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Results for “Microinjection”

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PubMed1986

Transient correction of excision repair defects in fibroblasts of 9 xeroderma pigmentosum complementation groups by microinjection of crude human cell extracts.

Crude extracts from human cells were microinjected into the cytoplasm of cultured fibroblasts from 9 excision-deficient xeroderma pigmentosum (XP) complementation groups. The level of UV-induced unscheduled DNA synthesis (UDS) was measured to determine the effect of the extract on the repair capacity of the injected cells. With a sensitive UDS assay procedure a (transient) increase in UV-induced UDS level was found in fibroblasts from all complementation groups after injection of extracts from repair-proficient (HeLa) or complementing XP cells (except in the case of XP-G), but not after introduction of extracts from cells belonging to the same complementation group. This indicates that the phenotypic correction is exerted by complementation-group-specific factors in the extract, a conclusion that is in agreement with the observation that different levels of correction are found for different complementation groups. The XP-G-correcting factor was shown to be sensitive to proteolytic degradation, suggesting that it is a protein like the XP-A factor.

Cell Fusion↗

PubMed1990

Electrophysiological study of dyskinesia produced by microinjection of picrotoxin into the striatum of the rat.

The neuronal mechanism of dyskinesia of the contralateral forelimb produced by microinjection of picrotoxin (PTX), a GABA antagonist, into the caudoputaminal unit (CPU) was analyzed electrophysiologically. PTX injection resulted in production of sharp, negative field potentials with or without preceding or succeeding positivity in the CPU and cerebral cortex (CX). These spike potentials first appeared in the CPU, thereafter within the CX, and were finally accompanied by dyskinesia indicated by electromyogram activity of the forelimb in association with fully developed CX spike potentials. Dyskinesia disappeared reversibly by cooling, and irreversibly by ablation, of the CX, indicating the crucial participation of the CX in the manifestation of dyskinesia. CPU spike potentials remained even after isolation of the CPU from its major afferents. Grouped discharges of extracellularly recorded single-unit spikes were observed in the CPU in association with the development of CPU spike potentials. Single-unit spikes of the pars reticulata of the substantia nigra were inhibited, and those of the ventromedial nucleus (VM) of the thalamus were excited in association with CPU spike potentials. We therefore propose that the primary origin of the dyskinesia is the CPU and that the inhibitory CPU efferent, as well as the nigrothalamic, pathway plays a basic role in the manifestation of the dyskinesia.

Action Potentials↗

PubMed1993

Effects of microinjection of a GABA antagonist into the periaqueductal gray upon electrically-induced vocalization in decerebrate cats.

The effects of the GABA antagonist bicuculline methiodide (BIC), microinjected into the ventrolateral periaqueductal gray (PAG) on the stimulus threshold of electrically-induced vocalization were examined in unanesthetized precollicular-postmamillary decerebrate cats. To induce vocalization, repetitive electrical stimulation (0.2 ms, 100 Hz, 5-10 s duration) was delivered to the caudal portion of the PAG (30 to 300 microA) or the pontine call site (PCS) (10 to 60 microA) in the ventrolateral pontine reticular formation. Injection of 0.1 microliter of 2 mM BIC into the caudal portion of the PAG decreased the stimulus thresholds of the PCS and the injection site for about 1 h. Injection of BIC into the reticular formation near the PAG, where the electrical stimulation induced vocalization, did not decrease the stimulus thresholds of the PCS or the injection site. These results indicate that GABAergic inhibition regulates the excitability of the cells within the ventrolateral PAG, which exerts an excitatory effect on the lower brain structures that produce vocalization.

Animals↗

PubMed1991

Suppression of feeding induced by phenylephrine microinjections within the paraventricular hypothalamus in rats.

Rats were treated with the alpha-2 agonist clonidine (4, 20 and 50 nMol) and with the alpha-1 agonist 1-phenylephrine (50, 100, 200 and 400 nMol). Phenylpropanolamine (PPA) is a phenythylamine anorectic drug that exerts direct agonist effects predominantly on alpha-1 adrenergic receptors, with some alpha-2 adrenergic activity. We recently reported that injection of PPA significantly suppressed feeding in rats. Prior studies have noted that into the paraventricular hypothalamus (PVN) microinjections of the alpha-2 adrenergic receptor agonist clonidine into the PVN induced feeding behavior in satiated rats. However, the effect on feeding of administration of alpha-1 adrenergic agonists within the PVN remains unknown. In the present study, unilateral guide cannulae aimed at the PVN were surgically implanted in adult male rats. In an initial 60 min feeding test conducted under free-feeding ("non-deprived") conditions, each rat was found to eat significantly more food after injection of 25 nMol norepinephrine (NE) into the PVN. In subsequent tests, the feeding increased significantly to 4 nMol clonidine; however, feeding was suppressed by 50 nMol clonidine. Food intake after 20 nMol clonidine was not significantly different from that recorded after vehicle. In contrast, phenylephrine (100-400 nMol) reliably suppressed feeding behavior. In the final phase of the study, the rats ate significantly less food after injection of 160 nMol PPA into the PVN but consumed significantly more food after a final injection of 25 nMol NE into the PVN. These results suggest that the anorexic action of PPA may be linked to activation of alpha-1 adrenergic receptors within the PVN.

Analysis of Variance↗

PubMedDate not supplied

Increases in heart rate and blood pressure produced by microinjections of atrial natriuretic factor into the AV3V region of rat brain.

Recent studies have provided evidence for the dense localization of atrial natriuretic factor (ANF) in the anteroventral third ventricle (AV3V) region of the rat brain. This area is currently thought to be involved in the regulation of blood pressure and fluid and electrolyte balance. To investigate whether ANF may play a role in central cardiovascular regulation, the effects of microinjection of ANF into the preoptic suprachiasmatic nucleus (POSC), which is located in the AV3V region of the brain, were examined in the present study. Low doses of ANF (2-4 pmol) produced modest elevations in systolic and diastolic pressures, approximately 10-14%, and a small rise in HR of roughly 7%. Higher doses of ANF (20-40 pmol) produced significant increases in systolic (15-19%), mean arterial (12-14%) and pulse (25-36%) pressures. In addition, much larger increases in HR, approximately 20%, were produced by these higher doses of ANF. The onset of effects produced by ANF on BP and HR was seen 15-45 min after injection. Peak effects were usually observed approximately 60-150 min after onset, and the duration of the effect was 2-4 hours, after which time values usually returned to baseline. These studies indicate that ANF produces significant increases in BP and HR when injected at pmol doses into the POSC, and lends support to the idea that this peptide may play an important role in central cardiovascular regulatory mechanisms.

Animals↗

PubMedDate not supplied

Cardiovascular effects produced by microinjection of calcitonin gene-related peptide into the rat central amygdaloid nucleus.

Recent studies have provided evidence for a dense localization of calcitonin gene-related peptide (CGRP) and its receptors within the central amygdaloid nucleus (Ce) in rat brain. Since this nucleus has been thought to play a role in central cardiovascular regulation, the present study examined the cardiovascular effects subsequent to the microinjection of CGRP into the Ce. Doses of 50-500 pmol of CGRP produced a significant elevation of 11-15% in systolic, diastolic and mean arterial pressures. Heart rate was significantly elevated by 16-18% by these doses of CGRP. The time course of the effects of CGRP revealed that onset of action occurred after 15-20 min, peak effects were seen at approximately 30-40 min after onset and the effects of the peptide usually lasted for at least 2 hr, after which time BP and HR values returned to baseline. The present study demonstrates that CGRP produces significant increases in both BP and HR when pmol doses of the peptide are injected into the Ce. It is suggested that in the Ce, CGRP plays a neuromodulatory role in cardiovascular function.

Amygdala↗

PubMedDate not supplied

Propranolol and methylatropine antagonize the cardiovascular effects produced by microinjection of the TRH analog MK-771 into the preoptic suprachiasmatic nucleus.

Thyrotropin-releasing hormone (TRH) has been shown to increase heart rate as well as blood pressure when administered into rat brain. The present study investigated the mechanism by which the TRH analog MK-771 produces these effects when injected into the preoptic suprachiasmatic nucleus (POSC). MK-771, at a dose of 125 pmol (50 ng), produced significant increases in both heart rate and blood pressure. These effects occurred within 5 minutes of microinjection and lasted approximately 20-30 minutes. Pretreatment with either the beta-adrenergic antagonist propranolol or the muscarinic antagonist methylatropine, administered into the POSC, significantly altered the response produced by MK-771. Propranolol, at a dose of 7 nmol, and methylatropine at a dose of 0.5 nmol, significantly inhibited the tachycardia produced by MK-771. In addition, methylatropine, at a dose of 0.5 nmol, significantly reduced the increase in diastolic pressure produced by the TRH agonist. These results are consistent with the idea that TRH agonists, when administered centrally, produce cardiovascular alterations through the autonomic nervous system.

Animals↗

PubMedDate not supplied

In vivo conversion of vasopressin after microinjection into limbic brain areas of rats.

The nonapeptide [Arg8]vasopressin was rapidly degraded with a half-life of lower than 1 minute after local administration into the hippocampus. During the conversion of vasopressin C-terminal fragments were transiently generated. The profile of these metabolites indicated that they were formed by aminopeptidase activity. The aminopeptidase inhibitor amastatin partially inhibited the conversion of vasopressin. A minor pathway involved cleavages in the C-terminus. The results indicate a predominant involvement of aminopeptidase activity in the in vivo metabolism of exogenous vasopressin in the brain. Since products of this metabolic route have been shown to have potent behavioral activities, the behavioral effects seen after microinjection of vasopressin in the brain may be partially due to generation of vasopressin fragments.

Amino Acid Sequence↗

PubMed1995

Psychostimulant-like effect of central microinjection of neurotensin on brain stimulation reward.

The curve shift method and the brain stimulation reward paradigm were used to dissociate reward and performance changes and determine whether unilateral ICV microinjection of neurotensin (3, 10, and 30 micrograms/10 microliters) produces neuroleptic- or psychostimulant-like effect on a dopamine-dependent behavior. At the highest dose tested, neurotensin potentiated brain stimulation reward, producing a significant time-dependent decrease in frequency threshold. Neurotensin also suppressed maximal rate of responding at every dose tested, suggesting that it was more effective at attenuating performance capability. These results suggest that a centrally acting neurotensin receptor agonist may specifically stimulate dopamine-dependent behaviors, producing psychostimulant-like effect that can be attenuated or masked by a suppression of performance capability.

Animals↗

PubMed1979

Rapid behavioural and biochemical effects of tetanus toxin microinjected into the substantia nigra: a dual role for GABA?

Tetanus toxin (200--250 mouse lethal doses) microinjected unilaterally into the substantia nigra produced rapid behavioural and biochemical effects. If the toxin was injected into the rostral part of the substantia nigra (SN), contralateral turning was observed. Raised ipsilateral striatal levels of the dopamine (DA) metabolite, homovanillic acid (HVA), indicated that this turning was due to activation of the nigro-striatal dopamine system. Caudal nigral injections of tetanus toxin produced ipsilateral turning. Biochemical estimations suggest that this behaviour change was mediated by a non-dopamine (non-DA) pathway.

Animals↗

PubMed1979

Hypotensive response in spontaneously hypertensive rats following microinjection of alpha-methylnoradrenaline in the caudal brain-stem.

Local microinjection of 1.25 nmol (-)-alpha-methylnoradrenaline in the A2-region of the nucleus tractus solitarii (NTS) caused a decrease of blood pressure and heart rate in both spontaneous hypertensive rats (SHR) and Wistar-Kyoto (W/K) rats. Although the maximal responses in both strains did not differ, the decrease in blood pressure lasted longer in the SHR. These results do not support the concept of a diminished sensitivity of catecholaminergic receptors in the NTS of SHR to alpha-methylnoradrenaline.

Animals↗

PubMed1979

Antinociceptive action following microinjection of methionine-enkephalin in the nucleus raphe magnus of the rat.

The analgesic effect of the microinjection of low doses of methione-enkephalin (20 micrograms in 0.5 microliter) into the caudal brain stem of the unrestrained rat was investigated by means of one vocalisation test. Immediate short duration significant increases in threshold (21%) were seen from sites in the nucleus raphé magnus (NRM). Delayed effects were seen from sites immediately adjacent to this nucleus; sites more lateral produced no significant effect. These results lend further support to the postulated role of NRM in antinociception.

Analgesics↗

PubMed1983

Formation of a glial scar following microinjection of fetal neurons into the hippocampus or midbrain of the adult rat: an immunocytochemical study.

Raphe tissue (minced or dissociated) from fetal rat was microinjected into adult hippocampus or midbrain, and the response of astrocytes observed by immunocytochemical staining for the astrocyte specific marker, glial fibrillary acidic protein (GFA). Astrocytes were observed to form a border around the transplanted cells. This border was visible as early as 7 days post-transplant and was still present up to 6 months later. The transplanted serotonergic cells, identified by immunocytochemical staining with a primary antibody to serotonin, appeared at the edge of the border but not beyond. This border may be responsible for preventing the complete integration of the transplanted cells with the adult host hippocampal and midbrain tissue.

Animals↗

PubMed1984

Haemodynamic effects of arginine-vasopressin microinjections into the nucleus tractus solitarius: a comparative study of vasopressin, a selective vasopressin receptor agonist and antagonist, and oxytocin.

Arginine-vasopressin (AVP) and related peptides were administered by microinjection into the nucleus tractus solitarius of the rat. AVP produced a rise both in mean arterial pressure and in heart rate. This effect was abolished by pretreatment with a specific antagonist of V1 receptors and was not seen either after injections of oxytocin or of the V2 agonist deamino-D-arginine-vasopressin. This study provides evidence for a specific action of vasopressin on the cardiovascular system in the nucleus of the tractus solitarius, which is mediated neither by V2 nor oxytocin receptors.

Animals↗

PubMed1984

Suppression of arterial pressure, heart rate and cardiac contractility following microinjection of kainic acid into the nucleus ambiguus of the rat.

In pentobarbital anesthetized rats, unilateral microinjection (500 ng) of the selective perikaryal excitotoxin, kainic acid, into the nucleus ambiguus promoted a significant suppression of arterial pressure, heart rate and cardiac contractility. The degree of such cardiovascular depression followed the order of heart contractility reduction (50.7%) greater than hypotension (28.9%) greater than bradycardia (20.8%) at the end of a 60-min postinjection period. We concluded that the nucleus ambiguus may exert its control on cardiac activities by both negative chronotropic and inotropic effects on the heart.

Animals↗

PubMed1985

Pulmonary edema as a cause for fulminant death following microinjection of kainic acid into the rat medulla oblongata.

The present study confirmed histopathologically the suggestion that pulmonary edema may underlie the fulminant death following microinjection of kainic acid into many medullary sites in rats anesthetized with pentobarbital sodium. We also observed a sustained elevation in systemic arterial pressure, cardiac contractility and heart rate before the animal succumbed to kainate neurotoxicity. It is suggested that the increased systemic hydrostatic pressure may retrogradely promote pulmonary hypertension that precipitates pulmonary edema.

Animals↗

PubMed1987

Microinjected clonidine inhibits noradrenergic neurons of the locus coeruleus in freely moving cats.

Microinjection of the alpha 2-adrenoceptor agonist, clonidine (CLON; 1.0 microgram/0.1 microliter) effected a virtually complete suppression of the spontaneous activity of noradrenergic neurons of the locus coeruleus in freely moving cats. This effect lasted for approximately 90 min and was reversible by systemic administration of the alpha 2-adrenoceptor antagonist, yohimbine. In contrast, CLON had no consistent effect on the activity of neighboring non-noradrenergic neurons. These results provide additional evidence for the direct inhibition of central noradrenergic neurons by CLON by demonstrating such effects independent of anesthesia or the behavioral effects of systemic drug administration. More generally, these findings demonstrate the usefulness of a technique in which small amounts of drug can be applied in small volumes to produce a neuropharmacologically specific effect upon locally recorded neurons in behaving animals.

Action Potentials↗

PubMed1988

Elicitation of intraspecific defence reactions in the rat from midbrain periaqueductal grey by microinjection of kainic acid, without neurotoxic effects.

Microinjection of 40 pmol of the neuroexcitotoxin, kainic acid (KA) in the midbrain periaqueductal grey region (PAG) evoked a significant increase in both defensive and immobile behaviours in rats tested in a social situation. The evoked reactions appeared identical to the rat's natural defensive reaction to attack by a conspecific, although they were evoked by the presence, rather than the attack, of another rat. The long duration and natural appearance of the KA-evoked reactions stand in contrast to the short, 'explosive' reactions evoked by injection in the PAG of other excitant amino acids. There was no behavioural evidence of a diminution in the effect of repeated injections of KA in the PAG, nor was there any histological evidence of neurotoxicity.

Animals↗