Microdialysis guide cannula implantation surgery v1 (protocols.io.bszxnf7n)

protocols.io ◽  
2021 ◽  
Author(s):  
Christiana.bjorkli not provided
Keyword(s):  
Guide Cannula

Central blockade of vasopressin V1receptors attenuates postexercise hypotension

2001 ◽  
Vol 281 (2) ◽  
pp. R375-R380 ◽  
Author(s):  
Heidi L. Collins ◽  
David W. Rodenbaugh ◽  
Stephen E. DiCarlo
Keyword(s):  
Central Administration ◽  
Guide Cannula ◽  
Spontaneously Hypertensive ◽  
Single Bout ◽  
Before And After ◽  
The Central Nervous System ◽  
Postexercise Hypotension ◽  
The Right ◽  
Carotid Arterial ◽  
Lateral Cerebral Ventricle

We tested the hypothesis that central arginine vasopressin (AVP) mediates postexercise reductions in arterial pressure (AP) and heart rate (HR). To test this hypothesis, nine spontaneously hypertensive rats (SHR) were instrumented with a 22-gauge stainless steel guide cannula in the right lateral cerebral ventricle and with a carotid arterial catheter. After the rats recovered, AP and HR were assessed before and after a single bout of dynamic exercise with the central administration of vehicle or the selective AVP V1-receptor antagonist d(CH3)5Tyr(Me)-AVP (AVP-X). AP and HR were significantly decreased below preexercise values with central administration of vehicle [ P < 0.05, change (Δ)−21 ± 4 mmHg and Δ−20 ± 6 beats/min, respectively]. In sharp contrast, after exercise with central administration of AVP-X, both AP (Δ+8 ± 5 mmHg) and HR (Δ+24 ± 9 beats/min) were not significantly different from preexercise values ( P > 0.05). Furthermore, AVP-X at rest did not significantly alter AP (181 ± 11 vs. 178 ± 11 mmHg, P > 0.05) or HR (328 ± 24 vs. 331 ± 22 beats/min, P > 0.05). Thus central blockade of AVP V1 receptors prevented postexercise reductions in AP and HR. These data suggest that AVP, acting within the central nervous system, mediates postexercise reductions in AP and HR in the SHR.

Stereoencephalography Electrode Placement Accuracy and Utility Using a Frameless Insertion Platform Without a Rigid Cannula

2019 ◽  
Author(s):  
Erin D’Agostino ◽  
John Kanter ◽  
Yinchen Song ◽  
Joshua P Aronson
Keyword(s):  
Electrode Placement ◽  
Target Point ◽  
Localization Error ◽  
Drug Resistant ◽  
Guide Cannula ◽  
Lateral Entry ◽  
Accurate Localization ◽  
Depth Electrodes ◽  
Rigid Frame ◽  
Drug Resistant Epilepsy

Abstract BACKGROUND Implantation of depth electrodes to localize epileptogenic foci in patients with drug-resistant epilepsy can be accomplished using traditional rigid frame-based, custom frameless, and robotic stereotactic systems. OBJECTIVE To evaluate the accuracy of electrode implantation using the FHC microTargeting platform, a custom frameless platform, without a rigid insertion cannula. METHODS A total of 182 depth electrodes were implanted in 13 consecutive patients who underwent stereoelectroencephalography (SEEG) for drug-resistant epilepsy using the microTargeting platform and depth electrodes without a rigid guide cannula. MATLAB was utilized to evaluate targeting accuracy. Three manual coordinate measurements with high inter-rater reliability were averaged. RESULTS Patients were predominantly male (77%) with average age 35.62 (SD 11.0, range 21-57) and average age of epilepsy onset at 13.4 (SD 7.2, range 3-26). A mean of 14 electrodes were implanted (range 10-18). Mean operative time was 144 min (range 104-176). Implantation of 3 out of 182 electrodes resulted in nonoperative hemorrhage (2 small subdural hematomas and one small subarachnoid hemorrhage). Putative location of onset was identified in all patients. We demonstrated a median lateral target point localization error (LTPLE) of 3.95 mm (IQR 2.18-6.23), a lateral entry point localization error (LEPLE) of 1.98 mm (IQR 1.2-2.85), a target depth error of 1.71 mm (IQR 1.03-2.33), and total target point localization error (TPLE) of 4.95 mm (IQR 2.98-6.85). CONCLUSION Utilization of the FHC microTargeting platform without the use of insertion cannulae is safe, effective, and accurate. Localization of seizure foci was accomplished in all patients and accuracy of depth electrode placement was satisfactory.

2-Deoxy-D-glucose and insulin modify release of norepinephrine from rat hypothalamus

1982 ◽  
Vol 242 (5) ◽  
pp. R596-R603 ◽  
Author(s):  
M. L. McCaleb ◽  
R. D. Myers
Keyword(s):  
Saline Control ◽  
Base Line ◽  
Noradrenergic Neurons ◽  
Guide Cannula ◽  
Hypothalamic Area ◽  
Individual Site ◽  
Artificial Cerebrospinal Fluid ◽  
Modify Release ◽  
Kinetics Of ◽  
Hypothalamic Level

Both 2-deoxy-D-glucose (2-DG) and insulin, administered systemically, evoke spontaneous feeding in the satiated animal. To determine whether hypothalamic norepinephrine (NE) could be involved in this eating response, we examined the effect of the two compounds on the kinetics of NE release from this structure in the unrestrained rat. An individual site in the hypothalamus of the rat was radiolabeled by 1.0-2.0 microCi of [14C]NE microinjected in a volume of 0.5-1.0 microliters through a permanently implanted guide cannula. Then 30 min later, the NE-labeled tissue was perfused, by means of push-pull cannulas, with an artificial cerebrospinal fluid at a rate of 25 microliters/min. The duration of each perfusion was 5.0 min with a 5.0-min interval between successive perfusions. After two base-line samples were collected, a saline control injection or either 40 mg/kg 2-DG or 20 U/kg insulin was given intraperitoneally; then the perfusion sequence was continued for an additional 1-h period. Aliquots of the collected samples of perfusate were analyzed by combined scintillation spectrometry and high-pressure liquid chromatography. 2-DG enhanced the release of NE at sites in the medial hypothalamus, whereas insulin generally caused a suppression of catecholamine efflux particularly at sites within the lateral hypothalamic area. The changes in NE efflux were morphologically specific. Taken together with the differences in amine release, these results suggest that 2-DG and insulin modify feeding by independent neurochemical mechanisms that may involve noradrenergic neurons at the hypothalamic level.

scholarly journals Perivascular Microapplication of Endothelin-1: A New Model of Focal Cerebral Ischaemia in the Rat

1993 ◽  
Vol 13 (5) ◽  
pp. 865-871 ◽  
Author(s):  
John Sharkey
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischaemia ◽  
Dorsal Hippocampus ◽  
Focal Cerebral Ischaemia ◽  
Local Cerebral Blood Flow ◽  
Guide Cannula ◽  
Conscious Rat ◽  
Endothelin 1 ◽  
Arterial Blood

In the present study, we describe the effects of perivascular microapplication of the potent vasoconstrictor peptide endothelin-1 (Et-1; (120 pmol in 3 μl), delivered via a guide cannula stereotaxically positioned above the left cerebral artery (MCA) of the conscious male Sprague–Dawley rat. Ten minutes after the administration of Et-1, mean arterial blood pressure had increased by 20% and profound reductions in local cerebral blood flow (up to 93%) were observed within those brain areas supplied by the MCA. In addition, significant increases in local cerebral blood flow were observed within the globus pallidus (100%), substantia nigra pars reticulata (48%), ventrolateral thalamus (65%), and dorsal hippocampus (74%) ipsilateral to the insult. Twenty-four hours following the insult, the pattern of ischaemic damage was similar to that reported previously following permanent occlusion of the rat MCA. It is suggested that perivascular microapplication of Et-1 may provide a useful model for the study of the functional disturbances associated with focal cerebral ischaemia in the conscious rat.

Endoscopic-guided percutaneous radiofrequency cordotomy

2010 ◽  
Vol 113 (3) ◽  
pp. 524-527 ◽  
Author(s):  
Erich Talamoni Fonoff ◽  
Ywzhe Sifuentes Almeida de Oliveira ◽  
William Omar Contreras Lopez ◽  
Eduardo Joaquim Lopes Alho ◽  
Nilton Alves Lara ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Blood Vessels ◽  
Cervical Spinal Cord ◽  
Ventral Root ◽  
Csf Leak ◽  
Clinical Implementation ◽  
Guide Cannula ◽  
Entry Zone ◽  
Root Entry Zone ◽  
Dentate Ligament

The authors present the first clinical implementation of an endoscopic-assisted percutaneous anterolateral radiofrequency cordotomy. The aim of this article is to demonstrate the intradural endoscopic visualization of the cervical spinal cord via a percutaneous approach to refine the spinal target for anterolateral cordotomy, avoiding undesired trauma to the spinal tissue or injury to blood vessels. Initially, a lateral puncture of the spinal canal in the C1–2 interspace is performed, guided by fluoroscopy. As soon as CSF is reached by the guide cannula (17-gauge needle), the endoscope can be inserted for visualization of the spinal cord and its surrounding structures. The endoscopic visualization provided clear identification of the pial surface of the spinal cord, arachnoid membrane, dentate ligament, dorsal and ventral root entry zone, and blood vessels. The target for electrode insertion into the spinal cord was determined to be the midpoint from the dentate ligament and the ventral root entry zone. The endoscopic guidance shortened the fluoroscopy usage time and no intrathecal contrast administration was needed. Cordotomy was performed by a standard radiofrequency method after refining of the neurophysiological target. Satisfactory analgesia was provided by the procedure with no additional complications or CSF leak. The initial use of this technique suggests that a percutaneous endoscopic procedure may be useful for particular manipulation of the spinal cord, possibly adding a degree of safety to the procedure and improving its effectiveness.

Morphine Inhibits Acetylcholine Release in Rat Prefrontal Cortex When Delivered Systemically or by Microdialysis to Basal Forebrain

2005 ◽  
Vol 103 (4) ◽  
pp. 779-787 ◽  
Author(s):  
Nadir I. Osman ◽  
Helen A. Baghdoyan ◽  
Ralph Lydic
Keyword(s):  
Prefrontal Cortex ◽  
Basal Forebrain ◽  
Acetylcholine Release ◽  
Sprague Dawley ◽  
Guide Cannula ◽  
Microdialysis Probe ◽  
Prefrontal Cortical ◽  
Substantia Innominata ◽  
Morphine Administration ◽  
Intravenous Morphine

Background Cortical acetylcholine originates in the basal forebrain and is essential for maintaining normal cognition and arousal. Morphine impairs these cholinergically mediated cortical functions. The current study tested the hypothesis that morphine decreases prefrontal cortical acetylcholine release by acting at the level of the basal forebrain. Methods Adult male Sprague-Dawley rats (n = 18) were anesthetized with isoflurane. One microdialysis probe was placed in the substantia innominata region of the basal forebrain and perfused with Ringer's solution (control) followed by one concentration of morphine (1, 10, 100, or 1,000 microm) or morphine (1,000 microm) plus naloxone (100 microm). A second microdialysis probe was placed in the prefrontal cortex for measuring acetylcholine. In a second series of experiments, rats (n = 6) were implanted with electrodes for recording states of arousal, a guide cannula positioned above the prefrontal cortex for inserting a microdialysis probe, and an indwelling jugular vein catheter. The effects of administering intravenous morphine (30 mg/kg) versus normal saline (0.9%) on prefrontal cortical acetylcholine release, cortical electroencephalographic power, and behavior were quantified. Results Dialysis delivery of morphine to the substantia innominata caused a concentration-dependent, naloxone-sensitive decrease in acetylcholine release within the prefrontal cortex. The maximal decrease in acetylcholine was 36.3 +/- 11.5%. Intravenous morphine administration significantly decreased cortical acetylcholine release, increased electroencephalographic power in the 0.5- to 5-Hz range, and eliminated normal wakefulness. Conclusion Morphine causes obtundation of arousal and may cause cognitive impairment by acting at the level of the substantia innominata to disrupt cortical cholinergic neurotransmission.

scholarly journals A novel variable delay Go/No-Go task to study attention, motivation and working memory in the head-fixed rodent

F1000Research ◽  
2013 ◽  
Vol 2 ◽  
pp. 125 ◽  
Author(s):  
Samuel D Dolzani ◽  
Shinya Nakamura ◽  
Donald C Cooper
Keyword(s):  
Working Memory ◽  
Brain Regions ◽  
Electrophysiological Recording ◽  
Variable Delay ◽  
Guide Cannula ◽  
Data Set ◽  
Behavioral Paradigm ◽  
Ongoing Behavior ◽  
Lever Pressing ◽  
The Subject

In order to parse the causal elements underlying complex behaviors and decision-making processes, appropriate behavioral methods must be developed and used in concurrence with molecular, pharmacological, and electrophysiological approaches. Presented is a protocol for a novel Go/No-Go behavioral paradigm to study the brain attention and motivation/reward circuitry in awake, head-restrained rodents. This experimental setup allows: (1) Pharmacological and viral manipulation of various brain regions via targeted guide cannula; (2) Optogenetic cell-type specific activation and silencing with simultaneous electrophysiological recording and; (3) Repeated electrophysiological single and multiple unit recordings during ongoing behavior. The task consists of three components. The subject first makes an observing response by initiating a trial by lever pressing in response to distinctive Go or No-Go tones.  Then, after a variable delay period, the subject is presented with a challenge period cued by white noise during which they must respond with a lever press for the Go condition or withhold from lever pressing for the duration of the cue in the No-Go condition. After correctly responding during the challenge period (Challenge) and a brief delay, a final reward tone of the same frequency as the initiation tone is presented and sucrose reward delivery is available and contingent upon lever pressing. Here, we provide a novel procedure and validating data set that allows researchers to study and manipulate components of behavior such as attention, motivation, impulsivity, and reward-related working memory during an ongoing operant behavioral task while limiting interference from non task-related behaviors.

Epidermal growth factor enhances spontaneous sleep in rabbits

1998 ◽  
Vol 275 (2) ◽  
pp. R509-R514 ◽  
Author(s):  
Tetsuya Kushikata ◽  
Jidong Fang ◽  
Zutang Chen ◽  
Ying Wang ◽  
James M. Krueger
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Eye Movement ◽  
Brain Temperature ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Sleep Regulation ◽  
Guide Cannula ◽  
Epidermal Growth

Several growth factors are implicated in sleep regulation. Epidermal growth factor (EGF) is found in the brain, and it influences the production of several sleep-promoting substances. We determined, therefore, whether administration of exogenous EGF affected spontaneous sleep in rabbits. Twenty-five rabbits were implanted with electroencephalographic electrodes, a brain thermistor, and an intracerebroventricular guide cannula. Three doses of EGF (0.5, 5, and 25 μg) were used. The animals were injected intracerebroventricularly with saline as control and one dose of EGF on 2 separate days. Five and twenty-five micrograms of EGF enhanced non-rapid eye movement sleep and increased brain temperature. The 25-μg dose of EGF also inhibited rapid eye movement sleep across the 23-h postinjection recording period. Results are consistent with the hypothesis that EGF, like other growth factors, could be involved in sleep regulation.

Iodide and thiocyanate efflux from brain following injection into rat caudate nucleus

1978 ◽  
Vol 235 (4) ◽  
pp. F331-F337 ◽  
Author(s):  
H. F. Cserr ◽  
B. J. Berman
Keyword(s):  
Caudate Nucleus ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Common Mechanism ◽  
Efflux System ◽  
Guide Cannula ◽  
Blood Brain ◽  
The Central Nervous System ◽  
Loading Estimates ◽  
The Brain

Mechanisms and pathways of 125I and 35SCN efflux from the brain were investigated in anesthetized rats. Tracers were injected into the caudate nucleus through a guide cannula implanted 1 wk previously and concentrations of isotope in brain and cerebrospinal fluid (CSF) were determined at various times after injection. 125I clearance from the brain followed a single exponential curve. In control rats 36.2% of the 125I remained in the brain 30 min after injection and 60.4% in rats pretreated with perchlorate. Comparable values for 35SCN were 25.8% in control rats, 41.0% with perchlorate, and 39.7% with iodide loading. Estimates of 125I and 35SCN effluxes from the brain via the blood-brain barrier and CSF pathways suggest that greater than 95% of efflux crosses the blood-brain barrier. These results indicate that 1)iodide and thiocyanate are transported across the blood-brain barrier by a common mechanism, and 2) this efflux system is an important factor in the control of the distributions of iodide and thiocyanate in the central nervous system.

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