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Biomedical subjects

Marie L Schulte

Publications and source records attributed to Marie L Schulte.

3 recordsLinked to original sources

Digit tapping model of functional activation in the rat somatosensory cortex.

To establish a non-invasive model for functional activation of the rat somatosensory cortex, the forepaw digits of halothane-anesthetized rats were tapped while the blood flow (laser-Doppler flow, LDF) and somatosensory evoked potential (SSEP) responses in the forelimb area of the somatosensory cortex (S1FL) were measured. The distal phalanges of the forepaw digits were lightly tapped for 10s with an aluminum bar at frequencies between 1 and 40 Hz, with 0.4 cm total bar displacement. The LDF signal was normalized to the baseline preceding each stimulus block and averaged. The LDF response to digit tapping in the contralateral, but not ipsilateral S1FL, commenced within 1s, peaked at 11+/-0.5% (S.E.M.) above baseline within 2-3s, decreased to a plateau of 5+/-0.3% for the duration of the stimulation, and returned to baseline within 5-10s following tapping cessation. The LDF peak and plateau were not significantly different at different tapping frequencies. In the contralateral, but not ipsilateral, S1FLs, tapping produced an SSEP with positive (P1) and negative (N1) peaks at 27+/-0.5 and 47+/-0.2m s, respectively, after onset of the tap stimulation. As the tapping frequency increased from 1 to 20 Hz, the P1-N1 peak-to-peak amplitude decreased. At 30 and 40 Hz, the shortened interstimulus interval entrained the individual SSEPs into a steady-state evoked response. This study demonstrates that a robust functional activation of the forelimb region of primary somatosensory cortex of halothane-anesthetized rats can be produced by non-invasively tapping the forepaw digits and quantified with LDF and SSEP.

Analysis of Variance↗

Functional hyperemic response in the rat visual cortex under halothane anesthesia.

To establish a model for functional hyperemia in the rat visual cortex, cortical blood flow responses to flash stimulation were measured with the laser Doppler flow (LDF) technique at various levels of halothane anesthesia. The concentration-dependent effect of halothane on arterial pressure and its consequent effect on the hyperemic response were also investigated. Using a stroboscopic light source, 10 flashes at 1 min intervals were delivered to the left eye of 12 Sprague-Dawley rats. LDF responses were measured bilaterally in the monocular primary visual cortex (V1M) at steady state halothane concentrations between 0.4 and 1.4%. In six rats, methoxamine (MX) was infused to prevent halothane-induced hypotension; the remaining rats did not receive MX. In all rats, LDF response to flash commenced within 1s and peaked at 2.5s in the contralateral V1M, but not in ipsilateral V1M. The maximum LDF response was 25% at 0.5% halothane and 12% at 1.4% halothane. In rats without MX infusion, mean arterial pressure (MAP) fell from 138 to 90 mmHg when halothane increased from 0.4 to 1.4%. MX infusion prevented the hypotension, but did not influence the LDF response, suggesting that the halothane's effect was direct rather than pressure-mediated. We demonstrate for the first time, a robust functional hyperemic response to discrete flash stimuli in the primary visual cortex of halothane-anesthetized albino rats that can be measured with LDF over a wide range of halothane concentrations and is not fully suppressed at surgical levels of halothane anesthesia.

Anesthetics, Inhalation↗

20-HETE contributes to the acute fall in cerebral blood flow after subarachnoid hemorrhage in the rat.

This study examined the effects of blocking the formation of 20-hydroxyeicosatetraenoic acid (20-HETE) on the acute fall in cerebral blood flow after subarachnoid hemorrhage (SAH) in the rat. In vehicle-treated rats, regional cerebral blood flow (rCBF) measured with laser-Doppler flowmetry fell by 30% 10 min after the injection of 0.3 ml of arterial blood into the cisterna magna, and it remained at this level for 2 h. Pretreatment with inhibitors of the formation of 20-HETE, 17-octadecynoic acid (17-ODYA; 1.5 nmol intrathecally) and N-hydroxy-N'-(4-butyl-2-methylphenyl)formamidine (HET0016; 10 mg/kg iv), reduced the initial fall in rCBF by 40%, and rCBF fully recovered 1 h after induction of SAH. The concentration of 20-HETE in the cerebrospinal fluid rose from 12 +/- 2 to 199 +/- 17 ng/ml after SAH in vehicle-treated rats. 20-HETE levels averaged only 15 +/- 11 and 39 +/- 13 ng/ml in rats pretreated with 17-ODYA or HET0016, respectively. HET0016 selectively inhibited the formation of 20-HETE in rat renal microsomes with an IC(50) of <15 nM and human recombinant CYP4A11, CYP4F2, and CYP4F3 enzymes with an IC(50) of 42, 125, and 100 nM, respectively. These results indicate that 20-HETE contributes to the acute fall in rCBF after SAH in rats.

Amidines↗