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C Aoki

Publications and source records attributed to C Aoki.

At least 55 records · Page 3Linked to original sources
PubMed1992

C-terminal tail of beta-adrenergic receptors: immunocytochemical localization within astrocytes and their relation to catecholaminergic neurons in N. tractus solitarii and area postrema.

beta-Adrenergic receptors (beta AR) in the medial nuclei of tractus solitarii (m-NTS) and area postrema (AP) may bind to catecholamines released from neurons, whereas only the AP has fenestrated capillaries allowing access to circulating catecholamines. Since varied autonomic responses are seen following beta AR activation of the dorsal vagal complex, including the m-NTS and AP, we hypothesized that there might be a cellular basis for varied responses to beta AR stimulation that depends on the differential access to circulating catecholamines. Therefore, we comparatively examined the ultrastructural localization of the beta AR in relation to catecholaminergic neurons in these regions. An antibody directed against the C-terminal tail (amino acids 404-418) of hamster beta-adrenergic receptor (beta AR404) was used in this study. The localization of beta AR404 was achieved by the avidin-biotin peroxidase complex (ABC) technique in combination with a pre-embed immunogold labeling method to localize tyrosine hydroxylase (TH), the catecholamine-synthesizing enzyme. Within m-NTS and at subpostremal border, labeling for beta AR404 was evident along the intracellular surface of plasma membranes of small, apparently distal, astrocytic processes. Astrocytic processes with beta AR404-immunoreactivity formed multiple, thin lamellae around TH-labeled and non-TH neuronal cell bodies and dendrites. beta AR404-immunoreactive astrocytes also extended end-feet around blood vessels and surrounded groups of axon terminals that were directly juxtaposed to each other. Some, but not all, of these axons demonstrated TH-immunoreactivity. Fewer beta AR404-immunoreactive astrocytes were detected in AP, regardless of their proximity to catecholaminergic processes or blood vessels. The present astrocytic localization of beta AR404, together with the earlier, neuronal localization of beta AR's third intracellular loop, suggest that the beta AR may be substantially different between neurons and astrocytes. The regional difference in the prevalence of beta AR404-immunoreactive astrocytes suggests that these receptive sites may either: (i) be preferentially activated by catecholamines released from terminals rather than circulating catecholamines; or (ii) be down-regulated in AP due to blood-born substances, such as catecholamines. The extensive localization of beta AR in the border between m-NTS and AP also suggests that catecholaminergic activation of these astrocytes may dictate the degree of diffusion of catecholamines which are of neuronal or vascular origin. The specific localization of beta AR404-immunoreactivity to the more distal portions of astrocytes suggests the possibility that astrocytes have restrictive distributions of beta AR and that the beta-adrenergic activation lead to morphological or chemical changes that are also localized to the distal portions of astrocytes.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

Cholinergic terminals in the cat visual cortex: ultrastructural basis for interaction with glutamate-immunoreactive neurons and other cells.

Acetylcholine (ACh) is one of the transmitters utilized by extra-thalamic afferents to modulate stimulus-driven neurotransmission and experience-dependent plasticity in the visual cortex. Since these processes also depend on the activation of glutamatergic receptors, cholinergic terminals may exert their effects via direct modulation of excitatory neurotransmission. The objective of this study was to determine whether the ultrastructural relationships between cholinergic terminals, glutamate-immunoreactive neurons, and other unlabeled cells support this idea. Sections from aldehyde-fixed visual cortex (area 17) of adult cats were immunolabeled for the following molecules: (1) choline acetyltransferase (ChAT), the acetylcholine-synthesizing enzyme; (2) L-glutamate; or (3) ChAT simultaneously with L-glutamate by combining electron-microscopic immunogold and immunoperoxidase techniques. None of the cortical terminals were dually labeled, suggesting that (1) the labeling procedure was free of chemical or immunological cross reactions; and (2) glutamate immunoreactivity probably reflects the transmitter, and not metabolic, pool of L-glutamate. Comparisons between cholinergic and noncholinergic axons revealed that (1) ChAT-immunoreactive axons formed fewer identifiable synaptic contacts within single ultrathin sections (P less than 0.01 using chi-square test); and (2) more of the cholinergic axons occurred directly opposed to other terminals (P less than 0.0015 by chi-square test), including 21% of which resided directly across asymmetric, axo-spinous junctions. Dual labeling showed that a third of the synaptic targets for cholinergic terminals contained detectable levels of glutamate immunoreactivity. Some of the axo-spinous junctions juxtaposed to cholinergic axons also exhibited glutamate immunoreactivity presynaptically. These observations provide ultrastructural evidence for direct, cholinergic modulation of glutamatergic pyramidal neurons within the mammalian neocortex. Prevalence of juxtapositions between cholinergic terminals and axo-spinous synapses supports the following ideas: (1) ACh may modulate the release of noncholinergic transmitters, including Glu; (2) Glu may modulate ACh release; and (3) these processes may be concurrent with cholinergic modulation of glutamatergic synapses at postsynaptic sites.

Animals↗
PubMed1992

Changes in bone mineral density and fracture prevalence in Japanese women after oophorectomy.

The bone changes after gynecological surgery during the early phase of recovery were examined. The subjects were randomly selected from women who had undergone bilateral oopho-hysterectomies (OOX, n = 98, 46.0 +/- 5.0 year-old) or hysterectomies (HX, n = 75, 43.6 +/- 4.6 year-old) within 4 years prior to entering the study. The ovarian functions in the HX group were presumed to be intact following the hysterectomies, judging from the cytological evaluation of the vaginal pap smears. The bone morphological changes in both groups were examined to measure the cortical thickness of the metacarpal bone (MCI) on hands X-ray film using microdensitometry, and the posterior/anterior height ratios (P/A ratio) of the entire vertebral bodies, on vertebral X-ray films using a digitizer. The changes in bone mineral densities in both groups were measured by dual energy X-ray absorptiometry at lumbar vertebrae (L2-4 BMD) and by microdensitometry at the metacarpal cortical bone; the bone densities of metacarpal bone were referenced by the density of aluminum step wedge on the same X-ray films. The prevalence of vertebral body fractures (P/A ratio greater than 1.4) in the OOX group (5.1%) was 3.9 times higher than that in the HX group (1.3%). There was a significant decrease in MCI in the OOX group compared with the HX group (p less than 0.01). L2-4 BMD in the OOX and HX group were 1.07 +/- 0.15 and 1.16 +/- 0.13 g/cm2, respectively (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Immunocytochemical study of GnRH and GnRH-associated peptide in male Syrian hamsters as a function of photoperiod and gonadal alterations.

Hypothalamic luteinizing-hormone-releasing hormone (GnRH) and gonadotropin-releasing-hormone-associated peptide (GAP) biosynthesis and storage were estimated by immunocytochemistry in male golden hamsters maintained in different photoperiods. Intact or castrated male hamsters with subcutaneously inserted testosterone implants were exposed to long-day (14:10) or short-day photoperiods (10:14) for 4-8 weeks. Exposure to short photoperiod for 4 weeks, an interval characterized by a suppression of gonadotropin secretion but not gonadal regression, was associated with an increase in the number of GnRH- and GAP-immunoreactive cells in the diagonal band of Broca/medial septum. Furthermore, morphometric analysis revealed that these animals displayed significantly more GnRH but not GAP immunoreactivity in the median eminence as opposed to hamsters exposed to long-day photoperiods. In additional studies, gonadally regressed hamsters exposed to short day lengths for 8 weeks had equal numbers of GnRH cells as did the long-day controls. These patterns suggest that reproductive quiescence in golden hamsters is not the result of depletions of neuronal GnRH stores available for secretion.

Animals↗
PubMed1992

Beta-adrenergic receptors: astrocytic localization in the adult visual cortex and their relation to catecholamine axon terminals as revealed by electron microscopic immunocytochemistry.

It has long been recognized that noradrenaline, the most abundant catecholamine within the visual cortex, plays important roles in modulating the sensitivity of cortical neurons to visual stimuli. However, whether or not these noradrenaline effects are confined to a discrete synaptic specialization or mediated by diffuse modulation of a group of synapses has remained an issue open for debate. The aim of this study was to examine the cellular basis for noradrenaline action within the visual cortex of adult rats and cats. To this end, I used electron microscopic immunocytochemistry to examine the relationship between (1) catecholamine axon terminals and beta-adrenergic receptors (beta AR), which, together, may define the effective sphere of noradrenaline modulation; and then (2) these putative sites for catecholamine modulation and axospinous asymmetric junctions where excitatory neurotransmission is likely to dominate. Antibodies against beta AR were used at light and electron microscopic levels on the visual cortex of rat and cat. Rat visual cortex was also labeled simultaneously for beta AR and the catecholamine-synthesizing enzyme, tyrosine hydroxylase (TH), to determine the ultrastructural relationships between catecholamine terminals and beta AR. Immunoperoxidase labeling revealed that beta AR404, a polyclonal antibody directed against the C-terminal tail of hamster lung beta AR (beta 2-type), recognized astrocytic processes predominantly. In contrast, beta AR248, a polyclonal antibody directed against the third cytoplasmic loop, recognized neuronal perikarya as observed in previous studies. Dual labeling for beta AR404 and TH revealed that catecholamine axon terminals that contained numerous vesicles formed direct contacts with astrocytic processes exhibiting beta AR404 immunoreactivity. However, some catecholamine axon terminals that lacked dense clusters of vesicles were positioned away from beta AR404-immunoreactive astrocytes. Frequently, beta AR-immunoreactive astrocytic processes surrounded asymmetric axospinous junctions while also contacting catecholamine axon terminals. These observations support the possibility that, through activation of astrocytic beta AR, noradrenaline modulates astrocytic uptake mechanism for excitatory amino acids, such as L-glutamate. Astrocytic beta AR might also define the effective sphere of catecholamine modulation through alterations in the morphology of distal astrocytic processes and the permeability of gap junctions formed between astrocytes.

Animals↗
PubMed1991

Identification of mitochondrial and non-mitochondrial glutaminase within select neurons and glia of rat forebrain by electron microscopic immunocytochemistry.

Antibodies against the mitochondrial enzyme glutaminase (EC 3.5.1.2), have been used in previous immunocytochemical studies to help identify glutamate-releasing neurons among all glutamate-containing neurons. The studies were based on the idea that glutaminase is enriched within the releasable "transmitter" pools of glutamate. However, evidence is also available to suggest that the enzyme does not occur exclusively within glutamate-releasing neurons. Thus we sought to determine whether glutaminase was immunocytochemically detectable within presynaptic terminals forming asymmetric (putatively excitatory) synapses or, alternatively, occurs in association with mitochondria throughout the cell. For this purpose, we examined the cellular and subcellular distribution of glutaminase- immunoreactivity in neocortical (visual and somatosensory) areas known to contain glutamatergic perikarya. This localization was compared with the distribution in striatal (caudate-putamen and nucleus accumbens) regions recognized to contain high densities of glutamatergic terminals but fewer, if any, glutamatergic perikarya. Glutaminase-immunoreactive perikarya were numerous within the infragranular laminae of neocortex (approximately 1 per 1,000 microns 2 tissue area) but sparse within the caudate-putamen nuclei and accumbens nuclei (less than 1 per 20,000 microns 2.). In addition, heterogeneous distribution of small (less than 1 microns) punctate immunoreactive structures was notable. Relatively high densities of these punctate structures occurred within the supragranular laminae of neocortex, dorsolateral quadrant of the caudate-putamen nuclei, and surrounding certain groups of myelinated fiber bundles throughout the striatum. Electron microscopy revealed diffusely distributed peroxidase immunoreactivity in a select population of dendritic spines, glial processes, and axons. Eight percent of all synapses within the supra-granular laminae were formed by terminals labeled for glutaminase. These principally formed asymmetric junctions on spiny processes. When tissue was incubated with the antibody in the presence of a permeabilizing agent, Photo-flo, high levels of glutaminase immunoreactivity was detectable by electron microscopy within select mitochondria of neocortical (4%) and striatal (8%) perikarya and dendrites, while the diffuse distribution of immunoreactivity within axons and glia was greatly diminished. The differential ultrastructural conditions provide direct demonstration that glutaminase in brain occurs in at least two forms discriminable by their diffuse distribution within non-mitochondrial cytoplasm versus discrete localization within mitochondria. The morphological characteristics of synapses formed by axons exhibiting diffuse distributions of glutaminase immunoreactivity are consistent with the idea that glutaminase-enriched terminals mediate excitatory chemical transmission via the release of glutamate. Because glia containing glutaminase occur juxtaposed to the asymmetric junctions, the glia may utilize neuronally released glutamate for energy metabolism.

Animals↗
PubMed1991

[Changes in bone mineral density and bone turnover within 12 months after oophorectomy: a prospective study compared with hysterectomized controls].

Nineteen patients (pts) with stage Ib to IIb uterine cervical cancer were studied for changes in bone mineral density and bone turnover within 12 months after radical hysterectomy and pelvic lymphadenectomy. Eleven out of 19 pts also underwent oophorectomy (OX), and the other 8 pts without OX were studied as controls. A significant increase in FSH and decrease in E2 (p less than 0.01) in OX pts indicated the completeness of oophorectomy, whereas no significant change in those levels showed retained ovarian function in the controls. In OX pts significantly increased serum alkaline phosphatase (p less than 0.01), urine-calcium/creatinine (p less than 0.05) and hydroxyproline/creatinine ratio (p less than 0.01) indicating high bone turnover after the oophorectomy were observed. However, a transient but significant (p less than 0.05) rise in these levels in the 3rd month in the controls was noted. In OX pts the spinal bone mineral density (BMD) measured by dual photon absorptiometry was significantly reduced to approximately 10% (p less than 0.05) within 12 months after oophorectomy, while in the controls loss of BMD was also observed up to 6 months, and it appeared to have returned towards baseline levels at 12 months after hysterectomy. These data suggest that a rapid and considerable loss of spinal BMD was mainly accelerated by the oophorectomy, but in part was contributed to by the stress or reduced physical activity for up to 6 months after radical hysterectomy.

Alkaline Phosphatase↗
PubMed1990

Optimization of differential immunogold-silver and peroxidase labeling with maintenance of ultrastructure in brain sections before plastic embedding.

The limited success of immunogold labeling for pre-embedding immunocytochemistry of neuronal antigens is largely attributed to poor penetration of large (5-20 nm) colloidal gold particles. We examined the applicability of using silver intensification of 1 nm colloidal gold particles non-covalently bound to goat anti-rabbit immunoglobulin (1) for single labeling of a rabbit antiserum against the catecholamine synthesizing enzyme, tyrosine hydroxylase (TH), and (2) for immunogold localization of rabbit anti-TH simultaneously with immunoperoxidase labeling of a mouse monoclonal antibody against the opiate peptide, leucine-enkephalin (LE). Vibratome sections were collected from acrolein fixed brains of adult rats. These sections were immunolabeled without use of freeze-thawing or other methods that enhance penetration, but damage ultrastructure. By light microscopy, incubations in the silver intensifier (Intense M, Janssen) for less than 10 min at room temperature resulted in a brownish-red reaction product for TH. This product was virtually indistinguishable from that seen using diaminobenzidine reaction for detection of peroxidase immunoreactivity. Longer incubations produced intense black silver deposits that were more clearly distinguishable from the brown immunoperoxidase labeling. However, by light microscopy, the gold particles seen by electron microscopy were most readily distinguished from peroxidase reaction product with shorter silver intensification periods. The smaller size of gold particles with shorter periods of silver intensification also facilitated evaluation of labeling with respect to subcellular organelles. Detection of the silver product did not appear to be appreciably changed by duration of post-fixation in osmium tetroxide. In dual-labeled sections, perikarya and terminals exhibiting immunogold-silver labeling for TH were distinct from those containing immunoperoxidase labeling for LE. These results (1) define the conditions needed for optimal immunogold-silver labeling of antigens while maintaining the ultrastructural morphology in brain, and (2) establish the necessity for controlled silver intensification for light or electron microscopic differentiation of immunogold-silver and peroxidase reaction products and for optimal subcellular resolution.

Animals↗
PubMed1990

Neuropeptide Y in cortex and striatum. Ultrastructural distribution and coexistence with classical neurotransmitters and neuropeptides.

NPY-neurons in the striatum and cortex have many morphological and chemical features in common. They are intrinsic, medium sized, aspiny and exhibit ultrastructural characteristics typical of neurons undergoing active synthesis and release of peptides. Most of the NPY-neurons in the two regions coexist with somatostatin, exhibit high levels of NADPH-diaphorase and are resistant to degeneration associated with Huntington's disease. Ultrastructural analysis suggests that the ensheathment by glia and sparsity of asymmetric (putatively excitatory) inputs may render NPY neurons resistant to excitotoxicity. Although NPY-neurons receive few inputs, they make numerous contacts with dendrites within a small region of the neuropil. Among their targets are GABAergic neurons. These NPY-receptive GABA neurons differ from other GABAergic neurons in the vicinity in that they receive few other inputs along their somata and proximal dendrites. This suggests that NPY may exert more influence on a specific class of GABAergic neurons. Many more of the NPY-terminals are found at sites that would be strategic for the simultaneous modulation of the release of transmitters and postsynaptic responses. The differences among NPY-neurons in the striatum versus cerebral cortex are mainly chemical. Most notably, the NPY-neurons are GABAergic in the cortex and not GABAergic in the striatum. In addition, some of the NPY-axons in the ventral portions of striatum and cerebral cortex may be catecholaminergic, and thus originate in brainstem areas recognized to contain NPY and epinephrine or norepinephrine. NPY- and catecholaminergic fibers converge onto same dendrites. Thus, the two transmitters may interact through intercellular biochemical pathways postsynaptically. Finally, the sites where the two fibers directly contact each other may be where NPY stimulates the turnover of dopamine.

Animals↗
PubMed1989

Cytoplasmic loop of beta-adrenergic receptors: synaptic and intracellular localization and relation to catecholaminergic neurons in the nuclei of the solitary tracts.

Pharmacological studies suggest that beta-adrenergic receptors (beta AR) in the medial nuclei of the solitary tracts (m-NTS) facilitate presynaptic release of catecholamines and also function at postsynaptic sites. We have localized the antigenic sites for a monoclonal antibody against a peptide corresponding to amino acids 226-239 of beta AR in the m-NTS of rat brain. By light microscopy, immunoperoxidase labeling for this antibody was detected in somata and proximal processes of many small cells that were distributed throughout the rostrocaudal extent of the m-NTS. Electron microscopy confirmed the cytoplasmic localization of beta AR in perikarya and proximal dendrites of neurons. Immunoreactivity occurred as discrete patches associated with cytoplasmic surfaces of plasma membrane and with irregularly-shaped saccules with clear lumen in the immediate vicinity. Select regions of nuclear envelopes, mitochondrial membranes, and rough endoplasmic reticulum were also immunoreactive along their cytoplasmic surfaces. In contrast, the Golgi apparatus was labeled, but infrequently. Immunoreactivity was also detected at numerous post- and occasional presynaptic membrane specializations of select axodendritic junctions. Dual labeling for the beta AR-antibody by the immunoperoxidase method and for a rabbit antiserum against the catecholamine-synthesizing enzyme, tyrosine hydroxylase (TH), by the immunoautoradiographic method within the same sections, further established the precise cellular relations between beta AR and catecholaminergic neurons. Immunoreactivity for beta AR was detected in numerous perikarya and proximal dendrites that did not show detectable levels of TH. However, a few cells were dually labeled for both antigens, as seen by both light and electron microscopy. The TH-labeled terminals formed synapses at junctions both with and without beta AR-like immunoreactivity. These results from the single and dual labeling studies: (1) confirm biochemical predictions that amino acids 226-239 of beta AR protein reside intracellularly; (2) provide the first ultrastructural evidence for beta AR localization within both pre- and postsynaptic membrane specializations of a subset of catecholaminergic synapses; and (3) suggest select intracellular sites that may be involved with synthesis and/or internalization and degradation of the receptor protein.

Animals↗
PubMed1989

Effects of metaraminol on the secretion of fluid and glycoproteins from the rat submandibular gland.

The actions of metaraminol on the secretion of fluid and glycoproteins from rat submandibular glands were investigated using phentolamine, propranolol and reserpine. Metaraminol at doses from 1 to 8 mg/kg (i.p.) increased the salivation and the amounts of protein in submandibular saliva in a dose-dependent manner. The salivation induced by metaraminol at 2 mg/kg was inhibited strongly by pretreatment with propranolol, whereas the salivation induced by metaraminol at 8 mg/kg was inhibited strongly by phentolamine. Reserpine inhibited the secretion of fluid caused by both doses of metaraminol. The electrophoretic profiles of saliva evoked by metaraminol at 2 mg/kg revealed two main bands of glycoprotein, I and IV, which originated from the acinus, and the intensities of these bands were decreased by treatment with propranolol, whereas the major band in saliva induced by 8 mg/kg of metaraminol was glycoprotein III, which originated from the granular tubules. The intensity of band III was decreased by pretreatment with phentolamine. These results suggest that metaraminol, at small doses, stimulates mainly the beta-adrenoceptor in the acinus, whereas at large doses, it prominently stimulates the alpha-adrenoceptors in the granular tubules, although metaraminol at small and large doses is able to stimulate alpha- and beta-adrenoceptors in rat submandibular gland.

Animals↗
PubMed1989

Effects of tachykinins on the secretion of fluid and glycoproteins from the submandibular glands of rat, mouse, hamster and guinea pig.

The effects of substance P, neurokinin A, physalamine, and eledoisin on the secretion of fluid and glycoproteins from the submandibular glands of various rodents were investigated. Following i.v. injection of each peptide at a dose of 20 micrograms/kg, the major glycoprotein species secreted from rats and guinea pigs were shown to be electrophoretically identical with those found in the acini. However, saliva was not elicited from the mice and hamsters. These results suggest that in both rats and guinea pigs, tachykinins act on the acinar cells of the submandibular gland only.

Animals↗
PubMed1989

Effects of autonomic agents on the secretion of glycoproteins from the secretory cells of the major salivary glands in rats.

The characteristics of the glycoproteins contained in the secretory segments of the three major salivary glands of adult male rats and the secretion of these various glycoproteins in response to autonomic agents were examined by micro-disc electrophoresis. Characterization of the glycoproteins showed that the acinar segments from the three major salivary glands and the segments of the convoluted granular tubules from the submandibular gland each contain characteristic species of glycoproteins. The glycoproteins characteristic of the acinus of the submandibular gland were secreted into saliva in response to carbachol or dobutamine, those characteristic of the parotid gland by carbachol, methoxamine, or dobutamine, and those of the sublingual gland by carbachol, whereas glycoproteins characteristic of the convoluted granular tubules of the submandibular gland were only elicited by methoxamine. The secretory response of carbachol, methoxamine and dobutamine, respectively, were almost completely reduced by pretreatment with atropine, prazosin and metoprolol. The relative proportions of glycoproteins secreted into the oral cavity from secretory cells of the three major glands varied significantly with the nature of the stimulant.

Animals↗
PubMed1989

Neuropeptide Y in the cerebral cortex and the caudate-putamen nuclei: ultrastructural basis for interactions with GABAergic and non-GABAergic neurons.

In the cerebral cortex and caudate-putamen (CP) nuclei, neuropeptide Y (NPY) immunoreactivity is detectable within 1-2% of all neurons. The NPY-immunoreactive neurons are interneuronal and are believed to be mostly GABAergic in the cerebral cortex but not in the CP nuclei. Thus NPY and GABA may play different roles in the circuitry within these 2 regions. We tested this possibility by comparing the ultrastructure of NPY-containing neurons between (1) cortex (somatosensory and anterior cingulate areas) versus dorsolateral CP; and (2) GABAergic versus non-GABAergic NPY neurons within each area. Single coronal sections through the rat forebrain were dually labeled for GABA and NPY by combining immunoautoradiography with the immunoperoxidase method. NPY-containing neurons with or without GABA occurred throughout the rostrocaudal portions of CP and all laminae of somatosensory and anterior cingulate cortex. Comparisons between the areas confirmed that somata and terminals dually labeled for GABA and NPY were more prevalent in the cortex. NPY terminals lacking detectable GABA immunoreactivity also were found within the cortex, thus suggesting additional heterogeneity in cortical NPY innervation. The ultrastructural features of NPY perikarya in both regions were morphologically similar regardless of whether the cells also contained GABA. Most synaptic inputs to NPY neurons occurred at distal dendrites. In comparison to neighboring neurons, synaptic inputs to proximal dendrites and somata of NPY neurons of cortex and CP were rare, suggesting that fewer and weaker inputs may modulate the excitability of NPY-containing neurons. In both regions, nearly all NPY- and NPY-GABA-labeled terminals formed symmetric junctions suggestive of inhibitory action. The majority of these junctions were with dendrites containing neither NPY nor GABA. NPY terminals formed few contacts on proximal dendrites and somata of GABAergic neurons (8% of 179 contacts in cortex; 12% of 73 contacts in CP) which, unlike most singly-labeled GABAergic neurons, were sparsely innervated. Thus, NPY may play a more prominent role in modulation of certain GABAergic neurons than would be predicted by the observed frequency of NPY-to-GABA contacts in the two regions. One notable regional difference was the greater prevalence in cortex of axoaxonic associations between NPY-immunoreactive terminals and other terminals, some of which also contained NPY. These nonsynaptic associations may be involved in the modulation of (1) the release of NPY by another transmitter or (2) NPY's modulation of release of other transmitters in cortex.

Animals↗
PubMed1988

Neuropeptide Y-containing neurons in the rat striatum: ultrastructure and cellular relations with tyrosine hydroxylase- containing terminals and with astrocytes.

The ultrastructural localization of neuropeptide Y (NPY) was comparatively examined in the dorsal (caudate-putamen) and ventral (nucleus accumbens) striatum using the peroxidase-antiperoxidase (PAP) method. In both striatal regions, NPY-like immunoreactivity (IR) was detected in perikarya, dendrites and axons. The labeled perikarya were 15-25 microns in a diameter and contained large, deeply and multiply indented nuclei and prominent Nissl bodies. The labeled dendrites contained a few large (80-150 nm) dense-core vesicles, lacked detectable spines and received few afferents. These morphological characteristics of NPY-IR neurons in both areas are in close accord with previous descriptions for the medium aspiny intrinsic neurons. Axon terminals with terminals with NPY-like IR contain primarily small clear round vesicles, as seen in single or serial sections. These terminals formed junctions that lacked recognizable pre- or post- synaptic densities, but showed parallel spacing between apposed plasmalemmas at presumed synaptic clefts. Targets of the axon terminals with NPY-like IR included unlabeled somata, unlabeled proximal dendrites and labeled and unlabeled distal dendrites. The NPY-IR neurons in the caudate-putamen differed from those in the nucleus accumbens in that (1) there were no recognized appositions between labeled dendrites and labeled terminals, and (2) fewer terminals contained large dense-core vesicles. These findings are consistent with the concept that in the nucleus accumbens, the excitability of the NPY-IR neurons may be more directly modulated by NPY or another transmitter co-existing in the terminals. Catecholamines are known to co-exist with NPY in certain rostrally projecting brainstem nuclei. Therefore, in the two striatal regions, we additionally sought to determine (1) whether the NPY-IR neurons might be modulated by catecholaminergic afferents and (2) whether NPY might co-exist with catecholamines in terminals. Goat antiserum against NPY and rabbit antiserum against tyrosine hydroxylase (TH), the catecholamine-synthesizing enzyme, were simultaneously localized in single sections by PAP and immunoautoradiographic methods, respectively. Quantitative analysis in dually labeled sections from both striatal areas revealed few, if any, direct synaptic contacts between TH-labeled terminals and dendrites containing NPY-like IR. However, there was convergence of separate NPY- and TH-IR terminals on unlabeled dendrites. A few terminals in the nucleus accumbens, but not in the dorsal striatum, showed immunoreactivity methods, to TH and also contained dense-core vesicles with NPY-like IR.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Effects of dobutamine and terbutaline on the secretion of glycoproteins from the acinar cells of the rat submandibular gland.

The actions of dobutamine (DOB) and terbutaline (TER) on the secretion of marker glycoprotein (GP) from the secretory cells of the glands and secretion of fluid from rat submandibular gland (SMG) were investigated in combination with two antagonists, metoprolol (MET) and ICI-118551 (ICI). The ED50 value of fluid secretion was 8.7 mg/kg for DOB and 5.9 mg/kg for TER. MET, administered prior to either agonists at a dose of 40 mg/kg, inhibited the fluid secretion. However, the blocking effects of ICI were considerably lower than those of MET. The electrophoretic profiles of GP in DOB-evoked saliva were similar to those in TER-evoked saliva, and included two characteristic main bands of GP I (130 KDa) and GP IV (21.5 KDa) from the acinar cells and a minor band of GP III (31 KDa) which originated in the cells of the granular tubules. When MET was administered at a dose of 5 mg/kg prior to DOB, the intensity of band I decreased, whereas that of band III did not change. These results showed that the SMG of rats contains both beta 1- and beta 2-adrenoceptors and that beta-receptors which mediate the secretion of GP from the acinus and fluid from the gland are mainly of the beta 1-subtype.

Adrenergic beta-Antagonists↗
PubMed1988

A comparative study of the effects of four choline esters on the secretion of fluid and glycoprotein from rat submandibular glands.

The actions of four choline esters, acetylcholine (ACH), methacholine (MET), carbachol (CAR) and bethanechol (BET), on the secretion of saliva and the specific glycoprotein (GP) contained in the secretory cells of the submandibular gland (SMG) of the rat were compared under conditions with and without physostigmine (PHY). The ED50 values with respect to salivation were 17 mg/kg for ACH, 1060 micrograms/kg for BET, 810 micrograms/kg for MET and 75 micrograms/kg for CAR, whereas after pretreatment with PHY, ED50 values were lowered to 7.5 mg/kg for ACH and 212 micrograms/kg for MET, but remained unchanged for CAR and BET. SDS-polyacrylamide gel electrophoresis demonstrated that the saliva from the SMG elicited by the four choline esters contained GP I (130 KDa) and GP IV (21.5 KDa), characteristic of the acinus, and a band of GP III (31 KDa), which originates from the granular tubules. The order of intensity of these bands was band I much greater than band III = band IV. Among these bands, band I increased in intensity in a dose-dependent manner. These results suggest that the four choline esters act mainly on the acinar cells, but exert some effects on the granular tubules of the rat SMG.

Acetylcholine↗