Cerebral ventricular infusions in unrestrained rats.

Goodrich, Cecilie A.; Greehey, B; Miller, T.; Pappenheimer, J. R.

doi:10.1152/jappl.1969.26.1.137

Cited by 41 publications

(17 citation statements)

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“…Surgical procedures for implantation of ventricular guide tubes and electroencephalogram (EEG)/EOG electrodes have been described (9,10). Calibrated glass bead thermistors (Fenwall; 1.2-mm outside diameter, 50 fl/'C) were implanted through burr holes in frontal bone: the thermistor leads were buried in a mound 6fdental cement that also insulated the screw electrodes and supported a 9-pin miniature electrical connector.…”

Section: Methodsmentioning

confidence: 99%

“…Chemical and physiological properties ofthe urinary factor resemble those of the sleep factor found in sterile cerebrospinal fluid and in acid/acetone extracts of brains from sleep-deprived animals (2,3). In rabbits, intraventricular infusion of10 pmol ofthe pure factor induces excess slow-wave sleep (SWS) for [5][6][7][8][9][10] hr after the infusion. The effects are primarily on the duration of SWS and on the amplitude of cortical slow waves; there is relatively little effect on rapid eye movement (REM) sleep.…”

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confidence: 99%

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Sleep-promoting effects of muramyl peptides.

Krueger¹,

Pappenheimer²,

Karnovsky³

1982

Proc. Natl. Acad. Sci. U.S.A.

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171

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following editorial errors should be corrected. On p. 6105, in Table 2, lines 5 and 6 should read "AcMur-L-Ala-D-Gln Me ester" and "AcMur-L-Ala-D-Gln n-Bu ester," respectively, and the last sentence in the legend should read "The amount of glutamic acid released by hydrolysis was used to calculate the dose." On the same page, in the right-hand column, line 28 should read "esters and the N-Me derivative of AcMur-Ala-Gln.-Proc. Nati, Acad. Sci. USA Vol. 79, pp. 6102-6106, Contributed by John R. Pappenheimner, June 28, 1982 ABSTRACT A muramyl peptide that induces excess slowwave sleep in rats, rabbits, and cats has recently been isolated from human urine. We now report that synthetic acetylmuramyl-L-alanyl-D-isoglutamine ("muramyl dipeptide") and its lysyl derivative (acetylmuramyl-L-alanyl-D-isoglutaminyllysine) can mimic the somnogenic effects of the natural peptide. Both compounds are also pyrogenic and may cause other disturbances ofautonomic function. The pyrogenic effects of intravenously administered muramyl dipeptide can be suppressed by previous treatment with acetaminophen without blocking the sleep-promoting effects.

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

Sleep-promoting effects of muramyl peptides.

Krueger¹,

Pappenheimer²,

Karnovsky³

1982

Proc. Natl. Acad. Sci. U.S.A.

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171

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“…31 Although this method is clearly convenient, infusion rates and the resistance to flow through the cannula can cause a significant artifactual reading of measured CSFP using this technique. Therefore, in the present study, two cannulas were inserted into the third ventricle, and these cannulas were used simultaneously for ACSF infusion and CSFP measurements, respectively.…”

Section: Measurements Of Cerebrospinal Fluid Pressurementioning

confidence: 99%

Pressor response to small elevations of cerebroventricular pressure in conscious rats.

1987

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SUMMARY Acute relationships between cerebrospinal fluid hydrostatic pressure and arterial pressure were quantified in conscious rats. The rats were catheterized with a left femoral artery catheter, and a double set of catheters was implanted into the third cerebral ventricle. In three groups of rats, artificial cerebrospinal fluid with various sodium concentrations (142,152, and 162 mM) was infused into the third ventricle for 3 hours at 1.0 /xl/min. Mean arterial pressure (MAP) and third ventricular pressure were monitored simultaneously, and both increased progressively over the 3-hour infusion period; the rate of rise was significantly greater with infusion of the hypertonic solution. There were no significant differences between the rat groups infused with low, normal, or high artificial cerebrospinal fluid sodium in either the slope or the intercept of the regression equation relating cerebrospinal fluid pressure and MAP: a 1 cm H 2 O rise of cerebrospinal fluid pressure was always associated with nearly a 1 mm Hg rise in MAP. In other rats, changes in both cerebrospinal fluid pressure and MAP were shown to be highly dependent on the rate of ventricular infusion. We conclude that elevations of systemic arterial pressure are associated with only small elevations of cerebrospinal fluid pressure and that physiological changes of cerebrospinal sodium (±10 mM) influence arterial pressure by altering intravascular hydrostatic pressure rather than sodium or osmosensitive receptors in the cerebral ventricles. T HE present studies evolved from our interest in the mechanisms whereby the body senses changes in daily sodium intake and initiates homeostatic mechanisms for the control of body sodium content and arterial blood pressure. There is particular interest in this question at the present time, since many forms of hypertension are aggravated by increased sodium intake, which indicates that the ability of the body to either detect or respond to changes in sodium intake is altered. 12Central nervous system structures in the wall of the third cerebral ventricle influence fluid-electrolyte homeostasis and arterial pressure.3 " 7 Cerebroventricular infusion of hypertonic NaCl is known to elicit pressor and natriuretic responses in various species.3 ' 4 -6 "" The proposed mechanisms for this pressor response include

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“…A preliminary account of this work was communicated previously (Pappenheimer, 1976 Goodrich, Greehey, Miller & Pappenheimer (1969). Stainless steel screw electrodes 192 SLEEP AND RESPIRATION DURING HYPOXIA were implanted in holes drilled through the skull; each rat was provided with symmetrically placed epidural electrodes over right and left frontal and occipital cortex.…”

Section: Introductionmentioning

confidence: 99%

Sleep and respiration of rats during hypoxia.

Pappenheimer¹

1977

The Journal of Physiology

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162

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Addition of C02 to inspired gas failed to prevent the reduction of SWS during hypoxia. C02 in normal 02 did not alter sleep significantly. The effects of hypoxia on sleep therefore depend upon changes in 02 pressure rather than upon changes in C02.4. The effect of SWS on respiration of rats breathing air was to decrease frequency and minute volume by 10-20%. In hypoxia, however, the frequency increased markedly when the animals entered SWS; minute volume was not significantly changed. It follows that stimulation of breathing by hypoxia is greater during SWS than during wakefulness.5. The anomalous increase of respiratory frequency when hypoxic rats entered SWS was abolished by addition of C02 to the hypoxic gas mixture.6. Steady-state gaseous metabolism (J02, GO2) was decreased 18 + 3 % during hypoxia and was increased 31 + 4 % during exposure to 5 % C02.The implications ofthese changes for interpretation ofrespiratory responses to 02 and C02 are discussed.

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Cerebral ventricular infusions in unrestrained rats.

Cited by 41 publications

References 0 publications

Sleep-promoting effects of muramyl peptides.

Sleep-promoting effects of muramyl peptides.

Pressor response to small elevations of cerebroventricular pressure in conscious rats.

Sleep and respiration of rats during hypoxia.

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