Social defeat impairs plasma corticosterone response to the 5-HT1A agonist 8-OH-DPAT in the rat.
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8-Hydroxy-2-(di-n-propylamino)tetralin↗
Biomedical subjects
B Buwalda
Publications and source records attributed to B Buwalda.
Induction of enhanced postnatal expression of immunoreactive calbindin-D28k in rat forebrain by the calcium antagonist nimodipine.
The early postnatal development of immunoreactive calbindin-D28k (CaB-ir) containing neuronal systems in hippocampus and parietal cortex was studied in offspring of Wistar rats chronically treated with either the Ca(2+)-channel antagonist nimodipine or placebo food. The drug was applied to the mother animals during the last week of gestation and continued until the end of the experiment. The CaB-ir was investigated in the period of the highest rate of hippocampal and cortical fiber growth at postnatal days (PD), 5, 7, 10 and 20. In the dorsal hippocampus from PD5 to 20, the dentate granule cells and their mossy fiber connection expressed increasing CaB-ir in a topographically organized manner. In the parietal cortex at PD5, 7 and 10 interneurons and a few pyramidal cells gradually appeared immunoreactive for CaB with progressively increasing intensity and approached their adult-like pattern at PD20. Chronic nimodipine treatment resulted in a transient and markedly enhanced ir-CaB expression up to the age of PD10, which was quantified by cell counts and image analysis. Nimodipine induced a more than twofold increase in the number of CaB-ir neurons in the cortex at PD5-PD10. The developmental enhancement in the hippocampus appeared slightly earlier mainly at PD5 and 7. The findings indicate that the antihypoxic effect of nimodipine, previously found in the perinatal age, may be associated with an increased Ca2+ buffering capacity of neurons due to an enhanced expression of ir-CaB during the early postnatal period.
Animals↗
Life-spanning behavioural and adrenal dysfunction induced by prenatal hypoxia in the rat is prevented by the calcium antagonist nimodipine.
The long-term behavioural effects of prenatal chronic anaemic hypoxia were investigated in young (5 months old), late adult (19 months) and aged Wistar rats (23-26 months). Sodium nitrite (2 g/l) offered in the drinking water during the second half of pregnancy served to evoke prenatal hypoxia. In parallel to nitrite treatment the Ca2+ channel blocker nimodipine (10 mg/kg) or vehicle alone was administered intragastrically once daily. Open-field activity, intermale social behaviour, learning ability in a black-white discrimination paradigm and fear-induced emotionality were assessed at different ages. Plasma corticosterone response to novelty stress was measured by blood sampling through chronic venous canulas at the age of 28 months. The nitrite-exposed 5-month-old offspring started exploration in a novel open-field with considerable delay. This delayed start-latency was augmented in 19- and 23-month-old rats, pointing to exaggerated suppression of behavioural arousal. Nitrite-induced hypoxia decreased the duration of social interactions during ageing. Aged rats exposed to nitrite were unable to learn a black-white discrimination but showed a normal generalized conditioned fear response (immobility) to the test situation as a whole. The conditioned fear-induced vocalization was more frequent among hypoxic aged animals. The aged hypoxic rats displayed a prolonged plasma corticosterone stress response and had higher adrenal weight than their controls. The abnormal open-field, social, learning and emotional behaviours, as well as the altered plasma corticosterone response, were prevented by prenatal nimodipine treatment.
Adrenal Insufficiency↗
Nimodipine accelerates the postnatal development of parvalbumin and S-100 beta immunoreactivity in the rat brain.
The effects of chronic maternal perinatal nimodipine treatment on the immunocytochemical distribution of the Ca(2+)-binding proteins parvalbumin (PV) and S-100 beta in neocortex and hippocampus were studied at the age of postnatal day (PD) 5, 7, 10, 14 and 20. The Ca2+ antagonist nimodipine (1000 ppm BAY e 9736 in daily food) was administered to pregnant rats starting at postconceptual day 11. The expression of PV exemplified in layer V of parietal and retrosplenial cortex and in all hippocampal layers of CA1 and CA3 was enhanced by more than two-fold in the offspring of nimodipine-treated dams at PD 10 compared with placebo-treated animals. The difference was no longer present at PD 14 and 20. Nimodipine administration also significantly increased the number of S-100 beta-immunopositive glial cells in upper neocortical layers I-III at PD 5 and 7. Again, the difference between nimodipine and placebo-treated animals disappeared after PD 10. The data indicate an accelerated development of PV and S-100 immunoreactivity in the postnatal forebrain as a result of perinatal blockade of the L-type Ca2+ current.
Aging↗
Postnatal development of hippocampal and neocortical cholinergic and serotonergic innervation in rat: effects of nitrite-induced prenatal hypoxia and nimodipine treatment.
Postnatal development of ingrowing cholinergic and serotonergic fiber patterns were studied in the rat hippocampus and parietal cortex employing a histochemical procedure for acetylcholinesterase as a cholinergic fiber marker, and immunocytochemistry of serotonin for serotonergic fiber staining. The rat pups were killed at postnatal days 1, 3, 5, 7, 10, and 20. The development of cholinergic and serotonergic innervation was described and the fiber density quantified under normal conditions and after long-term prenatal anemic hypoxia induced by chronic exposure to sodium nitrite. Furthermore, a third group was studied in which the nitrite hypoxia was combined with a simultaneous treatment with the Ca(2+)-entry blocker nimodipine to test the neuroprotective potential of this drug. Quantitative measurement of fiber density from postnatal day 1 to day 20 yielded the following results: (i) both neurotransmitter systems revealed an age-dependent and an anatomically-organized developmental pattern; (ii) the serotonergic innervation of the dorsal hippocampus preceded that of cholinergic afferentation in postnatal days 1-3; (iii) prenatal hypoxia induced a transient delay in the innervation of parietal neocortex and dentate gyrus for both neurotransmitter systems, but left the innervation of the cornu ammonis unaffected; and (iv) the hypoxia-induced retardation of cholinergic and serotonergic fiber development was prevented by concomitant application of the Ca(2+)-antagonist nimodipine during the hypoxia. The results indicate that prenatal hypoxia evokes a temporary delay in the cholinergic and serotonergic fiber outgrowth in cortical target areas in a region-specific manner. The hypoxia-induced growth inhibition is prevented by the calcium antagonist nimodipine, which supports the importance of the intracellular Ca2+ homeostasis of cells and growth cones in regulating axonal proliferation.
Acetylcholinesterase↗
The neurohypophysial peptides, learning, and memory processing.
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Adrenal Medulla↗
Neuroendocrine and behavioral effects of vasopressin in resting and mild stress conditions.
Neuroendocrine and behavioral effects of subcutaneously administered AVP (6 micrograms/kg b.wt.) were determined in resting conditions and after the mild stress of transportation to and placement in a novel environment. In resting conditions, systemic administration of AVP caused a rapid increase in blood glucose level and a long-lasting increase in CORT secretion. A decrease in circulating plasma NE level was observed. AVP did not affect adrenal medullary E secretion. The stress-induced sympathetic activation, as reflected in plasma NE level, was inhibited 60 min after AVP administration. Stress-induced increases in blood glucose, CORT, and E secretion were not influenced by AVP. In resting condition, AVP caused a 60-min lasting increase in grooming behavior with a concomitant decrease in time spent resting. Sixty minutes after administration, the behavioral activation after the stress of transportation and placement in a novel environment was more rapidly terminated in AVP-treated rats than in vehicle-treated control rats. The state- and time-dependent modulation of spontaneous behavior suggests that AVP has arousing properties shortly after administration when marked pressor and endocrine effects are apparent. In a later phase, AVP may facilitate dearousal mechanisms following stress-induced behavioral activation.
Animals↗
In situ blotting: a novel method for direct transfer of native proteins from sectioned tissue to blotting membrane: procedure and some applications.
We describe a novel technique for direct transfer of native proteins from unfixed frozen tissues sections to an immobilizing matrix, e.g., nitrocellulose, polyvinyliden difluoride, or positively charged nylon membranes. Proteins are directly blotted onto the membrane, providing optimal accessibility for molecular detection but retaining the anatomic localization at the cellular level. Within 10 min a maximum protein transfer is achieved independent of the protein molecular weight. The total protein bound was 80% of the maximal binding capacity of the blotting membrane and independent of the section thickness. These results indicate that the proteins that bind to the membrane originate from the cut cell monolayer that has direct contact with the blotting membrane. This in situ blotting method provides direct protein mapping from a single cell layer of a tissue section. The procedure includes cryosectioning at 20 microns and collecting sections on a dry blotting membrane at -20 degrees C. For protein transfer the blotted sections are thawed and incubated for 10 min with Tris buffer. After incubation the sections are removed from the membrane by high-pressure spray. The blotted membranes can be subjected to several detection assays. In the present study the presence of several proteins was demonstrated in brain and thymus by immunochemical and enzyme histochemical procedures.
Animals↗
Synaptic plasticity in the dentate gyrus of aged rats is altered after chronic nimodipine application.
We examined ultrastructural correlates of synaptic plasticity in the hippocampus of young (3 months) vs aged (30 months) Wistar rats and established the effects of the calcium antagonist nimodipine in animals chronically treated from 24 to 30 months. The effects of nimodipine was studied since this compound improves hippocampal neuronal physiology and enhances cognitive function during aging. In the supragranular layer of the dentate gyrus we found a 24% decrease in synaptic density (Nv) in aged animals, while synaptic size (S) was not significantly altered. After nimodipine treatment Nv in aged rats was not significantly different from young adults, thus being significantly increased compared to age-matched controls. The size of synapses was not significantly altered after nimodipine administration. Total synaptic surface area (Sv) in nimodipine-treated animals was significantly increased compared to aged controls, however, Sv remained significantly lower than in young adults. These data indicate that chronic administration of nimodipine enables granular cells in the dentate gyrus to maintain its number of synaptic contacts during the aging process. Furthermore, the presented influence of nimodipine on synaptic plasticity processes may underlie previously reported improved cognitive functioning of aged animals treated similarly with nimodipine.
Aging↗
Immunocytochemical localization of muscarinic acetylcholine receptors in the rat endocrine pancreas.
Immunocytochemical application of the antimuscarinic acetylcholine receptor antibody M35 to pancreas tissue revealed the target areas for the parasympathetic nervous system. Immunoreactivity in the endocrine pancreas was much higher than that in the exocrine part. Moreover, the endocrine cells at the periphery of the islets of Langerhans displayed the highest level of immunoreactivity. Based on these findings in the mantle of the islets, two types of islets have been distinguished: type-I islets with intensely stained mantle cells, and type-II islets with a much lower concentration of these cells. On average, type-I islets were larger (244.8 microns +/- 6.1 SEM) than type-II islets (121.5 microns +/- 3.8 SEM). M35-immunoreactivity was present on the majority of D cells, which were characterized by their immunoreactivity to somatostatin [of 446 D cells 356 (79.8%) were M35-immunopositive]. However, only a small proportion of the intensely stained mantle cells belonged to the D cell population. Therefore, it is concluded that the majority of the intensely stained mantle cells represent glucagon-secreting A and/or pancreatic polypeptide-secreting F cells. The intensity of M35-immunoreactivity at the periphery and central core of the islets paralleled the density of cholinergic innervation, suggesting a positive correlation between the intensity of cholinergic transmission and the number of muscarinic acetylcholine receptors at the target structures. The present study further revealed some striking parallels for the muscarinic acetylcholine receptor characteristics between the (endocrine) pancreas and the central nervous system.
Animals↗
Conditioned neuroendocrine and cardiovascular stress responsiveness accompanying behavioral passivity and activity in aged and in young rats.
Mean arterial pressure (MAP), heart rate (HR), plasma epinephrine (E), plasma norepinephrine (NE), and plasma corticosterone (CORT) were measured in 3-month- and 24-month-old male Wistar rats exposed to a conditioned emotional stress response (CER) paradigm and a conditioned defensive burying (CDB) paradigm. In the CER situation blood samples were taken during reexposure to the training environment one day after a single inescapable footshock (0.6 mA, AC for 3 s) had been administered. In the CER paradigm the young rats displayed passive behavior (immobility) accompanied by an increase in plasma levels of CORT and E, whereas both the control and conditioned animals showed increased NE responses. Previously shocked aged rats exhibited an attenuated plasma NE response, whereas levels of E remained elevated to a greater extent. Aged animals showed elevated basal levels of CORT one day after footshock administration. Stress-induced immobility was preserved in the aged rats. These animals had an increase in basal MAP values and a decrease in basal HR values compared to young ones. In the CDB paradigm, rats were exposed to a nonelectrified probe 1 day after the repeated shock (2 mA/contact) procedure. Young rats displayed defensive burying accompanied by increments in MAP, HR, CORT, and NE. The aged animals showed similar hormonal, autonomic, and behavioral stress responses. Thus, the age-related alterations in neuroendocrine and autonomic response patterns are apparent in stressed animals during behavioral passivity in absence of control (CER) rather than during active control (defensive burying).
Adaptation, Psychological↗
Behavioral and cardiac responses to mild stress in young and aged rats: effects of amphetamine and vasopressin.
Young (3-month-old) male Wistar rats showed a relative decrease in heart rate to a sudden silence superimposed on low intensity background noise. This bradycardia was accompanied by immobility behavior. In 26-month-old rats the magnitude of the heart rate response was reduced while immobility behavior remained in the same order of magnitude as in young controls. In the aged rats a shift in autonomic regulation of heart rate in the direction of increased sympathetic influence was indicated by the results obtained by blocking the autonomic input with atropine methyl-nitrate (0.5 mg/kg) or atenolol (1 mg/kg) given subcutaneously (SC) 30 min prior to testing. Pretest (30 min) administration of amphetamine (0.5 mg/kg SC) reinstated the bradycardiac response in aged rats to a level seen in young ones. Arginine-vasopressin (AVP, 10 micrograms/kg SC), administered 60 min before the experiment, markedly facilitated the cardiac response in young animals but failed to restore cardiac responses in aged ones. The immobility behavior in the peptide-treated aged rats was also absent. The present findings suggest that a diminished central aminergic drive in aged rats is causing a reduction of the parasympathetic cardiac response to stress of sudden silence. The results also indicate an age-related vasopressinergic modulation of behavioral and cardiac responses to mild stress.
Aging↗
Vasopressin prolongs behavioral and cardiac responses to mild stress in young but not in aged rats.
In young male Wistar rats sudden silence superimposed on low intensity background noise evokes a relative decrease in heart rate. This bradycardia is accompanied by immobility behavior. In the present study, involving young (3 month), late-adult (14 month), aged (20 month), and senescent (25 month) rats the magnitude of the stress-induced bradycardia shows an age-related reduction while the behavioral immobility response remained unchanged during the process of aging. Arginine-8-vasopressin (AVP, 6 micrograms/kg SC) administered 60 min prior to the experiment led to a prolonged behavioral and cardiac stress response in young and late-adult rats, but not in aged and senescent animals. The peripheral and central mechanisms possibly involved in the failure of systemically applied AVP to improve bradycardiac stress responses in aged rats are discussed.
Aging↗
Effects of neonatal administration of vasopressin on cardiac and behavioral responses to emotional stress in adult male rats.
Arginine-8-vasopressin (AVP) was administered subcutaneously on postnatal days 3-7 in a high (10 micrograms/100 g b.wt.) or a low dose (1 microgram/100 g b.wt.) to male Wistar rats. Control pups were untreated or saline injected. Behavioral observations in a complex maze after maturation indicated that neonatal administration of AVP increases exploratory behavior in this novel environment in a dose-dependent way. Cardiac monitoring during the conditioned emotional stress of fear of inescapable electric footshock showed that only the high dose of AVP attenuates the bradycardiac stress response. The analysis of cardiac responses also suggested an adult hyposensitivity to AVP in rats treated neonatally with AVP. In addition, the low dose of neonatal AVP was impairing the retention of a passive avoidance behavior. The data indicate that the neonatal administration of AVP exerts long-term effects upon the behavioral adaptation to novelty and memory processes related to emotional stress. That neonatal AVP is less effective in influencing adult vagally mediated cardiac stress responses suggests differences in the developmental sensitivity ("critical periods") of the central vasopressinergic systems involved in the regulation of behavior and autonomic functioning.
Animals↗
Reduced preabsorptive insulin response in aged rats: differential effects of amphetamine and arginine-vasopressin.
The experiments presented here have been designed to investigated whether the age-related attenuation of the vagal reactivity to emotional stressors and its modulation by amphetamine (Amph) or arginine-vasopressin (AVP) can be generalized for other physiological response patterns. We therefore studied the vagal control of the endocrine pancreas during food intake. Young (3 months old) and aged (27 months old) male Wistar rats were provided with permanent cardiac catheters allowing free movement and repeated, stress-free blood sampling. The vagally mediated preabsorptive insulin response (PIR) in relation to food intake as seen in young rats was reduced in aged ones. Blood glucose increments were the same at both ages. Administration of Amph (0.5 mg/kg; s.c.) 30 min before, or AVP (10 micrograms/kg; s.c.) 60 min before presentation of a test meal led to an elevation of the magnitude of insulin secretion in young rats but reduced the response in aged rats. Moreover, the PIR was not reinstated in aged rats. Blood glucose increments were not influenced by the treatments. The results are interpreted in terms of age-related general reduction of parasympathetic reactivity. The differential effect of amphetamine and AVP treatment on the insulin response suggests that the central aminergic or peptidergic drive of vagal output to the endocrine pancreas is also age-related.
Aging↗
Immunocytochemical applications in neuroanatomy. Demonstration of connections, transmitters and receptors.
In the present paper we review immunocytochemical methods for anterograde tracing with the lectin Phaseolus vulgaris-leucoagglutinin (PHA-L), combined PHA-L tracing - neurotransmitter immunocytochemistry, and the immunocytochemical localization of receptor proteins. These methods will be mainly illustrated by examples from tracing- and neurotransmitter studies on the cholinergic basal forebrain system. The morphology of PHA-L labeled neurons strongly resembles that of Golgi impregnated neurons. The complete axonal trajectories and patterns of presynaptic endings of PHA-L labeled neurons are visualized, both for light- and electron microscopic application. PHA-L-tracing can very well be combined with second immunocytochemical labeling procedures. In this way, traced pathways can be studied in their relation to chemically identified fiber systems or target neurons. Application of immunocytochemistry for the localization of the muscarinic acetylcholine receptor, albeit in its early stages, holds great promise for the near future.
Fluorescent Antibody Technique↗
Effect of low amphetamine doses on cardiac responses to emotional stress in aged rats.
In young Wistar rats conditioned emotional stress can be characterized by a learned bradycardiac response to an inescapable footshock. In aged rats this bradycardiac response is attenuated and accompanied by suppressed behavioral arousal in response to novelty. In the present study, cardiac responses to emotional stress and behavioral reactivity to a novel experience in an open field were tested in aged and young rats under the influence of a low dose of d-amphetamine (AMPH, 0.5 mg/kg IP). AMPH administration in 27-month-old rats reinstated the bradycardiac response to emotional stress, while it failed to influence the resting heart rate in the home cage. Age-associated differences in open-field ambulation, present in drug-free conditions, were antagonized by low doses of AMPH (0.25-1.0 mg/kg). It is concluded that enhanced arousal by aminergic stimulation with AMPH in the aged rat invoked cardiac and behavioral response patterns resembling those at younger ages.
Aging↗
Long-term cholinergic denervation caused by early postnatal AF64A lesion prevents development of muscarinic receptors in rat hippocampus.
The effect of early postnatal (day 8) intracerebroventricular injections of the putative cholinotoxin ethylcholine aziridinium mustard (AF64A) on development of cholinergic innervation and postsynaptic muscarinic acetylcholine receptors in the rat hippocampus was examined. The cholinotoxin applied at this stage of development leads to a permanent denervation of cholinergic fibres in the hippocampus in adulthood demonstrated by (immuno)histochemical methods and biochemical assays. Muscarinic receptor expression in the principal neurons of dentate gyrus and cornu ammonis was strongly reduced as studied by immunostaining with antibodies against muscarinic receptor proteins and binding assays with the muscarinic antagonist quinuclidinyl benzilate. Cholinoceptive interneurons and somatostatinergic interneurons are not affected by the developmental cholinergic lesion. Immunoreactivity to protein kinase C type I as a marker for inositolphosphate-related cellular activation systems slightly decreased in the apical dendrites of the hippocampal principal neurons. These findings indicate that damage to ingrowing cholinergic terminals in the hippocampus in the early postnatal period is a critical hazard for development of the muscarinic receptor system in the hippocampal principal neurons. These results are discussed for their significance to the neural mechanisms that underlie perinatal brain damage and associated cognitive dysfunction.
Animals↗