Rhythmic Activity of Cat Pial Vessels in vivo

1981 ◽  
Vol 20 (6) ◽  
pp. 448-468 ◽  
Author(s):  
L.M. Auer ◽  
B. Gallhofer
Keyword(s):  
Rhythmic Activity ◽  
Pial Vessels

Hypothermia Attenuates the Vasodilator Effects of Dexmedetomidine on Pial Vessels in Rabbits In Vivo

2004 ◽  
pp. 477-482 ◽  
Author(s):  
Hiroki Iida ◽  
Mami Iida ◽  
Hiroto Ohata ◽  
Kiyoshi Nagase ◽  
Shuji Dohi
Keyword(s):  
Pial Vessels

scholarly journals Circadian modulation of neurons and astrocytes controls synaptic plasticity in hippocampal area CA1

2019 ◽  
Author(s):  
John P. McCauley ◽  
Maurice A. Petroccione ◽  
Lianna Y. D’Brant ◽  
Gabrielle C. Todd ◽  
Nurat Affinnih ◽  
...  
Keyword(s):  
Cognitive Processing ◽  
Temporal Dynamics ◽  
Rhythmic Activity ◽  
Surface Expression ◽  
Receptor Activation ◽  
Cellular Mechanisms ◽  
Functional Changes ◽  
Area Ca1 ◽  
Hippocampal Area

SummaryMost animal species operate according to a 24-hour period set by the suprachiasmatic nucleus (SCN) of the hypothalamus. The rhythmic activity of the SCN is known to modulate hippocampal-dependent memory processes, but the molecular and cellular mechanisms that account for this effect remain largely unknown. Here, we show that there are cell-type specific structural and functional changes that occur with circadian rhythmicity in neurons and astrocytes in hippocampal area CA1. Pyramidal neurons change the surface expression of NMDA receptors, whereas astrocytes change their proximity to synapses. Together, these phenomena alter glutamate clearance, receptor activation and integration of temporally clustered excitatory synaptic inputs, ultimately shaping hippocampal-dependent learningin vivo. We identify corticosterone as a key contributor to changes in synaptic strength. These findings identify important mechanisms through which neurons and astrocytes modify the molecular composition and structure of the synaptic environment, contribute to the local storage of information in the hippocampus and alter the temporal dynamics of cognitive processing.

Direct Effects of α1-and α2-AdrenergicAgonists on Spinal and Cerebral Pial Vessels in Dogs 

1999 ◽  
Vol 91 (2) ◽  
pp. 479-485 ◽  
Author(s):  
Hiroki Iida ◽  
Hiroto Ohata ◽  
Mami Iida ◽  
Yukinaga Watanabe ◽  
Shuji Dohi
Keyword(s):  
Topical Administration ◽  
Vessel Diameter ◽  
Dependent Manner ◽  
Adrenergic Agonists ◽  
Concentration Dependent Manner ◽  
Cranial Window ◽  
Pial Vessels ◽  
Cerebral Arterioles ◽  
Pial Vessel

Background The effects of adrenergic agonists, often used as local anesthetic additives or spinal analgesics, on spinal vessels have not been firmly established. The authors investigated the effects of alpha2- and alpha1-adrenergic agonists on spinal and cerebral pial vessels in vivo. Methods Pentobarbital-anesthetized dogs (n = 28) were prepared for measurement of spinal pial-vessel diameter in a spinal-window preparation. The authors applied dexmedetomidine, clonidine, phenylephrine, or epinephrine in three different concentrations (0.5, 5.0, and 50 microg/ml; [2.1, 1.9, 2.5, and 2.3] x [10(-6), 10(-5), and 10(-4)] M, respectively) under the window (one drug in each dog) and measured spinal pial arteriolar and venular diameters in a sequential manner. To enable the comparison of their effects on cerebral vessels, the authors also administered these drugs under a cranial window. Results On topical administration, each drug constricted spinal pial arterioles in a concentration-dependent manner. Phenylephrine and epinephrine induced a significantly larger arteriolar constriction than dexmedetomidine or clonidine at 5 microg/ml (8%, 11%, 0%, and 1%, respectively). Spinal pial venules tended to be less constricted than arterioles. In cerebral arterioles, greater constrictions were induced by dexmedetomidine and clonidine than those induced by phenylephrine and epinephrine (14%, 8%, 0%, and 1%, respectively). Cerebral pial venules tended to exhibit larger constrictions than cerebral arterioles (unlike in spinal vessels). Conclusion Dexmedetomidine and clonidine constricted spinal vessels in a concentration-dependent manner, but such vasoconstrictions were smaller than those induced by phenylephrine and epinephrine.

Nasal Trigeminal Inputs Release the A5 Inhibition Received by the Respiratory Rhythm Generator of the Mouse Neonate

2004 ◽  
Vol 91 (2) ◽  
pp. 746-758 ◽  
Author(s):  
Jean-Charles Viemari ◽  
Michelle Bévengut ◽  
Patrice Coulon ◽  
Gérard Hilaire
Keyword(s):  
Trigeminal Nerve ◽  
Respiratory Rhythm ◽  
Rhythmic Activity ◽  
Electrolytic Lesion ◽  
Burst Frequency ◽  
Neuronal Tracing ◽  
Rhythm Generator ◽  
Trigeminal Nerve Stimulation

Experiments were performed on neonatal mice to analyze why, in vitro, the respiratory rhythm generator (RRG) was silent and how it could be activated. We demonstrated that in vitro the RRG in intact brain stems is silenced by a powerful inhibition arising from the pontine A5 neurons through medullary α2 adrenoceptors and that in vivo nasal trigeminal inputs facilitate the RRG as nasal continuous positive airway pressure increases the breathing frequency, whereas nasal occlusion and nasal afferent anesthesia depress it. Because nasal trigeminal afferents project to the A5 nuclei, we applied single trains of negative electric shocks to the trigeminal nerve in inactive ponto-medullary preparations. They induced rhythmic phrenic bursts during the stimulation and for 2–3 min afterward, whereas repetitive trains produced on-going rhythmic activity up to the end of the experiments. Electrolytic lesion or pharmacological inactivation of the ipsilateral A5 neurons altered both the phrenic burst frequency and occurrence after the stimulation. Extracellular unitary recordings and trans-neuronal tracing experiments with the rabies virus show that the medullary lateral reticular area contains respiratory-modulated neurons, not necessary for respiratory rhythmogenesis, but that may provide an excitatory pathway from the trigeminal inputs to the RRG as their electrolytic lesion suppresses any phrenic activity induced by the trigeminal nerve stimulation. The results lead to the hypothesis that the trigeminal afferents in the mouse neonate involve at least two pathways to activate the RRG, one that may act through the medullary lateral reticular area and one that releases the A5 inhibition received by the RRG.

scholarly journals Phase-dependent closed-loop modulation of neural oscillations in vivo

2020 ◽  
Author(s):  
Colin G. McNamara ◽  
Max Rothwell ◽  
Andrew Sharott
Keyword(s):  
Brain Function ◽  
Single Channel ◽  
Rhythmic Activity ◽  
Electronic System ◽  
Normal Brain ◽  
Beta Band ◽  
Phase Estimate ◽  
Neuronal Computation ◽  
Stimulation Of

AbstractNormal brain function is associated with an assortment of oscillations of various frequencies, each reflecting the timing of separate computational processes and levels of synchronization within and between brain areas. Stimulation accurately delivered on a specified phase of a given oscillation provides the opportunity to target individual aspects of brain function. To achieve this, we have developed a highly responsive system to produce a continuous online phase-estimate. In addition to stable oscillations, the system accurately tracks the early cycles of short, transient oscillations and can operate across the frequency range of most established neuronal oscillations (4 to 250 Hz). Here we demonstrate bidirectional modulation of the pathologically elevated parkinsonian beta-band oscillation (around 35 Hz) in 6-OHDA hemi-lesioned rats. Beta phase, monitored using a single channel electrocorticogram above secondary motor cortex, was used to drive electrical stimulation of the globus pallidus on one of eight phases spanning the oscillation cycle. Stimulation of the early ascending phase suppressed the oscillation whereas stimulation of the early descending phase was amplifying. By implementing a rule that prevented stimulation when the phase estimate was unstable, we achieved a system that could adapt stimulation rate and pattern to respond to the changes produced in the target oscillation. This allowed the electronic system to create and maintain a state of equilibrium with the biological system resulting in continuous stable modulation of the target oscillation over time. These results demonstrate the feasibility of phase locked stimulation as a more refined strategy for remediation of pathological beta oscillations in the treatment of the motor symptoms of Parkinson’s disease. Furthermore, they establish the utility of our algorithm and allow for the potential to assess the contribution of rhythmic activity in neuronal computation across a number of brain systems.

In Vivo Rat Closed Spinal Window for Spinal Microcirculation: Observation of Pial Vessels, Leukocyte Adhesion, and Red Blood Cell Velocity

Neurosurgery ◽  
1999 ◽  
Vol 44 (1) ◽  
pp. 156-161 ◽  
Author(s):  
Mami Ishikawa ◽  
Eiichi Sekizuka ◽  
Shuzo Sato ◽  
Noriyuki Yamaguchi ◽  
Katsuyoshi Shimizu ◽  
...  
Keyword(s):  
Blood Cell ◽  
Red Blood Cell ◽  
Leukocyte Adhesion ◽  
Pial Vessels ◽  
Cell Velocity ◽  
Red Blood Cell Velocity

scholarly journals Rhythmic patterns in the thoracic nerve cord of the stick insect induced by pilocarpine

1995 ◽  
Vol 198 (2) ◽  
pp. 435-456 ◽  
Author(s):  
A Büschges ◽  
J Schmitz ◽  
U Bässler
Keyword(s):  
Phase Transitions ◽  
Nerve Cord ◽  
Rhythmic Activity ◽  
Stick Insect ◽  
Burst Duration ◽  
Cycle Period ◽  
Muscarinic Agonist ◽  
Thoracic Nerve ◽  
Similar Range

Bath application of the muscarinic agonist pilocarpine onto the deafferented stick insect thoracic nerve cord induced long-lasting rhythmic activity in leg motoneurones. Rhythmicity was induced at concentrations as low as 1x10(-4) mol l-1 pilocarpine. The most stable rhythms were reliably elicited at concentrations from 2x10(-3) mol l-1 to 5x10(-3) mol l-1. Rhythmicity could be completely abolished by application of atropine. The rhythm in antagonistic motoneurone pools of the three proximal leg joints, the subcoxal, the coxo-trochanteral (CT) and the femoro-tibial (FT), was strictly alternating. In the subcoxal motoneurones, the rhythm was characterised by the retractor burst duration being correlated with cycle period, whereas the protractor burst duration was almost independent of it. The cycle periods of the rhythms in the subcoxal and CT motoneurone pools were in a similar range for a given preparation. In contrast, the rhythm exhibited by motoneurones supplying the FT joint often had about half the duration. The pilocarpine-induced rhythm was generated independently in each hemiganglion. There was no strict intersegmental coupling, although the protractor motoneurone pools of the three thoracic ganglia tended to be active in phase. There was no stereotyped cycle-to-cycle coupling in the activities of the motoneurone pools of the subcoxal joint, the CT joint and the FT joint in an isolated mesothoracic ganglion. However, three distinct 'spontaneous, recurrent patterns' (SRPs) of motoneuronal activity were reliably generated. Within each pattern, there was strong coupling of the activity of the motoneurone pools. The SRPs resembled the motor output during step-phase transitions in walking: for example, the most often generated SRP (SRP1) was exclusively exhibited coincident with a burst of the fast depressor trochanteris motoneurone. During this burst, there was a switch from subcoxal protractor to retractor activity after a constant latency. The activity of the FT joint extensor motoneurones was strongly decreased during SRP1. SRP1 thus qualitatively resembled the motoneuronal activity during the transition from swing to stance of the middle legs in forward walking. Hence, we refer to SRPs as 'fictive step-phase transitions'. In intact, restrained animals, application of pilocarpine also induced alternating activity in antagonistic motoneurone pools supplying the proximal leg joints. However, there were marked differences from the deafferented preparation. For example, SRP1 was not generated in the latter situation. However, if the ipsilateral main leg nerve was cut, SRP1s reliably occurred. Our results on the rhythmicity in leg motoneurone pools of deafferented preparations demonstrate central coupling in the activity of the leg motoneurones that might be incorporated into the generation of locomotion in vivo.

scholarly journals Dynamics of pial vessels reactivity after brief cerebral ischemia

2015 ◽  
Vol 14 (1) ◽  
pp. 74-78 ◽  
Author(s):  
O. P. Gorshkova ◽  
M. V. Lensman ◽  
A. I. Artem'eva ◽  
D. P. Dvoretsky
Keyword(s):  
Cerebral Ischemia ◽  
Brain Perfusion ◽  
Artery Occlusion ◽  
Global Cerebral Ischemia ◽  
Pial Arteries ◽  
Pial Vessels ◽  
Transient Global Cerebral Ischemia ◽  
Pial Vessel ◽  
Arteries And Veins

Cerebral blood vessel reactivity is one of the main determinants of final outcome of brain ischemia. Most of studies on the vascular mechanisms of ischemic brain injury, however, focus on the acute changes within ischemic period or several hours after it. Dilatatory capacity of cerebral arterioles (perfusion reservoir) is considered as an important factor of brain perfusion elevation in critical situations.The aim of the present study was to examine the pial vessel reactivity in response to hypercapnia in rats, subjected to transient global cerebral ischemia, at 7, 14 and 21 days after ischemia. Materials and methods. Transient global cerebral ischemia was induced in anesthetized Wistar rats by bilateral common carotid artery occlusion for 12 min with simultaneous controlled hypotension to 45±3 mm Hg, followed by blood reinfusion and recovery from anesthesia. Three different groups of rats were re-anesthetized at 7, 14 or 21 days after ischemia and subjected to microvascular reactivity studies using in vivo video microscopy. Hypercapnia was caused by i.v. injection of acetazolamide. The changes in diameter of pial arteries and veins in response to hypercapnia were measured. Results and discussion. Global cerebral ischemia led to marked decrease in pial vessels (both arteries and veins) reactivity in response to hypercapnia, caused by i.v. injection of acetazolamide. In intact rats, i.v. injection of acetazolamide led to pial arteries dilation and pial veins constriction; in animals subjected to ischemia-reperfuion. the numbers of dilated large arteries and constricted small veins were much less, as well as the extent of arterial dilation. Reactivity changes were observed in all time points studied. Conclusions. Thus, transient global cerebral ischemia cause marked and long lasting (3 weeks) decrease in pial vessel reactivity in response to hypercapnia.

scholarly journals Effects of increased blood content of fibrinogen on mouse pial vessels in vivo

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Nino Muradashvili ◽  
Reeta Tyagi ◽  
Neetu Tyagi ◽  
Richard L Benton ◽  
Andrew M Roberts ◽  
...  
Keyword(s):  
Blood Content ◽  
Pial Vessels
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