SEARCH · PubMed Health

Results for “Microinjection”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 865 records · Page 48Linked to original sources

PubMedDate not supplied

Microinjection of human placenta. II: Biological application.

Using microinjection of probes detectable by epifluorescence light microscopy and electron microscopy we have provided direct evidence that syncytiotrophoblast is a true syncytium. We have investigated the freedom of movement of probes injected into the syncytiotrophoblast. These probes appear to move relatively extensively within the cytosolic compartment which forms a 'maze' through the membrane-bounded organelles and reticula of the syncytium. Thus mathematical models of certain forms of transepithelial transport based on simple mean and harmonic mean histologically measured thickness of epithelia are unlikely to describe the transepithelial transport pathway of at least some larger molecules, particulates and organelles with great accuracy. Microinjection of probes directly into the mesenchymal core of chorionic villi has been used to demonstrate extensive freedom of movement in that compartment which is the region where exchange with elements contained in the fetal vascular tree takes place.

Chorion↗

PubMed1997

Behavioral effects of angiotensin II microinjected into CA1 hippocampal area.

The behavioral responses of rats to bilateral microinjections of angiotensin II (ATII) at doses of 0.1, 0.5 and 1.0 microg into the hippocampal CA1 area of male Sprague-Dawley rats were studied. ATII affected locomotor activity (the number of horizontal and vertical movements) in a dose-related U-shaped manner. In the elevated plus-maze experiments, ATII at a dose of 0.1 microg microinjected bilaterally into the CA1 hippocampal area increased the number of entries into the open arms, suggesting some anxiolytic effect.

Analysis of Variance↗

PubMed2001

A simple method to microinject solid neural tracers into deep structures of the brain.

We have developed an instrument to perform microinjections of solid neural tracers into deep structures of the brain. The instrument consists of a thin hypodermic needle equipped with a movable internal rod, which is connected to a pressure chamber. When a pressure pulse is applied to the chamber, the rod moves forward and back inside the needle, pushing out a solid load previously packed inside the needle tip. By attaching a microelectrode to the instrument, it is also possible to have electrophysiological control of the injection placement. To test the instrument, we microinjected DiI and rhodamine crystals into selected structures of the visual system of pigeons. The results show small, well-defined injection sites, accurately located in the desired targets, together with well-developed anterogade and retrograde transport, selectively originated from the injection sites. This method extends the usage of solid tracers to most structures in the brain and may, in certain cases, be more advantageous than the conventional method of injecting tracer solutions.

Animals↗

PubMed2003

A novel method for marking microinjection sites using methylene blue and diaminobenzidine.

A number of different compounds have been microinjected into the brains of animals for the purpose of marking injection sites. In the present study, we describe a novel method for visualising and permanently preserving sites in the brainstem of rats marked by microinjections of methylene blue. Subsequent exposure of the sections to diaminobenzidine (DAB) tetrahydrochloride in the presence of glucose oxidase or infrared light produced an insoluble black precipitate at the injection site. A major advantage of this method is that the injection sites are marked simultaneously with immunohistochemical processing.

3,3'-Diaminobenzidine↗

PubMed2001

Effect of cholecystokinin-8 microinjection into ventral tegmental area on dopamine release in nucleus accumbens of rats: an in vivo voltammetric study.

1. Effects of microinjection of cholecystokinin-8 (CCK-8) into the rat ventral tegmental area were studied on dopamine (DA) release from nucleus accumbens (Acb), using fast cyclic voltammetry and carbon fibre microelectrode. 2. DA release was evoked by electrical stimulation of the medial forebrain bundle (MFB). DA release from Acb was increased with increasing intensity or frequency of electrical stimulation in a dose-dependent manner and was inhibited by microinjection of CCK-8 (0.5 microg/kg) into the ventral tegmental area. 3. The release of DA was clearly reduced at all the intensities (0.25, 0.5, 0.75 and 1.0 mA) tested following CCK injection into the VTA, which was statistically significant (P<0.05). But the reduced percentage of DA release did not show significant changes between the data obtained with stimuli of different intensities (P>0.05). 4. While no change could be found with the stimuli of 10Hz, the DA release was significantly suppressed by injection of CCK-8 at the other three frequencies tested (50 Hz, 100 Hz and 250 Hz). Furthermore, although the differences in the reduced amounts of DA release obtained at 50 Hz, 100 Hz and 250 Hz were statistically significant, the reduced percentage seemed to be not closely related to the frequency applied (P>0.05). 5. These results indicate that CCK-8 is involved in the regulation of midbrain DA neurotransmission, and thereby implicated in disorders, such as Parkinson's disease, that involve malfunctions of the basal ganglion DA neuronal systems.

Animals↗

PubMed1998

Intrathecal methysergide antagonizes the antinociception, but not the hyperalgesia produced by microinjection of baclofen in the ventromedial medulla of the rat.

Microinjection of baclofen, a gamma-aminobutyric acidB (GABA[B]) receptor agonist, in the nucleus raphe magnus (NRM) or nucleus reticularis gigantocellularis pars alpha (NGCpalpha) of the rat produces antinociception at doses of 0.1-1.0 ng and hyperalgesia at doses of 30-150 ng in the tail-flick test. The antinociception is proposed to result from disinhibition of spinally-projecting neurons in this region that contain serotonin. The hyperalgesia is proposed to result either from inhibition of these neurons or from disinhibition of a serotonergic pain facilitatory pathway that also originates in this area of the ventromedial medulla. To determine the involvement of bulbospinal serotonergic pathways in the biphasic effects of baclofen, rats were pretreated intrathecally with either 30 microg of methysergide or saline. Ten minutes later, either saline, 0.5 ng or 150 ng of baclofen was microinjected in the NRM and NGCpalpha, and alterations in nociceptive threshold were assessed by the tail-flick and hot-plate tests. Intrathecal pretreatment with methysergide prevented the increase in tail-flick latency produced by 0.5 ng of baclofen, but did not prevent the decrease in tail-flick latency produced by 150 ng of baclofen. Neither dose of baclofen altered hot-plate latency and this lack of effect was unchanged by methysergide. These data support the idea that the antinociceptive effect of low doses of baclofen in the tail-flick test is mediated by disinhibition of a bulbospinal serotonergic projection and release of serotonin in the spinal cord. These data also suggest that the hyperalgesia produced by high doses of baclofen does not result from disinhibition of a serotonergic pain facilitatory pathway, but rather from direct inhibition of tonically-active pain inhibitory neurons in the NRM and NGCpalpha.

Analgesics↗

PubMed1998

Neuropeptide Y release in the paraventricular nucleus is decreased during transient hyperphagia induced by microinjection of colchicine into the ventromedial nucleus of rats.

Disruption of neural signaling in the ventromedial nucleus (VMN) of rats by microinjection of the neurotoxin colchicine (COL) results in transient hyperphagia accompanied by enhanced weight gain. We tested the hypothesis that release of neuropeptide Y (NPY), a potent orexigenic signal is augmented within the paraventricular nucleus (PVN) of COL-treated hyperphagic rats. Adult male rats were microinjected bilaterally with either COL (4 microg/0.5 microl in saline) or saline in the VMN and a push-pull guide cannula aimed at the PVN was implanted for analysis of extra-cellular NPY. COL-injected rats gained 37.8+/-6.1 g while the saline-injected rats lost 9.3+/-3.4 g during the 4 days following surgery. On day 4, post-injection, the PVN of these rats was perfused with artificial cerebrospinal fluid via the push-pull cannula. NPY levels in perfusates collected at 10 min intervals from hyperphagic, COL-injected rats were markedly diminished. Cumulative NPY efflux over the 180 min sampling period was significantly less in COL-treated (27.7+/-6.0 pg) versus saline-injected control rats (110.6+/-32.2 pg; P < 0.05). These results show that impairment of neural signaling in the VMN by COL suppressed NPY release in the PVN. These observations taken together with previous studies showing diminution in preproNPY mRNA in the arcuate nucleus (ARC) and NPY levels in the PVN are in accordance with the thesis that the VMN normally exerts a facilitatory influence on NPYergic signaling in the ARC-PVN axis.

Animals↗

PubMed1999

Calcitonin microinjection into the periaqueductal gray impairs contextual fear conditioning in the rat.

We have previously proposed that behavioral alterations induced by salmon calcitonin in the rat provide an animal model of depression. As depression is characterized by context-related anxiety, behavioral inhibition and alterations in memory processing, we tested the effects of microinjections of salmon calcitonin into the periaqueductal gray matter (PAG) on contextual fear conditioning in the rat. In a first experiment, calcitonin or saline were microinjected into the PAG before the training phase and before the testing phase of a conditional fear testing procedure. In a second experiment, calcitonin or saline were injected before and immediately after the training phase. When given before the training phase, calcitonin had no effects on immediate postshock freezing but produced significant deficits in contextual freezing (24 h after footshock) in comparison with controls. When given immediately after the footshocks, calcitonin impaired contextual fear. These results suggest that calcitonin receptor stimulation in the PAG can alter the acquisition and consolidation of contextual fear behavior processes.

Animals↗

PubMed1997

Vasoactive intestinal polypeptide microinjections into the oral pontine tegmentum enhance rapid eye movement sleep in the rat.

Rapid eye movement sleep can be elicited in the rat by microinjection of the cholinergic agonist carbachol into the oral pontine reticular nucleus. Intracerebroventricular administration, during the light period, of vasoactive intestinal peptide enhances rapid eye movement sleep in several species. Since this peptide is co-localized with acetylcholine in many neurons in the central nervous system, it was assumed that the oral pontine tegmentum could also be one target for vasoactive intestinal peptide to induce rapid eye movement sleep. This hypothesis was tested by recording the sleep-wakefulness cycle in freely-moving rats injected with vasoactive intestinal peptide or its fragments (1-12 and 10-28) directly into the oral pontine reticular nucleus. when administered into the posterior part of this nucleus, vasoactive intestinal peptide at 1 and 10 ng (in 0.1 microliter of saline), but not its fragments, induced a 2-fold enhancement of rapid eye movement sleep during 4 h, at the expense of wakefulness. At the dose of 10 ng, a significant increase in rapid eye movement sleep persisted for up to 8 h. Moreover, when the peptide was injected into the centre of the positive zone, rapid eye movement sleep was enhanced during three to eight consecutive days. These data provide the first evidence that rapid eye movement sleep can be elicited at both short- and long-term by a single intracerebral microinjection of vasoactive intestinal peptide. Peptidergic mechanisms, possibly in association with cholinergic mechanisms, within the caudal part of the oral pontine reticular nucleus may play a critical role in the long-term regulation of rapid eye movement sleep in rats.

Animals↗

PubMed2001

Microinjection of arginine vasopressin into the central nucleus of amygdala suppressed nociceptive jaw opening reflex in freely moving rats.

This study was performed to examine the antinociceptive effect after microinjection of arginine vasopressin (AVP) into the central nucleus of amygdala. We recorded the jaw opening reflex in freely moving rats. After injection of 0.2 or 0.4 nM AVP into the central nucleus of amygdala, digastric electromyogram (dEMG) was suppressed to 55 +/- 5% or 88 +/- 3 of the control. Artificial cerebrospinal fluid had no effects on the basal dEMG activity. V(1) vasopressin receptor antagonist blocked the suppressive effect produced by microinjection of 0.4 nM AVP from 53 +/- 3 to 81 +/- 3% of the control. However, V(2) vasopressin receptor antagonist did not affect changes in dEMG. We observed dEMG activity after intracerebroventricular injection of naloxone, methysergide, or phentolamine. All drugs did not affect the basal dEMG activity at our dose. Naloxone blocked the suppressive effect of 0.4 nM AVP from 42 +/- 4 to 79 +/- 5% of the control. Methysergide also inhibited the suppression of dEMG from 44 +/- 3 to 83 +/- 6% of the control. However, phentolamine, an alpha-adrenergic receptor antagonist, did not affect the suppression of dEMG. These results indicate AVP in the central nucleus of amygdala has potent analgesic effects in the orofacial area. The antinociception of central AVP seems to be mediated by opioid and serotonergic pathways.

Adrenergic alpha-Antagonists↗

PubMed1997

Effects of microinjections of substance P into the suprachiasmatic nucleus region on hamster wheel-running rhythms.

The suprachiasmatic nucleus (SCN) receives a direct retinal projection, which in rats includes substance P (SP)-immunoreactive retinal ganglion cells. While SP has been shown to have neurophysiological effects on SCN cells in Syrian hamsters and rats, it is not known what effects SP in the SCN has on circadian rhythms in hamsters. We examined this question using male Syrian hamsters that were implanted with cannulas aimed at the SCN region and maintained in constant dim red lighting conditions. Hamsters received 0.5 microl microinjections of saline or SP (500 pmol in saline) at a variety of circadian times (CT). Saline injections had little or no phase-shifting effects at any phase tested. SP had no significant effects at CT4-8, 16-20, or 20-24, but did cause small phase delays of -23.7 +/- 7 min (mean +/- sem) at CT12-16. In order to examine the dose-response relations of this effect, hamsters were also microinjected with 50 and 2500 pmol of SP at CT12-16. Both the 50 and 2500 pmol doses induced very small phase delays (-14.2 +/- 7 min and -18.2 +/- 5 min, respectively), indicating no obvious dose dependence within this range. These results do not suggest that SP alone in the SCN mimics light effects on circadian rhythms or is a key neurotransmitter involved in photic entrainment. It remains to be determined whether SP interacts with other transmitters in the SCN to modulate their effects on rhythm phase.

Animals↗

PubMed2000

Behavioral and c-fos expression changes induced by nitric oxide donors microinjected into the dorsal periaqueductal gray.

The dorsolateral periaqueductal gray matter (DLPAG) is a key structure in behavioral and autonomic expression of defensive reactions. Inhibitors of nitric oxide (NO) synthase microinjected into the DLPAG are anxiolytic. The purpose of the present study was to evaluate the behavioral effects produced by administration of two NO donors, SIN-1 or DEA/NO, into the DLPAG. We also employed the detection of Fos-like immunoreactivity (FLI) to reveal brain areas activated by SIN-1 administration. Male Wistar rats (n = 7-11/group) received intra-DLPAG injection of SIN-1 (150 or 300 nmol), DEA/NO (150, 300, or 600 nmol), or saline (0.5 microl), and their behavior was observed in an open arena during 15 min. For the FLI assay, the animals (n = 3-5/group) were sacrificed 2.25 h after the drug. In a second experiment, rats (n = 5-7/group) received a first intra-DLPAG injection of saline or methylene blue (MB, 30 nmol), an NO antagonist, followed by saline or SIN-1 (300 nmol). SIN-1 (300 nmol) induced a flight response characterized by coordinated running and oriented jumps with escape attempts. Similar but short-lasting changes were seen after the administration of DEA/NO. FLI was dose-dependently induced by SIN-1 in several regions related to defensive reactions, including the periaqueductal gray, hypothalamic nuclei, medial amygdala, and cingulate cortex (analysis of variance, p < 0.05). A greater number of neurons showing FLI was found ipsilateral to the microinjection site. The drug effect was greater at this side in the bed nucleus of the stria terminalis, paraventricular and lateral hypothalamus, cingulate cortex, septohipoccampal nucleus, and horizontal limb of the diagonal band. The increase in SIN-1-induced FLI was attenuated by MB pretreatment in most regions. These results suggest that NO may participate in the modulation of defensive responses in the DLPAG.

Animals↗

PubMed2004

Effects of 5-HT1B receptor ligands microinjected into the ventral tegmental area on the locomotor and sensitizating effects of cocaine in rats.

The present study was aimed at finding out whether 5-HT(1B) receptors located in the ventral tegmental area (VTA) played a role in the locomotor hyperactivity induced by a single dose of cocaine and in the sensitization evoked by repeated exposure to the psychostimulant in rats. Male Wistar rats, implanted bilaterally with cannulae in the VTA, were microinjected with GR 55562 (an antagonist of 5-HT(1B) receptors) or CP 93129 (an agonist of 5-HT(1B) receptors). GR 55562 (0.3-3 microg/side) did not affect locomotor hyperactivity response to a single dose of cocaine (10 mg/kg). CP 93129 in a dose of 1 microg/side (but not lower), which stimulated basal locomotor activity, enhanced the cocaine-induced locomotor hyperactivity. The rats that were treated repeatedly (for 5 days) with cocaine (10 mg/kg) and then challenged with cocaine (10 mg/kg) after 5-day withdrawal period (day 10 of the experiment) showed significantly higher locomotor hyperactivity compared to the effect observed in saline-pretreated and cocaine-challenged rats. GR 55562 (a dose of 3 microg/side, but not lower), administered for 5 days into the VTA just prior to daily cocaine, attenuated cocaine sensitization. When injected for 5 days into the VTA, CP 93129 (0.03-0.1 microg/side) enhanced the development of cocaine sensitization. The enhancing effect of CP 93129 (0.1 microg/side) was blocked by GR 55562 (1 microg/side). To examine the effects of GR 55562 and CP 93129 on the expression of cocaine sensitization, the 5-HT(1B) receptor ligands were given acutely before the challenge dose of cocaine administered on day 10. No change in cocaine sensitization was observed after intra-VTA microinjections of GR 55562 (0.3-3 microg/side) or CP 93129 (0.1-1 microg/side). Our findings suggest that 5-HT(1B) receptors located in the VTA play a permissive role in the development of cocaine sensitization, but are not involved in the locomotor hyperactivity induced by a single dose of cocaine or in the expression of the sensitization to the psychostimulant.

Analysis of Variance↗

PubMed1982

Subcellular transport and ribosomal incorporation of microinjected protein S6 in oocytes from Xenopus laevis.

Protein S6 was isolated from 40S ribosomal subunits of Xenopus laevis oocytes, labeled with sodium boro[3H]hydride, and microinjected back into oocytes. In the first 4 h of incubation, the uptake of S6 into the nucleus increased to a maximum, with, however, no detectable incorporation into 40S ribosomal subunits. After this lag period, S6 was progressively integrated into the small ribosomal subunit. When rRNA transcription was inhibited by actinomycin D, the uptake of S6 into the nucleus and its consequent incorporation into the 40S subunit were significantly reduced. Moreover, when enucleated oocytes were microinjected, little or no S6 was found in the 40S subunits, also suggesting that integration of S6 into ribosomes is linked to rRNA precursor synthesis. In contrast to S6, the acidic protein eL12 isolated from Artemia salina or X. laevis oocyte 60S subunits was integrated into the large subunit independently of the nucleus or active rRNA synthesis.

Animals↗

PubMed1999

Isolation and microinjection of somatic cell-derived mitochondria and germline heteroplasmy in transmitochondrial mice.

At present, there are no means for creation of relevant animal models of human mitochondrial DNA (mtDNA)-based diseases in a directed fashion. As an initial step towards this end, we have developed a microinjection technique for transfer of isolated, viable mitochondria between two mouse species. Previously, we reported detection, by nested PCR with species-specific primer sets, of Mus spretus mtDNA in Mus musculus domesticus blastocyts following zygote microinjection and culture. We now report the production of transmitochondrial founder mice, and germline transmission of the heteroplasmic state in a maternal lineage. Heteroplasmic mice produced by this technique will be useful in the study of mitochondrial dynamics and may hasten the creation of animal models of human mtDNA-based diseases.

Animals↗

PubMedDate not supplied

The effects of microinjection of neurotensin into the caudate nucleus of the rat brain on the performance and extinction of a conditioned motor reflex.

The studies reported here demonstrate that microinjection of neurotensin into the caudate nucleus of the rat brain facilitated extinction of a conditioned motor reflex with reinforcement provided by drinking. Neurotensin had positive effects on the process of post-extinction inhibition in subsequent experiments. Neurotensin microinjections had no marked effect on the performance of the conditioned reflex, though it weakened the emotional tension of the animals in an "open field" test. It is concluded that the functional importance of neurotensin at the level of the caudate nucleus is associated less with the regulation of motor function than with optimizing the motivational-emotional state of the animal.

Animals↗

PubMed1997

Mitochondria transfer into mouse ova by microinjection.

A method for mitochondria isolation and interspecific transfer of mitochondria was developed in mice. Mitochondria were isolated from Mus spretus liver samples for microinjection into fertilized ova obtained from superovulated M. musculus domesticus females. Electron microscopic observations of mitochondria preparations used for microinjection demonstrated intact mitochondrial vesicles with little microsomal contamination. Species-specific nested PCR primers complementary to sequence differences in the mitochondrial DNA D-loop region revealed high rates of successful transfer of foreign mitochondria after isolation and injection into zygotes cultured through the blastocyst stage of embryonic development. Of 217 zygotes, 67 survived mitochondria injection and 23 out of 37 zygotes developed were at the blastocyst-stage of embryonic development after 4.5 days of in vitro culture. All 23 of these blastocysts contained detectable levels of foreign mitochondria. These results represent an initial step in developing a model system to study mitochondrial dynamics and development of therapeutic strategies for human metabolic diseases affected by aberrations in mitochondrial function or mutation.

Animals↗

PubMed1997

Microinjection of morphine into the nucleus accumbens impairs contextual learning in rats.

A unilateral microinjection of morphine into the amygdala impaired fear conditioning to both a conditioned stimulus (CS) paired with shock and the context where shock occurred, whereas a microinjection of morphine into the nucleus accumbens (NA) spared fear conditioning to the CS but impaired, in a dose-dependent and receptor-specific manner, fear conditioning to the context. Morphine in the NA also spared extinction and latent inhibition of a CS but abolished the context specificity of these effects and eliminated the increase in discriminability that results from preexposure to a to-be-shocked context. The results identify a role for the NA in the processes by which rats learn about a context and are discussed in terms of an opioid disruption of either within-context associations or of attentional processes that contribute to such associations.

Animals↗