Freehand cerebroventricular injection technique for unanesthetized rats

Verster, F. de Balbian; Robinson, C A; Hengeveld, C.; Bush, E Sanders

doi:10.1016/0024-3205(71)90268-2

Cited by 80 publications

(9 citation statements)

References 8 publications

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“…administration, stainless steel guide cannulae (20 gauge, hypodermic injection needle 1 / 1; Sato, Tokyo) were stereotaxically implanted in the skull of rats unilaterally, according to the method of de Balbian Vester et al (15), under pentobarbital anesthesia (50 mg / kg, i.p.). Stereotaxic coordinates were 2-mm left lateral to the sagittal suture and 1-mm caudal to the coronal suture.…”

Section: Experiments Proceduresmentioning

confidence: 99%

Activation of Spinal Anti-analgesic System Following Electroacupuncture Stimulation in Rats

et al. 2005

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Abstract. We evaluated the interaction between electroacupuncture (EA)-induced antinociception and an endogenous anti-analgesic system. EA was applied to the ST-36 acupoint for 45 min in male Sprague-Dawley rats, and pain thresholds were assessed by the hind-paw pressure test. EA produced a marked increase in pain thresholds and its antinociceptive action was completely reversed by naloxone (5 mg / kg). The analgesic effects of subcutaneous morphine (7 mg / kg) following EA stimulation were significantly attenuated. The attenuation of morphine analgesia was inversely proportional to the time intervals between EA termination and morphine injection, and the effect was not observed 120 min after EA stimulation. The analgesic effects of i.t. morphine (10 µg), but not i.c.v. morphine (25 µg), following EA were also attenuated. On the other hand, systemic morphine (7 mg / kg)-induced hyperthermia was not affected by EA. Moreover, i.c.v. morphine, but not i.t. morphine, produced hyperthermia. The i.c.v. morphineinduced hyperthermia was not affected by EA, similar to i.c.v. morphine analgesia. These results suggest that the attenuation of morphine analgesia following EA, that is, the activation of an endogenous anti-analgesic system, is closely related to the activation of an analgesic system by EA and that the spinal cord plays a critical role in the activation of the endogenous anti-analgesic systems.

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Section: Experiments Proceduresmentioning

confidence: 99%

Activation of Spinal Anti-analgesic System Following Electroacupuncture Stimulation in Rats

et al. 2005

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“…The endoscope, which was connected to a color camera (Toshiba)-digital AV mixer (Panasonic)-VCR (Panasonic) system, was lowered until an image of BV and the suture were in focus on a video monitor. A PE-20 polyethylene catheter, with a bulbous expansion as a stop (de Balbian Verster et al, 1971), was inserted into the injection hole extending 3.5 mm into the egg with the other end connected to a syringe mounted on an infusion pump (Harvard Apparatus, Millis, MA). The egg was allowed to acclimate for 5 min before a baseline (BL) video recording was made.…”

Section: Experiments 1: Blood Vessel Visualization Recording and Quamentioning

confidence: 99%

Vasoconstriction Caused by Cocaine is Enhanced by Sodium Salicylate: Is Inducible Nitric Oxide Synthase mRNA Related?

Mendoza-Baumgart

Pravetoni

Sparber

2004

Neuropsychopharmacol

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We have previously found that sodium salicylate (NaSal), injected into chicken eggs at nontoxic doses used for quantifying hydroxyl free radicals in hearts and brains of embryos, caused or exacerbated hemorrhages and dramatically reduced hatchability when combined with cocaine (Coc). It has also been reported that inducible nitric oxide synthase (iNOS) gene expression is altered in brain in response to vascular damage and inflammation. In this study we measured diameters of membrane-bound blood vessels (BV) before and after pretreatment with saline (NaCl) or NaSal (100 mg/kg egg), followed by infusion of either NaCl or Coc HCl (total of 67.5 mg/kg egg) during 15 min. Brains and hearts of the embryos were then analyzed for iNOS messenger RNA (mRNA) concentrations. Coc caused vasoconstriction that was significant 5 min postinfusion (5 min PI) of the entire dose (ie after 67.5 mg/kg egg). Significant vasoconstriction was evident within 5 min in the group injected with NaSal followed by infusion with Coc (ie after 22.5 mg Coc/kg egg). Expression of iNOS mRNA was significantly increased only in the brains of the group exposed to NaSal plus Coc, and the increase was inversely related to BV diameter. These data are discussed in relation to effects of salicylate upon prostanoid synthesis and/or nitric oxide synthesis via iNOS inhibition and their possible relationship to Coc-associated cerebral vascular and/or cardiovascular events in abusing humans.

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“…Port Washington. N.Y., USA) and implanted with an indwelling PE-20 cannula within the left lateral cerebral ven tricle [36], Eight days later, the same animals received, under light halothane anesthesia, intravenous catheters, manufactured from si lastic tubing (0.025 inch ID x 0.047 inch OD. Dow Corning, Mid land.…”

Section: Animalsmentioning

confidence: 99%

Antagonism of Type II, but Not Type I Glucocorticoid Receptors Results in Elevated Basal Luteinizing Hormone Release in Male Rats

Briski

Sylvester²

1994

Neuroendocrinology

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The present studies utilized a phaimacologic approach to evaluate the role of corticosterone-preferring mineralocorticoid receptors (type I or MR) versus classic glucocorticoid receptors (type II or GR) in the regulation of basal pituitary luteinizing hormone (LH) secretion in vivo in male rats. Animals bearing indwelling intracardiac venous catheters received a subcutaneous (s.c.) injection of either vehicle, the MR antagonist, RU 752 (0.5 or 5.0 mg/kg body weight), or the GR antagonist, RU 486 (0.5 or 5.0 mg/kg body weight). Additional groups of rats were implanted with indwelling intracerebroventricular (i.c.v.) cannulas and intravenous catheters for drug administration and blood withdrawal, respectively, and injected i.c.v. with vehicle or graded doses (0.1, 1.0 or 10.0 µg/rat) of RU 752 or RU 486. The MR RU 752 failed to alter plasma LH concentrations regardless of dose or route of administration. In contrast, the GR antagonist, RU 486, elicited significant, dose-dependent increases in circulating LH when given either s.c. or i.c.v. Animals injected s.c. with either 0.5 or 5.0 mg RU 486/kg body weight showed elevated plasma LH levels; while the magnitude of this secretory response was not different between the two drug-treated groups, hormone levels remained elevated over baseline for a longer period of time in rats given the higher dose. Central administration of RU 486 at a dose of either 1.0 or 10.0 µg also resulted in elevated LH release; both the magnitude and duration of this increase in plasma LH were dose-dependent. In additional experiments, groups of rats were pretreated with vehicle or the synthetic GR agonist, RU 362, before administration of RU 486. These studies showed that the stimulatory effect of RU 486 on peripheral LH was abolished by prior interaction of GR with the exogenous ligand. In summary, the ability of the GR antagonist, RU 486, to promote an increase in plasma LH concentrations in intact male rats suggests that endogenous glucocorticoids exert a tonic inhibitory tonus on in vivo LH release in these animals, and that GR mediate these suppressive effects. Observations that drug-induced elevations in circulating LH were abolished by pretreatment with the GR agonist, RU 362, suggest that the stimulatory effects of RU 486 on hormone release were achieved by an antiglucocorticoid action. The current findings that plasma LH was increased following intracranial administration of RU 486 implicate central GR in neuroendocrine mechanisms governing pituitary LH.

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Freehand cerebroventricular injection technique for unanesthetized rats

Cited by 80 publications

References 8 publications

Activation of Spinal Anti-analgesic System Following Electroacupuncture Stimulation in Rats

Activation of Spinal Anti-analgesic System Following Electroacupuncture Stimulation in Rats

Vasoconstriction Caused by Cocaine is Enhanced by Sodium Salicylate: Is Inducible Nitric Oxide Synthase mRNA Related?

Antagonism of Type II, but Not Type I Glucocorticoid Receptors Results in Elevated Basal Luteinizing Hormone Release in Male Rats

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