes by synaptophysin immunoreactivity. We conclude that newly generated neurons in the dentate gyrus have the correct immunohistochemical profile, send appropriate axonal projections to field CA3, and are surrounded by profiles containing synaptic vesicle proteins.

Animals↗
PubMed1999

Exacerbation of damage and altered NF-kappaB activation in mice lacking tumor necrosis factor receptors after traumatic brain injury.

Tumor necrosis factor alpha (TNFalpha) is widely expressed in both neurons and glia and has been shown to be upregulated after traumatic brain injury (TBI). TNFalpha receptor activation results in activation of the transcription factor nuclear factor kappaB (NF-kappaB), which may serve an antiapoptotic role via the induction of target genes manganese superoxide dismutase (MnSOD) and/or calbindin. In the present study, we used a controlled cortical impact model of TBI with pertinent lines of transgenic mice to combine both morphological characterization and molecular analysis to elucidate the role of TNFalpha after TBI. Measurements of both the lesion volume and the blood-brain barrier breach indicated exacerbations in mice rendered genetically deficient in both the p55 and p75 TNFalpha receptors (TNFR-KO) compared with wild-type animals. Additionally, animals genetically altered to overexpress MnSOD showed a significant decrease in lesion volume compared with that of control littermates, whereas no alterations were observed in mice lacking the calcium-binding protein calbindin D28k. Analysis of NF-kappaB activation and relative levels of MnSOD revealed delayed responses in the injured cortex of TNFR-KO animals compared with wild-type animals, implying that endogenous TNFalpha may be neuroprotective after TBI.

Animals↗
PubMed1998

[Neurotoxicity of antibody against motoneuron on cultured rat cortical neurons].

OBJECTIVE: In order to determine the role of antibody against motoneuron in the process of neuronal death. METHODS: Cultured rat cortical neurons growing in serum-free medium, were employed to observe the effects of antibody against motoneuron (anti-SMN) on the survival of these cultured neurons. RESULTS: (1) Exposure of the cultures in serum-free medium to anti-SMN with dilution of 1:50 results in death of 31%-41% of neurons for 24 hours incubation, 50%-67% for 48 hours and above 90% after 72 hours. The neurotoxicity induced by anti-SMN was accompanied by concentration-dependent release of lactate dehydrogenase into the culture medium. Cultures exposed to normal rat IgG as controls exhibited no such sign. (2) The cultured neurons exposed to anti-SMN (1:200) expressed markedly higher levels of immunoreactive Calbindin-D28k especially after 48 hours incubation with it. There was a reduction in the number of acetylcholinesterase-positive neurons compared to the normal control. CONCLUSIONS: The anti-SMN could directly initiate the process of cortical neuronal death and this effect was independent of complement. The alteration of Calbindin-D28k immunoreactivity implied that calcium may be involved in the neurotoxicity induced by anti-SMN.

Acetylcholinesterase↗
PubMed2002

Chemical coding and electrophysiology of enteric neurons expressing neurofilament 145 in guinea pig gastrointestinal tract.

Electrophysiologic recording and indirect immunofluorescence were combined to study localization of the medium-sized neurofilament 145 (NF145) component of the cytoskeleton in morphologically identified neurons in the myenteric and submucosal plexuses of the guinea pig enteric nervous system. Neuronal localization of chemical markers, including calbindin DK28, calretinin, nitric oxide synthase, choline-acetyltransferase, neuropeptide Y, serotonin, neurokinin 1 receptor protein, and somatostatin, was integrated with electrophysiologic and morphologic results for a more complete assessment. NF145 immunoreactivity (-IR) was present in ganglion cells with Dogiel type I morphology in the myenteric plexus of the stomach and small and large intestine. NF145-IR was not found in myenteric ganglion cells with Dogiel type II morphology. NF145-IR was not present in any of the ganglion cells in the submucosal plexus. NF145 was expressed in nerve fibers in both myenteric and submucosal plexuses. The majority of these fibers were identified as sympathetic postganglionic axons based on their disappearance in organotypic culture and on their expression of tyrosine hydroxylase. The myenteric ganglion cells with NF145-IR had electrophysiologic properties of S-type enteric neurons. NF145-IR was found in neurons with vasoactive intestinal peptide, serotonin, nitric oxide synthase, somatostatin, and neurokinin 1 receptor but not with neuropeptide Y or calbindin. The results in general suggest that NF145 is localized to distinct subsets of myenteric motor neurons and interneurons. Absence of NF145 from ganglion cells in the submucosal plexus is an example of differences between myenteric and submucosal components of the enteric nervous system.

Action Potentials↗
PubMed1992

GABAergic septal and serotonergic median raphe afferents preferentially innervate inhibitory interneurons in the hippocampus and dentate gyrus.

Postsynaptic targets of the GABAergic septohippocampal and the serotonergic raphe-hippocampal pathways were studied using anterograde tracing with Phaseolus vulgaris leucoagglutinin combined with pre- and postembedding immunocytochemistry in the rat. Two types of afferents were labeled in the hippocampus and dentate gyrus from the medial septum-diagonal band of Broca complex, one with large diameter varicosities and another with smaller terminals. The former type was shown to be immunoreactive for gamma-aminobutyric acid (GABA), and to innervate predominantly GABA-immunoreactive interneurons. Subsequently, these target interneurons were demonstrated to include all subpopulations of GABAergic cells which could be visualized by antisera against parvalbumin, calbindin D28k, calretinin, cholecystokinin, somatostatin, neuropeptide Y and vasoactive intestinal polypeptide. These types of interneurons have different afferent and efferent connections, and thus participate in different inhibitory processes in the hippocampal formation. The other subcortical pathway, the serotonergic projection from the median raphe nucleus, was also shown to establish synapses predominantly with GABAergic interneurons both in the hippocampus and in the dentate gyrus. In contrast to the septohippocampal projection, this pathway did not innervate all types of GABAergic neurons. They selected a particular subpopulation, i.e. those which contain calbindin D28k, and ignored those which contained parvalbumin or the other neurochemical markers. This suggests a strong functional specialization among local inhibitory circuits, as well as among the subcortical afferents originating in the septum and raphe. These findings suggest that a mechanism by which numerically small afferent pathways may have a profound global effect on the electrical activity of the hippocampal formation is the selective innervation of local interneurons. These GABAergic inhibitory cells, in turn, control the activity of large populations of principal cells. The level of GABAergic inhibition determines the degree of population synchrony and influences N-methyl-D-aspartate receptor-mediated epileptiform burst-firing. Thus, the specific subcortical modulation of hippocampal inhibitory circuits may also have fundamental implications for epileptogenesis.

Afferent Pathways↗
PubMed1997

Combinations of AMPA receptor subunit expression in individual cortical neurons correlate with expression of specific calcium-binding proteins.

The functional properties of AMPA-type glutamate receptors are determined by their subunit composition. We detected the expression of the AMPA receptor subunits (GluR1-GluR4) in neurons in the somatosensory cortex of adult rats by combining nonradioactive in situ hybridization using digoxigenin-labeled RNA probes of GluR1 and GluR2 with immunocytochemistry using specific antibodies against GluR1, GluR2/3, and GluR4. On the basis of differential expression of the GluR1 and GluR2 subunits, we classified the cortical neurons into four categories. To correlate the differential expression of AMPA receptor subunits in each neuron with that of two calcium-binding proteins, parvalbumin and calbindin-D28k, we used a triple-labeling method. The majority of cortical neurons ( approximately 2/3) showed expression of GluR2 and undetectable expression of GluR1. GluR1-/GluR2-expressing neurons and GluR1-expressing/GluR2-undetectable neurons comprised approximately 1/10 each. Regarding the morphology, most GluR1-undetectable/GluR2-expressing neurons were pyramidal cells in layers II/III, V, and VI, whereas most GluR1-expressing/GluR2-undetectable neurons were nonpyramidal cells in layers II-VI. The GluR1-/GluR2-expressing neurons were either pyramidal or nonpyramidal. The majority of GluR1-/GluR2-expressing nonpyramidal cells was intensely stained with monoclonal antibody against calbindin-D28k, and one-half of the GluR1-undetectable/GluR2-expressing pyramidal neurons in layer II/III were lightly stained with this antibody. Most of GluR1-expressing/GluR2-undetectable neurons possessed parvalbumin immunoreactivity. These results indicate that neurons in the rat somatosensory cortex express differential combinations of GluR subunits, which correlate with the specific expression of the calcium-binding proteins.

Animals↗
PubMed1998

Nicotinic receptor-induced apoptotic cell death of hippocampal progenitor cells.

Nicotine has many effects on CNS functions, presumably through its action on neuronal nicotinic acetylcholine receptors (AChRs). One subclass of AChRs that binds the snake venom toxin alpha-bungarotoxin (alpha-Bgt-AChRs) has been shown to modulate neurotransmission in the brain. We now show that alpha-Bgt-AChR activation by low doses of nicotine results in apoptotic cell death of both primary and immortalized hippocampal progenitor cells. In HC2S2-immortalized hippocampal progenitors, nicotine is cytotoxic to undifferentiated cells, whereas it spares the same cells once differentiation has been induced. The activation of alpha-Bgt-AChRs by nicotine results in the induction of the tumor suppressor protein p53 and the cdk inhibitor p21. The cytotoxic effect of nicotine is dependent on extracellular calcium levels and is probably attributable to the poor ability of undifferentiated progenitors to buffer calcium loads. The major calcium buffer in these cells, calbindin D28K, is present only after differentiation has been induced. Furthermore transfection of undifferentiated cells with calbindin results in dramatic protection against the cytotoxic effects of nicotine. These results show that nicotine abuse could have significant effects on the survival of progenitor populations in the developing and adult brain and also suggest an endogenous role for alpha-Bgt-AChRs in neuronal development and differentiation.

Animals↗
PubMed1998

Olfactory bulb development is altered in small-eye (Sey) mice.

Small-eye (Sey) is a spontaneous, semidominant murine mutation that results from a point mutation in the Pax-6 gene. Both the eyes and the olfactory system fail to develop in homozygotes and these animals die neonatally. Heterozygotes (Sey/+) have different degrees of eye abnormalities including decreased lens size and cataracts. In the present study, we examined whether one mutated allele of Pax-6 also affects olfactory system development. By 42 days of age, main olfactory bulb volume was significantly decreased in Sey/+ animals compared with wild-type littermates, and this effect was even more dramatic in 70-day-old animals. In contrast, there was no effect on accessory olfactory bulb, olfactory epithelial, or vomeronasal organ development at any age in Sey/+ animals, demonstrating the specificity of the effect. In the main olfactory bulb, the largest differences in laminar volume were found in the glomerular and granule cell layers. These layers contain the olfactory bulb interneurons, and a subpopulation of these cells were found to be Pax-6 immunoreactive. Examination of the neurochemical consequences of this mutation showed that the number of both tyrosine hydroxylase (TH)- and gamma-aminobutyric acid (GABA)-immunoreactive profiles were dramatically decreased in Sey/+ animals as compared with controls. In contrast, neither calretinin nor calbindin immunoreactivity was affected by this mutation. Dual-labeling immunohistochemistry showed that nearly all TH-immunoreactive cells and a subpopulation of GABA-immunoreactive cells coexpressed Pax-6. However, calretinin- and calbindin-immunoreactive cells were not Pax-6 immunopositive. These data indicate that two normal alleles of Pax-6 are required for normal olfactory bulb development and, as part of this effect, this gene may be involved in the development of specific neurotransmitter systems.

Aging↗
PubMed1996

Ventral striatopallidothalamic projection: IV. Relative involvements of neurochemically distinct subterritories in the ventral pallidum and adjacent parts of the rostroventral forebrain.

Retrograde and anterograde tract-tracing studies were carried out to determine whether the capacity of the nucleus accumbens to influence the thalamic mediodorsal nucleus via ventral striatopallidothalamic connections disproportionately favors the shell over the core subterritory. After injections of Fluoro-Gold into the mediodorsal thalamic nucleus, retrogradely labeled neurons were detected in sections also processed for calbindin-D 28-kD and neurotensin immunoreactivities to facilitate identification of subterritories in the ventral pallidum. Fluoro-Gold-labeled cells were counted in series of sections cut through the ventral pallidum, rostral globus pallidus, nucleus of the vertical limb of the diagonal band, preoptic region, lateral hypothalamus, and the sublenticular gray region, including parts of the extended amygdala. Data were expressed as cells/unit area and as percentages of all labeled forebrain cells. Mediodorsal nucleus-projecting rostroventral forebrain neurons were most numerous in the ventromedial part of the subcommissural ventral pallidum and pallidal parts of the olfactory tubercle. Few were observed in the dorsolateral part of the subcommissural ventral pallidum. In addition, following injections into the ventral pallidum, anterogradely transported biotinylated dextran amine was evaluated in sections processed for calbindin or tyrosine hydroxylase immunoreactivities. Injection into the ventromedial part of the subcommissural ventral pallidum resulted in robust anterograde labeling of the medial segment of the mediodorsal nucleus and ventral tegmental area and weak labeling of the substantia nigra and subthalamic nucleus. Conversely, after injection into the dorsolateral part of the subcommissural ventral pallidum, anterograde labeling was weak in the mediodorsal nucleus and ventral tegmental area, but robust in the substantia nigra and subthalamic nucleus. The results are consistent with a predominant accumbens shell influence on the mediodorsal nucleus and with cortico-ventral striatopallidal-thalamocortical pathways that begin and end in different parts of the frontal lobe.

Amines↗
PubMed2000

Neurochemical and connectional organization of the dorsal pulvinar complex in monkeys.

To investigate the organization of the dorsal pulvinar complex, patterns of neurochemical staining were correlated with cortico-pulvinar connections in macaques (Macaca mulatta). Three major neurochemical subdivisions of the dorsal pulvinar were identified by acetylcholinesterase (AChE) histochemistry, as well as immunostaining for calbindin-D(28K) and parvalbumin. The dorsal lateral pulvinar nucleus (PLd) was defined on histochemical criteria as a distinct AChE- and parvalbumin-dense, calbindin-poor wedge that was found to continue caudally along the dorsolateral edge of the pulvinar to within 1 mm of its caudal pole. The ventromedial border of neurochemical PLd with the rest of the dorsal pulvinar, termed the medial pulvinar (PM), was sharply defined. Overall, PM was lighter than PLd for AChE and parvalbumin and displayed lateral (PMl) and medial (PMm) histochemical divisions. PMm contained a central "oval" (PMm-c) that stained darker for AChE and parvalbumin than the surrounding region. The neurochemically defined PLd was labeled by tracer injections in the inferior parietal lobule (IPL) and dorsolateral prefrontal cortex but not the superior temporal gyrus (STG). Label within PMl was found after prefrontal and IPL and, to a lesser extent, after STG injections. The PMm was labeled after injections of the IPL and STG, but only sparsely following prefrontal injections. The histochemically distinct subregion or module of PMm, PMm-c, was labeled only by STG injections. Overlapping labeling was found in dorsal pulvinar divisions PMl and PLd following paired IPL/prefrontal, but not IPL/STG or these particular STG/prefrontal, injections. Thus, PLd may be a visuospatially related region whereas PM appears to contain several types of territories, some related to visual or auditory inputs, and others that receive directly converging input from posterior parietal and prefrontal cortex and may participate in a distributed cortical network concerned with visuospatial functions.

Acetylcholinesterase↗
PubMed2000

Visual cortical projections and chemoarchitecture of macaque monkey pulvinar.

We investigated the patterns of projections from the pulvinar to visual areas V1, V2, V4, and MT, and their relationships to pulvinar subdivisions based on patterns of calbindin (CB) immunostaining and estimates of visual field maps (P(1), P(2) and P(3)). Multiple retrograde tracers were placed into V1, V2, V4, and/or MT in 11 adult macaque monkeys. The inferior pulvinar (PI) was subdivided into medial (PI(M)), posterior (PI(P)), central medial (PI(CM)), and central lateral (PI(CL)) regions, confirming earlier CB studies. The P(1) map includes PI(CL) and the ventromedial portion of the lateral pulvinar (PL), P(2) is found in ventrolateral PL, and P(3) includes PI(P), PI(M), and PI(CM). Projections to areas V1 and V2 were found to be overlapping in P(1) and P(2), but those from P(2) to V2 were denser than those to V1. V2 also received light projections from PI(CM) and, less reliably, from PI(M). Neurons projecting to V4 and MT were more abundant than those projecting to V1 and V2. Those projecting to V4 were observed in P(1), densely in P(2), and also in PI(CM) and PI(P) of P(3). Those projecting to MT were found in P(1)- P(3), with the heaviest projection from P(3). Projections from P(3) to MT and V4 were mainly interdigitated, with the densest to MT arising from PI(M) and the densest to V4 arising from PI(P) and PI(CM). Because the calbindin-rich and -poor regions of P(3) corresponded to differential patterns of cortical connectivity, the results suggest that CB may further delineate functional subdivisions in the pulvinar.

Animals↗
PubMed2000

Age-related resistance to alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid-induced hippocampal lesion.

This study compares the effects of acute alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) administration in the hippocampus in adult (3 months) and middle-aged (15 months) rats at 15 days postinjection. Injection of 1 and 2.7 mM AMPA produced dose-dependent neurodegeneration, assessed by Nissl staining; a glial reaction shown by glial fibrillary acidic protein immunocytochemistry; and calcification, revealed by alizarin red staining. Furthermore, at both doses, these alterations were significantly greater in 3-month-old rats. Finally, at AMPA 2.7 mM, no significant changes in the density of hippocampal parvalbumin- or calbindin-immunoreactive neurons or in choline acetyltransferase, glutamate uptake, or GABA uptake activities were found in 15-month-old animals, whereas significant reductions in parvalbumin (-76%) and calbindin (-32%) immunostaining and in GABA uptake (-27%) were observed in 3-month-old animals compared to the respective sham-operated or control animals. In conclusion, this study clearly demonstrates that in rats the vulnerability of hippocampal neurons and the glial and calcification reactions to AMPA-induced injury decreased with age between 3 and 15 months. Our results also indicate that hippocampal cholinergic, glutamatergic, and GABAergic systems show an adaptive response to excitotoxic damage in both adult and middle-aged animals.

Aging↗
PubMed2000

Altered expression of calcium- and apoptosis-regulating proteins in multiple system atrophy Purkinje cells.

The expression patterns of the calcium binding proteins calbindin and parvalbumin and of the apoptosis modulating proteins Bcl-2, Bax, and Bcl-x were studied in the cerebellum of patients with multiple system atrophy (MSA). Calbindin and parvalbumin immunoreactivity was markedly decreased in MSA Purkinje cells whereas Bax and Bcl-x protein expression was increased. Bcl-2 expression was restricted to a subpopulation of granule neurons, but no decrease of Bcl-2 was evident in MSA. Additional DNA end-labeling (ISEL) studies revealed only one possible apoptotic Purkinje cell nucleus, but nuclei in the cerebellar white matter, probably oligodendrocytes, in the cerebellum of patients with MSA. The present results suggest that a diminished calcium binding capacity of MSA Purkinje cells might lead to a change in the regulation of proteins of the bcl-2 family that could favor the pathologic initiation of apoptosis.

Apoptosis↗
PubMed1991

Electrostatic interactions in protein solution--a comparison between Poisson-Boltzmann and Monte Carlo calculations.

The accuracy of the Poisson-Boltzmann (PB) approximation and its linearized version is investigated by comparison to results obtained from Monte Carlo simulations. The dependence of the calcium binding constant of the protein calbindin as a function of salt concentration and mutation is used as a test case. The protein is modeled as a collection of charged and neutral spheres immersed in the electrolyte solution. The PB equation is solved using a finite difference technique on a grid in a spherical polar coordinate system, which is the preferred choice for a globular protein like calbindin. Both MC and PB give quantitative agreement with experimental results. The linearized PB equation is almost as accurate, but it becomes less reliable in systems with divalent ions. However, the linearized PB equation fails to describe the concentration profiles for cations and anions outside the protein even in a 1:1 salt solution.

Anions↗
PubMed2005

Expression of type 1 corticotropin-releasing factor receptor in the guinea pig enteric nervous system.

Reverse transcription-polymerase chain reaction (RT-PCR), immunohistochemistry, electrophysiological recording, and intraneuronal injection of the neuronal tracer biocytin were integrated in a study of the functional expression of corticotropin-releasing factor (CRF) receptors in the guinea pig enteric nervous system. RT-PCR revealed expression of CRF1 receptor mRNA, but not CRF2, in both myenteric and submucosal plexuses. Immunoreactivity for the CRF1 receptor was distributed widely in the myenteric plexus of the stomach and small and large intestine and in the submucosal plexus of the small and large intestine. CRF1 receptor immunoreactivity was coexpressed with calbindin, choline acetyltransferase, and substance P in the myenteric plexus. In the submucosal plexus, CRF1 receptor immunoreactivity was found in neurons that expressed calbindin, substance P, choline acetyltransferase, or neuropeptide Y. Application of CRF evoked slowly activating depolarizing responses associated with elevated excitability in both myenteric and submucosal neurons. Histological analysis of biocytin-filled neurons revealed that both uniaxonal neurons with S-type electrophysiological behavior and neurons with AH-type electrophysiological behavior and Dogiel II morphology responded to CRF. The CRF-evoked depolarizing responses were suppressed by the CRF1/CRF2 receptor antagonist astressin and the selective CRF1 receptor antagonist NBI27914 and were unaffected by the selective CRF2 receptor antagonist antisauvagine-30. The findings support the hypothesis that the CRF1 receptor mediates the excitatory actions of CRF on neurons in the enteric nervous system. Actions on enteric neurons might underlie the neural mechanisms by which stress-related release of CRF in the periphery alters intestinal propulsive motor function, mucosal secretion, and barrier functions.

Action Potentials↗
PubMed1993

Acetylcholinesterase staining differentiates functionally distinct auditory pathways in the barn owl.

The aim of this study was to examine how the functional specialization of the barn owl's auditory brainstem might correlate with histochemical compartmentalization. The barn owl uses interaural intensity and time differences to encode, respectively, the vertical and azimuthal positions of sound sources in space. These two auditory cues are processed in parallel ascending pathways that separate from each other at the level of the cochlear nuclei. Sections through the auditory brainstem were stained for acetylcholinesterase (AChE) to examine whether nuclei that process different auditory cues stain differentially for this enzyme. Of the two cochlear nuclei, angularis showed more intense staining than nucleus magnocellularis. Nucleus angularis projects to all of the nuclei and subdivisions of nuclei that belong to the intensity processing pathway. Acetylcholinesterase stained all regions that contain terminal fields of nucleus angularis and thus provided discrimination between the time and intensity pathways. Moreover, staining patterns with acetylcholinesterase were complementary to those previously reported with an anti-calbindin antibody, which stains terminal fields of nucleus laminaris, and thus stains all the nuclei and subdivisions of nuclei that belong to the time pathway. Some of the gross staining patterns observed with AChE were similar to those reported with antibodies to glutamate decarboxylase. However, AChE is a more convenient and definitive marker in discriminating between these pathways than is calbindin or glutamate decarboxylase. Acetylcholinesterase staining of the intensity pathway in the owl may be related to encoding of sound intensity by spike rate over large dynamic ranges.

Acetylcholinesterase↗