A simplified intracranial cannula for chemical stimulation or long-term infusion of the brain

Myers, R.D.; Casaday, George; Holman, R. Bruce

doi:10.1016/0031-9384(67)90016-9

Cited by 29 publications

(7 citation statements)

References 8 publications

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“…(3) complications given in (2) often lead to manifestation of behavioral and motor deficits and even death in the animals (Yaksh and Rudy, 1976;Myers et al, 1966); (4) preparation of cannula systems and surgical procedure are time consuming (LoPachin et al, 1981;Yaksh and Rudy, 1976;Consiglio and Lucion, 2000;Myers et al, 1966). In comparison, the technique described here provides several advantages: it is less time consuming, less invasive, and has proven reliable for collecting sizable, uncontaminated volumes of CSF from rats.…”

Section: Discussionmentioning

confidence: 86%

Technique for collection of cerebrospinal fluid from the cisterna magna in rat

Pegg

Stroink

et al. 2010

Journal of Neuroscience Methods

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Section: Discussionmentioning

confidence: 86%

Technique for collection of cerebrospinal fluid from the cisterna magna in rat

Pegg

Stroink

et al. 2010

Journal of Neuroscience Methods

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“…The data were subjected to the two-tailed Student's t test for nonpaired samples. Myers, Casaday & Holman (1967), was introduced through the hole and its tip aimed at the coordinates 5.4 mm anterior, 2 mm lateral and 3 mm vertical (according to Pellegrino & Cushman, 1967), fixed to the skull with dental cement, and the skin sewn up. After the operation rats were housed individually, and used from the 10th post-operative day once or twice a week during four to five weeks.…”

Section: Chemical Estimationsmentioning

confidence: 99%

The Influence of Cerebral 5‐hydroxytryptamine on Catalepsy Induced by Brain‐amine Depleting Neuroleptics or by Cholinomimetics

Fuenmayor

Vogt

1979

British J Pharmacology

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1 Catalepsy was produced in rats and mice by the subcutaneous injection of either tetrabenazine or the butyrophenone U-32,802A (4'-fluoro-4-{[4-(p-fluorophenyl)3-cyclohexen-1-yl]aminoI butyrophenone hydrochloride). Catalepsy was evaluated by the duration of total immobility on a vertical grid.2 Pretreatment with p-chlorophenylalanine (PCPA) reduced the intensity of catalepsy by 50% or more, whereas its time course remained the same. 3 5-Hydroxytryptophan (5-HTP), 10 mg/kg, enhanced the catalepsy induced by U-32,802A or tetrabenazine, provided it was administered soon (45 min) after the neuroleptic; injections at 90 min had no effect. Otherwise untreated rats given this dose of 5-HTP behaved normally on the grid. 4 The anticataleptic effect of PCPA was reversed by 5-HTP.5 Measurable changes in 5-hydroxytryptamine (5-HT) metabolism in the rat forebrain accompanied the modification of catalepsy by 5-HTP and PCPA. 6 Methysergide (5 mg/kg) given 30 min before the neuroleptics to either mice or rats reduced the catalepsy, assessed 2.5 h after the methysergide. It also prevented the increase in neurolepticinduced catalepsy following 5-HTP, 10 mg/kg. 7 Tryptophan, like 5-HTP, increased the catalepsy seen in mice after U-32,802A and tetrabenazine, and increased the production of 5-hydroxyindol-3-ylacetic acid in the forebrain. 8 In the rat, intracerebroventricular injection of physostigmine produced catalepsy which was not modified by methysergide or PCPA but was abolished by atropine. Similarly, in the mouse, catalepsy induced by the subcutaneous injection of pilocarpine was abolished by atropine but not affected by either methysergide or 5-HTP. 9 Atropine greatly reduced the catalepsy induced by U-32,802A and tetrabenazine but lowered striatal homovanillic acid (HVA) only after U-32,802A. D,L-DOPA, 20 mg/kg, diminished the cataleptogenic effect of both neuroleptics and raised striatal HVA.10 The results support the view that there is a facilitating or permissive action of 5-HT-containing neurones on neuroleptic-induced catalepsy.

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“…The rats were anaesthetized with sodium pentobarbitone (50-60 mg/kg) and the cannulae implanted according to the stereotaxic coordinates of De Groot (1959): anterior 5 4, lateral 2-0 and vertical + 2 5. The cannula was a simplified version of that described earlier (Myers, Casaday & Holman, 1967): a piece was cut from the nozzle of a IP0 ml plastic syringe barrel to form a pedestal, the base of which was 7 mm wide and the overall height 5 mm. A 15 mm length of 21 gauge stainless steel tubing bevelled to a 300 angle at one end served as the outer guide.…”

Section: Methodsmentioning

confidence: 99%

Sleep produced by clonidine (2‐(2,6‐dichlorophenylamino)‐2‐imidazoline hydrochloride)

Holman

Shillito

Vogt

1971

British J Pharmacology

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Summary1. The dose of clonidine (given intravenously) required to elicit sleep in the young chick is 1/25th to 1/50th of an equiactive dose of noradrenaline. The approximate ED50 is 0-01 umol/kg. Phentolamine (10-15 mg/kg, but not 5 mg/kg) antagonizes the action of both clonidine and noradrenaline. 2. Intensive treatment with p-chlorophenylalanine (700 mg/kg for 3-4 days) does not prevent the hypnotic effect of clonidine in the chick, although brain 5-HT is reduced to 15% of normal. Neither is natural sleep modified.3. Sleep after clonidine is not affected by methysergide (0 1-1 ,umol/kg, i.m.), but prevented by LSD (0-1-03 Amol/kg). The effect of LSD is interpreted-as a physiological antagonism. 4. Clonidine (50 mg/kg) injected intravenously into adult rats causes sleep which is not abolished by phentolamine (5 mg/kg) or by p-chlorophenylalanine in doses which interfere with natural sleep. 5. When, per kg body weight, the same dose of clonidine is injected into the lateral cerebral ventricle of rats, sleep ensues in more than half the animals, and persistent eating in about a third; only one -of seventeen rats showed no change in behaviour. Eating and sleeping remained unaltered after p-chlorophenylalanine. The actual dose of clonidine injected into the lateral ventricle was 0 037 ,umol, amounting to about 0 15 ptmol/kg or 15 times the dose required intravenously in the chick. Noradrenaline 0S15 ttmol per (intraventricular) injection caused eating but no sleep, whereas higher doses produced ataxia and paresis. 6. The work suggests that clonidine does not elicit sleep by an action requiring the integrity of the 5-HT-containing neurones arising in the raphe nuclei, and that its action is not on tryptamine receptors. In the chick, sleep appears to be produced by a central sympathomimetic effect; it is possible, but not certain, that this also holds for the rat. 7. The intravenous hypnotic dose of clonidine for the cat is about the same as that for the rat, but injection is not accompanied by signs of peripheral sympathetic stimulation.

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A simplified intracranial cannula for chemical stimulation or long-term infusion of the brain

Cited by 29 publications

References 8 publications

Technique for collection of cerebrospinal fluid from the cisterna magna in rat

Technique for collection of cerebrospinal fluid from the cisterna magna in rat

The Influence of Cerebral 5‐hydroxytryptamine on Catalepsy Induced by Brain‐amine Depleting Neuroleptics or by Cholinomimetics

Sleep produced by clonidine (2‐(2,6‐dichlorophenylamino)‐2‐imidazoline hydrochloride)

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