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Results for “Microinjection”

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At least 1,369 records · Page 76Linked to original sources

PubMed1988

Neural control of blood glucose homeostasis; effect of microinjection of glucose into hypothalamic nuclei on efferent activity of pancreatic branch of vagus nerve in the rat.

Efferent discharges were recorded from the nerve filament dissected from the central cut end of the pancreatic branch of the vagus nerve in the rat. Microinjections of 5% glucose solution (100-200 nl) into the LHA caused an increase in efferent activity, however, those into VMH caused no change in discharge rate. The results of experiments indicate that activation of vagal pancreatic efferents in hyperglycemic situation is originated in LHA and transmitted to the vagal pancreatic motoneurons. The role played by the neural network on blood glucose homeostasis was also discussed.

Action Potentials↗

PubMed1992

Microinjection of the alpha 1-agonist methoxamine into the paraventricular hypothalamus induces anorexia in rats.

Adrenergic receptors within the paraventricular hypothalamus (PVN) play a prominent role in the control of food intake: stimulation of alpha 2-adrenoceptors induces food intake whereas stimulation of alpha 1-adrenoceptors suppresses food intake. This study further examines the role of PVN alpha 1-adrenoceptors by examining the effects on food and water intake of the alpha 1-adrenergic agonist methoxamine (100, 200, 400 nMol) microinjected into the rat paraventricular hypothalamus. Methoxamine suppressed food intake but not water intake. Doses of 100, 200, and 400 nMol methoxamine suppressed food intake by 47%, 64%, and 96%, respectively. These results further confirm the hypothesis that administration of alpha 1-agonists into the PVN acts to significantly suppress food intake; an action that is in opposition to the facilitory effects of alpha 2-adrenergic agonists on food intake.

Animals↗

PubMed1992

Lack of serotonin neurotoxicity after intraraphe microinjection of (+)-3,4-methylenedioxymethamphetamine (MDMA).

Systemic administration of 3,4-methylenedioxymethamphetamine (MDMA) produces depletions of serotonin (5-HT) and its primary metabolite, 5-hydroxyindoleacetic acid (5-HIAA), decreases 5-HT reuptake sites and diminishes tryptophan hydroxylase activity in various forebrain regions. MDMA has been shown to be neurotoxic to the fine fibers originating from dorsal raphe (DR) 5-HT neurons but not the beaded fibers from the median raphe (MR) nucleus. In the present experiment, MDMA was microinjected directly into the DR or MR to determine whether differential neurotoxicity developed in the DR versus MR fiber systems as measured by 5-HT levels and immunocytochemistry. Two weeks following stereotaxic injection with either vehicle or (+)MDMA (50 micrograms base in 2 microliters) into the DR or MR, rat brains were assayed for 5-HT and catecholamine content or 5-HT immunocytochemistry. HPLC analysis revealed no significant changes in monoamine or metabolite concentrations in the hippocampus and striatum of rats administered intra-DR or -MR (+)MDMA. Raphe sections stained for 5-HT also did not reveal any apparent neurotoxicity. A single cerebral injection of (+)MDMA does not produce neurotoxicity to 5-HT neuronal systems originating in the raphe, although neurotoxicity of multiple MDMA injections into these raphe nuclei cannot be ruled out.

3,4-Methylenedioxyamphetamine↗

PubMed1993

Axotomy-induced neurofilament phosphorylation is inhibited in situ by microinjection of PKA and PKC inhibitors into identified lamprey neurons.

Close axotomy of identified lamprey neurons induces phosphorylation of somatodendritic neurofilaments (NFs), followed by ectopic regeneration of neurofilamentous sprouts from the dendrites. We used in situ intracellular microinjection to study the mechanism of axotomy-induced NF phosphorylation. We found that inhibitors of protein kinase C (PKC) and protein kinase A (PKA) block somatodendritic NF phosphorylation for up to 15 days when injected at the time of axotomy. Injection of PKA catalytic subunit, diacylglycerol, or okadaic acid induces somatodendritic NF phosphorylation in intact neurons with the same time course as close axotomy. These results suggest that transient activation of PKC, PKA, and/or serine phosphatase inhibition by axotomy triggers persistent intracellular changes that may be related to polarity loss in these neurons.

Animals↗

PubMedDate not supplied

Induction of audiogenic seizures in normal and genetically epilepsy-prone rats following focal microinjection of an excitant amino acid into reticular formation and auditory nuclei.

An excitant amino acid (EAA), N-methyl-D-aspartate (NMDA), induces susceptibility to seizures when bilaterally microinjected into subcortical auditory nuclei of normal rats. Thirty-five percent of animals exhibit only audiogenic seizures (AGS) after infusions of NMDA into inferior colliculus (IC). Infusions into cochlear nucleus and medial geniculate body never produce susceptibility to AGS without non-audiogenic seizures (N-AGS). The overall seizure incidence (AGS and N-AGS) with IC infusions is 100%, but the incidence is less than 50% with infusions into cochlear nucleus or medial geniculate body. Although AGS susceptibility is induced by NMDA infusions in normal animals, the seizures are submaximal in severity and lack tonic components. Bilateral infusions of NMDA into IC or reticular formation of the substrain of genetically epilepsy-prone rats (GEPRs) that exhibits submaximal AGS (GEPR-3s) do not increase seizure severity. These data along with studies showing increased EAA levels and excitotoxic-like damage in the IC of the GEPR and blockade of AGS with an EAA receptor antagonist or synthesis inhibitor suggest that an EAA in the IC is involved in initiation of AGS in the GEPR. However, EAA action in the GEPR IC is not sufficient to induce the complete spectrum of seizure behaviors, and additional mechanisms may be required for induction of maximal severity audiogenic seizures.

Acoustic Stimulation↗

PubMed1990

Suppression of spontaneous generalized non-convulsive seizures in the rat by microinjection of GABA antagonists into the superior colliculus.

Intranigral injections of GABA agonists suppress spontaneous and chemically induced generalized non-convulsive seizures in the rat. In order to examine whether the GABAergic nigrotectal pathway could be involved in this suppression, bilateral injections of GABA antagonists were performed in the superior colliculus of rats with spontaneous generalized non-convulsive seizures. Bilateral microinjections into this structure of the GABA antagonists picrotoxin (20 and 40 ng/side) and bicuculline methiodide (5 ng/side) suppressed spike-and-wave discharges for 40 min and 20 min post injection, respectively. Unilateral injections of picrotoxin (40 ng) into the superior colliculus as well as bilateral injections of a GABA agonist (muscimol; 80 ng) did not induce significant modifications. These results show that blockade of the GABAergic transmission at the level of the superior colliculus results in a suppression of generalized non-convulsive seizures. These data support the hypothesis that the suppressive effect of intranigral injections of GABA agonists over generalized non-convulsive seizures involves, at least in part, the nigrotectal GABAergic pathway.

Animals↗

PubMed1994

Dendritic morphology in epileptogenic cortex from TRPE patients, revealed by intracellular Lucifer Yellow microinjection and confocal laser scanning microscopy.

Biopsy material was obtained from cortical epileptogenic zones (eight temporal, one occipital, one parietal and one frontal) of eleven patients aged 1.5-47 years with therapy-resistant partial epilepsy (TRPE) undergoing epilepsy surgery. Control autopsy material (two temporal, two occipital, one parietal and one frontal) was removed from six neurologically healthy cases within 6-10 hours postmortem delay. In each specimen, 100-300 pyramidal and non-pyramidal neurons were visualized by intracellular Lucifer Yellow microinjection. Single neurons were imaged using CLSM generated serial optical sections; 2-D reconstruction of each neuron was made using z-projection of serial optical images, and 3-D reconstructions and rotations were computerized. Neuronal maps from TRPE biopsies, compared to control autopsies, show markedly increased numbers of dendritic abnormalities of single pyramidal and non-pyramidal neurons in layers I, II-III, V-VII, and in the subcortical white matter. The abnormalities include: (1) increased number of non-pyramidal cells in layer I; (2) many pyramidal cells with two or three dendrites originating apically, rather than one single apical dendrite, in layers II-III; (3) atypical orientation of oblique apical and basal dendrites in pyramidal neurons of layers II-VII; (4) increased number of atypical 'dinosaur-like' and fusiform cells in layers V-VII; (5) numerous neurons in the white matter. These abnormalities may be etiological in cases with early onset, and predisposing in cases with late onset.

Adolescent↗

PubMed1989

Microinjection of T4 endonuclease V produced by a synthetic denV gene stimulates unscheduled DNA synthesis in both xeroderma pigmentosum and normal cells.

A structural gene for T4 endonuclease V was constructed by ligating synthetic oligonucleotides. The endonuclease V was overproduced in E. coli under control of the E. coli tryptophan promoter and purified to apparent homogeneity. The product had comparable DNA glycosylase and apurinic/apyrimidinic (AP) endonuclease activities to the natural enzyme in vitro. When this endonuclease V was microinjected into the cytoplasm of xeroderma pigmentosum (XP) cells of complementation group A, B, C, D, F, G or H, unscheduled DNA synthesis (UDS) above the residual level was detected in all the cells at a dose of about 10(3) molecules following UV irradiation. The gain numbers of UDS in these XP cells increased with increase in the dose of enzyme and reached a plateau at the normal cell level on introduction of about 10(4) molecules. Introduction of more enzyme into either XP cells or normal human cells did not increase the grain number under regular labelling conditions (2.5 h, 37 degrees C). In normal mouse cells, introduction of the enzyme increased the grain number more than 4-fold under the same conditions during at least 8.5 h following UV irradiation. Furthermore, with a labelling time of 30 min, the enzyme more than doubled the grain number even in normal human cells.

Animals↗

PubMed1989

Activity of maturation promoting factor in pig oocytes after microinjection and serial transfer of maturing cytoplasm.

Microinjection of 120 pl homologous or heterologous (mouse) maturing cytoplasm into immature pig oocytes resulted in germinal vesicle breakdown (GVBD) and chromosome condensation (CC) after 8 h of culture. In contrast, nearly all control oocytes remained at the germinal vesicle stage. Immature cytoplasm did not induce nuclear maturation of recipient oocytes when injected. The cytoplasm of the oocytes injected with maturing cytoplasm preserved the capacity to cause GVBD in the second recipients. These results suggest that the level of injected maturation promoting factor (MPF) must rise before GVBD can occur. When the pig oocytes injected with 120 pl of mouse maturing cytoplasm were cultured in cycloheximide for 8 h, the presence of GVBD was dramatically reduced. Thus, in pig oocytes the increase in active MPF up to the effective concentration requires protein synthesis.

Animals↗

PubMed1992

Changes in permissiveness for the expression of microinjected DNA during the first cleavages of mouse embryos.

LacZ DNA and LacZ RNA were microinjected during the first cleavages of embryos. LacZ DNA was not expressed before 18-19 h post insemination (hpi) but LacZ RNA was translated. Before 22 hpi LacZ DNA was expressed in the pronuclei of the one-cell embryos and the polypeptides of the minor, but not the major activation period of the genome were synthesized. This suggests a negative control of transcription before 18-19 hpi and demonstrates that its resumption is independent of the first cleavage and of the major activation of the genome. At the time of the minor activation the eggs contain the trans-acting elements to express a variety of genes that they do not express. It may indicate that, the minor and the major activation of the genome are differently controlled.

Animals↗

PubMed2005

Depressor responses to L-proline microinjected into the rat ventrolateral medulla are mediated by ionotropic excitatory amino acid receptors.

The essential amino acid L-proline produces a depressor response when microinjected into the caudal ventrolateral medulla (CVLM) of anesthetized rats. L-proline may activate some excitatory amino acid (EAA) receptors. The present study tested this hypothesis by investigating the effects of two ionotropic excitatory amino acid receptor antagonists on the depressor response to L-proline in the CVLM: the alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA)/kainate receptor-selective antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and the N-methyl-D-aspartate (NMDA) receptor-selective antagonist MK801. Urethane-anesthetized rats received arterial catheters and their ventrolateral medulla surface was exposed. Injections of the antagonists CNQX and MK801 (2 mM, 68 nl in each case) into the CVLM completely blocked depressor responses to subsequent administration of AMPA (2 pmol/34 nl) and NMDA (2 pmol/34 nl), respectively. The depressor response to L-proline (3.4 nmol/34 nl) was strongly inhibited by prior injection of CNQX (2 mM, 68 nl) and significantly attenuated by prior injection of a high dose (20 mM, 68 nl), but not a low dose (2 mM, 68 nl), of MK801. The results indicate that the depressor response to L-proline in the CVLM includes mechanisms of ionotropic excitatory amino acid receptors.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed2004

Effects of the 5-HT1A receptor ligands flesinoxan and WAY 100635 given systemically or microinjected into the laterodorsal tegmental nucleus on REM sleep in the rat.

The effects of flesinoxan, a selective 5-HT1A receptor agonist, and of WAY 100635, a selective high affinity 5-HT1A receptor antagonist, on spontaneous sleep were studied in adult rats implanted for chronic sleep recordings. Systemic administration of flesinoxan (0.03 and/or 0.06 micromol/kg, s.c.) increased waking (W) and sleep latencies and reduced REM sleep (REMS) and the number of REM periods during the first and/or second 2-h period after treatment. Systemic injection of WAY 100635 (0.46 and/or 0.92 micromol/kg, s.c.) augmented W and REMS latency and reduced REMS and the number of REM periods during the 6-h recording period. Microinjection of flesinoxan (0.03, 0.06 and/or 0.12 nmol) into the laterodorsal tegmental nucleus (LDT) reduced REMS and the number of REM periods, and augmented REMS latency during the first, second, and/or third 2-h recording period. Direct infusion of WAY 100635 (0.06 and/or 0.12 nmol) into the LDT increased REMS and the number of REM periods during the first and/or second 2 h of recording. It is proposed that the activation by flesinoxan of postsynaptic 5-HT1A receptors located in the LDT could be responsible for the REMS suppression. The increase in REMS after the blockade of postsynaptic 5-HT1A receptors in the LDT by WAY 100635 further supports our proposal. The effects of systemic flesinoxan on sleep variables may depend mainly on the activation of postsynaptic 5-HT1A receptors, whereas the effects corresponding to systemic WAY 100635 may be predominantly related to the blockade of presynaptic somatodendritic 5-HT1A autoreceptors.

Analysis of Variance↗

PubMed2005

Striatal microinjections of interleukin-2 and rat behaviour in the elevated plus-maze.

We showed that the relationship between cytokine mRNA in the rat brain and elevated plus-maze behaviour is site- (striatum, prefrontal cortex), and cytokine-specific (interleukin-2). Here, we investigated whether a striatal microinjection of interleukin-2 (1, 10, 25 ng) affects elevated plus-maze behaviour. Analyses showed no acute effects of IL-2 on open arm time, whereas dose-dependent differences in rearing activity, and open arm entries became apparent between IL-2 doses. Twenty-four hours later, a previous dose of 25 ng IL-2 showed a trend for more open arm time compared to vehicle. These behavioural changes are discussed in relation to anxiety-relevant and exploratory behaviour, and possible neurochemical mechanisms.

Analysis of Variance↗

PubMed2005

Microinjection of ritanserin into the CA1 region of hippocampus improves scopolamine-induced amnesia in adult male rats.

The effect of ritanserin (5-HT2 antagonist) on scopolamine (muscarinic cholinergic antagonist)-induced amnesia in Morris water maze (MWM) was investigated. Rats were divided into eight groups and bilaterally cannulated into CA1 region of the hippocampus. One week later, they received repeatedly vehicles (saline, DMSO, saline+DMSO), scopolamine (2 microg/0.5 microl saline/side; 30 min before training), ritanserin (2, 4 and 8 microg/0.5 microl DMSO/side; 20 min before training) and scopolamine (2 microg/0.5 microl; 30 min before ritanserin injection)+ritanserin (4 microg/0.5 microl DMSO) through cannulae each day. Animals were tested for four consecutive days (4 trial/day) in MWM during which the position of hidden platform was unchanged. In the fifth day, the platform was elevated above the water surface in another position to evaluate the function of motor, motivational and visual systems. The results showed a significant increase in escape latencies and traveled distances to find platform in scopolamine-treated group as compared to saline group. Ritanserin-treated rats (4 microg/0.5 microl/side) showed a significant decrease in the mentioned parameters as compared to DMSO-treated group. However, scopolamine and ritanserin co-administration resulted in a significant decrease in escape latencies and traveled distances as compared to the scopolamine-treated rats. Our findings show that microinjection of ritanserin into the CA1 region of the hippocampus improves the scopolamine-induced amnesia.

Amnesia↗

PubMed2004

Effects of rubral microinjections of muscimol and bicuculline in a genetic animal model of paroxysmal dystonia.

Previous studies suggested that GABAergic dysfunctions within the red nucleus are involved in stress-inducible paroxysmal dystonia of the dt(sz) mutant hamster. In the present study, rubral microinjections of the GABAA receptor agonist muscimol exerted only moderate antidystonic effects and the antagonist bicuculline failed to show significant effects on the severity of dystonia. These data indicate that disturbed rubral GABAergic inhibition is not important for the manifestation of dystonia in the dt(sz) mutant.

Animals↗

PubMed2004

Lesions of the periaqueductal gray disrupt input to the rostral ventromedial medulla following microinjections of morphine into the medial or basolateral nuclei of the amygdala.

Microinjections of morphine into the basolateral (BLa) and medial (MEa) nuclei of the amygdala differentially affect rostral ventromedial medulla (RVM) neuronal activity and nocifensive behaviors. PAG lesions attenuated or blocked the effects of both BLa and MEa morphine on RVM cell activity, and interfered with the behavioral antinociception produced by BLa infusions. These results demonstrate that the influences from both the BLa and MEa to the RVM are relayed via the PAG.

Action Potentials↗

PubMed2004

Microinjection of bicuculline into the central nucleus of the amygdala alters gustatory responses of the rat parabrachial nucleus.

The central amygdaloid nucleus (CeA) receives projection from the parabrachial nucleus (PBN) gustatory neurons and descendingly projects to the PBN, and taste responses in the PBN are significantly affected by stimulation or lesion of the CeA. To examine whether the GABA receptors within the CeA are involved in this modulation, the effects of microinjection of bicuculline, a GABA(A)-selective antagonist, into the CeA on the activities of PBN taste neurons were observed by using extracellular recording technique. In general, after bicuculline was administered to ipsilateral CeA, the responses of PBN neurons to four tastants all increased, with the magnitudes significantly higher than those obtained before drug administration (P<0.01), respectively. However, after bicuculline was delivered into the contralateral CeA, only the responses to NaCl, HCl and QHCl increased. According to the best-stimulus category, 47% NaCl-best (8/17), 64% HCl-best (7/11), 80% QHCl-best (4/5), and 33% sucrose-best (1/3) increased their responses to at least one basic taste stimulus after GABA(A) receptors within the ipsilateral CeA were blocked. After contralteral CeA injection, more NaCl-best neurons (6/8) increased responses than that after ipsilateral CeA injection, but other best-stimulus units showed no differences before and after drug injection into the contralateral CeA. Analyses of across-unit patterns indicated that the correlation coefficient of responses between NaCl and sucrose was apparently higher after drug administration to the CeA. However, after drug injection into the contralateral CeA, the correlations between NaCl and the other three tastants were higher than those before. These results indicate that the GABA(A) receptors within the CeA play an important role in modulating the gustatory activities of PBN neurons.

Amygdala↗

PubMed2005

Microinjections of nociceptin into the nucleus ambiguus elicit tachycardia in the rat.

Cardiovascular effects of activation of opioid receptor like receptors (ORL1 receptors) in the nucleus ambiguus were studied in urethane-anesthetized, adult male Wistar rats. Microinjections of nociceptin (0.31, 0.62, 1.25 and 2.25 mmol/L) into the nucleus ambiguus elicited increases in heart rate (17.5 +/- 4, 33.3 +/- 2.9, 16.5 +/- 1.5 and 13.9 +/- 2.7 beats/min, respectively) which were blocked by an ORL1 receptor antagonist. These results indicate that activation of ORL1 receptors in the nucleus ambiguus elicits tachycardia.

Animals↗