Observations on the development of descending pathways from the brain stem to the spinal cord in the clawed toad Xenopus laevis

1982 ◽  
Vol 163 (4) ◽  
pp. 461-473 ◽  
Author(s):  
H. J. Donkelaar ◽  
R. Boer-van Huizen
Keyword(s):  
Spinal Cord ◽  
Xenopus Laevis ◽  
Brain Stem ◽  
Descending Pathways ◽  
The Brain

Regional blood flow in the brain and spinal cord of hypothermic rats

1989 ◽  
Vol 257 (3) ◽  
pp. H785-H790
Author(s):  
T. Sakamoto ◽  
W. W. Monafo
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Brain Stem ◽  
Regional Blood Flow ◽  
Experimental Conditions ◽  
Pentobarbital Sodium ◽  
Arterial Blood ◽  
Group A ◽  
Group B ◽  
The Brain

[14C]butanol tissue uptake was used to measure simultaneously regional blood flow in three regions of the brain (cerebral and cerebellar hemispheres and brain stem) and in five levels of the spinal cord in 10 normothermic rats (group A) and in 10 rats in which rectal temperature had been lowered to 27.7 +/- 0.3 degrees C by applying ice to the torso (group B). Pentobarbital sodium anesthesia was used. Mean arterial blood pressure varied minimally between groups as did arterial pH, PO2, and PCO2. In group A, regional spinal cord blood flow (rSCBF) varied from 49.7 +/- 1.6 to 62.6 +/- 2.1 ml.min-1.100 g-1; in brain, regional blood flow (rBBF) averaged 74.4 +/- 2.3 ml.min-1.100 g-1 in the whole brain and was highest in the brain stem. rSCBF in group B was elevated in all levels of the cord by 21-34% (P less than 0.05). rBBF, however, was lowered by 21% in the cerebral hemispheres (P less than 0.001) and by 14% in the brain as a whole (P less than 0.05). The changes in calculated vascular resistance tended to be inversely related to blood flow in all tissues. We conclude that rBBF is depressed in acutely hypothermic pentobarbital sodium-anesthetized rats, as has been noted before, but that rSCBF rises under these experimental conditions. The elevation of rSCBF in hypothermic rats confirms our previous observations.

Visual Pathways for Postural Control and Negative Phototaxis in Lamprey

1997 ◽  
Vol 78 (2) ◽  
pp. 960-976 ◽  
Author(s):  
Fredrik Ullén ◽  
Tatiana G. Deliagina ◽  
Grigori N. Orlovsky ◽  
Sten Grillner
Keyword(s):  
Spinal Cord ◽  
Postural Control ◽  
Brain Stem ◽  
Light Response ◽  
Contralateral Side ◽  
Visual Pathways ◽  
Negative Phototaxis ◽  
Intact Side ◽  
Roll Control ◽  
The Brain

Ullén, Fredrik, Tatiana G. Deliagina, Grigori N. Orlovsky, and Sten Grillner. Visual pathways for postural control and negative phototaxis in lamprey. J. Neurophysiol. 78: 960–976, 1997. The functional roles of the major visuo-motor pathways were studied in lamprey. Responses to eye illumination were video-recorded in intact and chronically lesioned animals. Postural deficits during spontaneous swimming were analyzed to elucidate the roles of the lesioned structures for steering and postural control. Eye illumination in intact lampreys evoked the dorsal light response, that is, a roll tilt toward the light, and negative phototaxis, that is a lateral turn away from light, and locomotion. Complete tectum-ablation enhanced both responses. During swimming, a tendency for roll tilts and episodes of vertical upward swimming were seen. The neuronal circuitries for dorsal light response and negative phototaxis are thus essentially extratectal. Responses to eye illumination were abolished by contralateral pretectum-ablation but normal after the corresponding lesion on the ipsilateral side. Contralateral pretectum thus plays an important role for dorsal light response and negative phototaxis. To determine the roles of pretectal efferent pathways for the responses, animals with a midmesencephalichemisection were tested. Noncrossed pretecto-reticular fibers from the ipsilateral pretectum and crossed fibers from the contralateral side were transected. Eye illumination on the lesioned side evoked negative phototaxis but no dorsal light response. Eye illumination on the intact side evoked an enhanced dorsal light response, whereas negative phototaxis was replaced with straight locomotion or positive phototaxis. The crossed pretecto-reticular projection is thus most important for the dorsal light response, whereas the noncrossed projection presumably plays the major role for negative phototaxis. Transection of the ventral rhombencephalic commissure enhanced dorsal light response; negative phototaxis was retained with smaller turning angles than normal. Spontaneous locomotion showed episodes of backward swimming and deficient roll control (tilting tendency). Transections of different spinal pathways were performed immediately caudal to the brain stem. All spinal lesions left dorsal light response in attached state unaffected; this response presumably is mediated by the brain stem. Spinal hemisection impaired all ipsiversive yaw turns; the animals spontaneously rolled to the intact side. Bilateral transection of the lateral columns impaired all yaw turns, whereas roll control and dorsal light response were normal. After transection of the medial spinal cord, yaw turns still could be performed whereas dorsal light response was suppressed or abolished, and a roll tilting tendency during spontaneous locomotion was seen. We conclude that the contralateral optic nerve projection to the pretectal region is necessary and sufficient for negative phototaxis and dorsal light response. The crossed descending pretectal projection is most important for dorsal light response, whereas the noncrossed one is most important for negative phototaxis. In the most rostral spinal cord, fibers for lateral yaw turns travel mainly in the lateral columns, whereas fibers for roll turns travel mainly in the medial spinal cord.

Brain stem and spinal cord demyelination due to acute carbon monoxide poisoning

2021 ◽  
pp. 247-253
Author(s):  
Yan Lv ◽  
Yv Zhang ◽  
Shuyi Pam ◽  
Keyword(s):  
Spinal Cord ◽  
Carbon Monoxide ◽  
Brain Stem ◽  
Carbon Monoxide Poisoning ◽  
Recovery Period ◽  
Extended Period ◽  
Severe Case ◽  
Co Poisoning ◽  
Secondary Demyelination ◽  
The Brain

Demyelination throughout the brain stem and spinal cord caused by acute carbon monoxide (CO) poisoning has not been previously reported. Magnetic resonance imaging (MRI) has revealed that acute CO poisoning primarily affects the subcortical white matter of the bilateral cerebral hemispheres and basal ganglia. Here we report the case of a patient with delayed neuropsychological sequelae (DNS) due to acute CO poisoning. A 28-year-old man was admitted to our department following a suicide attempt by acute CO poisoning. After a six-month pseudo-recovery period, he was diagnosed with DNS, with MRI evidence of demyelinating change of the bilateral cerebral peduncles. Demyelination was identified throughout the brain stem, expanding from the bilateral cerebral peduncles to the medulla oblongata, occurring approximately six months after poisoning. One and a half years after acute CO poisoning, demyelination of the cervical and thoracic spine was observed, most notable in the lateral and posterior cords. It is evident that previously published research on this topic is extremely limited. Perhaps in severe cases of acute CO poisoning the fatality rate is higher, leading to fewer surviving cases for possible study. This may be because a more severe case of acute CO poisoning would result in the higher likelihood of secondary demyelination. This research indicates that clinicians should be aware of the risk of secondary demyelination and take increased precautions such as vitamin B supplementation and administration of low-dose corticosteroids for an extended period of time in order to reduce the extent and severity of demyelination.

Symptoms, Related Brain Regions, and Diagnosis

2013 ◽  
Author(s):  
J. Eric Ahlskog
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
Basal Ganglia ◽  
Brain Stem ◽  
Muscle Activation ◽  
Sensory Information ◽  
Brain Regions ◽  
Electrical Signal ◽  
Brain And Spinal Cord ◽  
The Brain

As a prelude to the treatment chapters that follow, we need to define and describe the types of problems and symptoms encountered in DLB and PDD. The clinical picture can be quite varied: problems encountered by one person may be quite different from those encountered by another person, and symptoms that are problematic in one individual may be minimal in another. In these disorders, the Lewy neurodegenerative process potentially affects certain nervous system regions but spares others. Affected areas include thinking and memory circuits, as well as movement (motor) function and the autonomic nervous system, which regulates primary functions such as bladder, bowel, and blood pressure control. Many other brain regions, by contrast, are spared or minimally involved, such as vision and sensation. The brain and spinal cord constitute the central nervous system. The interface between the brain and spinal cord is by way of the brain stem, as shown in Figure 4.1. Thought, memory, and reasoning are primarily organized in the thick layers of cortex overlying lower brain levels. Volitional movements, such as writing, throwing, or kicking, also emanate from the cortex and integrate with circuits just below, including those in the basal ganglia, shown in Figure 4.2. The basal ganglia includes the striatum, globus pallidus, subthalamic nucleus, and substantia nigra, as illustrated in Figure 4.2. Movement information is integrated and modulated in these basal ganglia nuclei and then transmitted down the brain stem to the spinal cord. At spinal cord levels the correct sequence of muscle activation that has been programmed is accomplished. Activated nerves from appropriate regions of the spinal cord relay the signals to the proper muscles. Sensory information from the periphery (limbs) travels in the opposite direction. How are these signals transmitted? Brain cells called neurons have long, wire-like extensions that interface with other neurons, effectively making up circuits that are slightly similar to computer circuits; this is illustrated in Figure 4.3. At the end of these wire-like extensions are tiny enlargements (terminals) that contain specific biological chemicals called neurotransmitters. Neurotransmitters are released when the electrical signal travels down that neuron to the end of that wire-like process.

Partial cloning of the rat choline acetyltransferase gene and in situ localization of its transcripts in the cell body of cholinergic neurons in the brain stem and spinal cord

1993 ◽  
Vol 17 (1-2) ◽  
pp. 101-111 ◽  
Author(s):  
Nozomu Mori ◽  
Yasutaka Tajima ◽  
Hironobu Sakaguchi ◽  
David J. Vandenbergh ◽  
Hiroyuki Nawa ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Brain Stem ◽  
Cell Body ◽  
Choline Acetyltransferase ◽  
Cholinergic Neurons ◽  
The Brain

Cervical spinal cord in experimental hydrocephalus

1972 ◽  
Vol 37 (5) ◽  
pp. 538-542 ◽  
Author(s):  
George J. Dohrmann
Keyword(s):  
Spinal Cord ◽  
Brain Stem ◽  
Cervical Spinal Cord ◽  
Central Canal ◽  
Content Type ◽  
Experimental Hydrocephalus ◽  
Physiological Pressure ◽  
The Brain ◽  
Shunting Procedure ◽  
Fine Print

✓ Adult dogs were rendered hydrocephalic by the injection of kaolin into the cisterna magna. One group of dogs was sacrificed 1 month after kaolin administration, and ventriculojugular shunts were performed on the other group. Hydrocephalic dogs with shunts were sacrificed 1 day or 1 week after the shunting procedure. All dogs were perfused with formalin at physiological pressure, and the brain stem and cervical spinal cord were examined by light microscopy. Subarachnoid granulomata encompassed the superior cervical spinal cord and dependent surface of the brain stem. Rarefaction of the posterior white columns and clefts or cavities involving the gray matter posterior to the central canal and/or posterior white columns were present in the spinal cords of both hydrocephalic and shunted hydrocephalic dogs. Predominantly in the dogs with shunts, hemorrhages were noted in the spinal cord in association with the clefts or cavities. A mechanism of ischemia followed by reflow of blood is postulated to explain the hemorrhages in the spinal cords of hydrocephalic dogs with shunts.

Excitation of lumbar motoneurons by the medial longitudinal fasciculus in the in vitro brain stem spinal cord preparation of the neonatal rat

1993 ◽  
Vol 70 (6) ◽  
pp. 2241-2250 ◽  
Author(s):  
M. K. Floeter ◽  
A. Lev-Tov
Keyword(s):  
Spinal Cord ◽  
Brain Stem ◽  
Short Latency ◽  
Medial Longitudinal Fasciculus ◽  
Paired Pulse ◽  
Long Latency ◽  
The Brain ◽  
Pulse Stimulation ◽  
Stimulation Of

1. The excitation of lumbar motoneurons by reticulospinal axons traveling in the medial longitudinal fasciculus (MLF) was investigated in the newborn rat using intracellular recordings from lumbar motoneurons in an in vitro preparation of the brain stem and spinal cord. The tracer DiI (1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine) was introduced into the MLF of 6-day-old littermate rats that had been fixed with paraformaldehyde to evaluate the anatomic extent of this developing pathway. 2. Fibers labeled from the MLF by DiI were present in the cervical ventral and lateral white matter and a smaller number of labeled fibers extended to the lumbar enlargement. Patches of sparse terminal labeling were seen in the lumbar ventral gray. 3. In the in vitro preparation of the brain stem and spinal cord, MLF stimulation excited motoneurons through long-latency pathways in most motoneurons and through both short-(< 40 ms) and long-latency connections in 16 of 40 motoneurons studied. Short- and longer-latency components of the excitatory response were evaluated using mephenesin to reduce activity in polysynaptic pathways. 4. Paired-pulse stimulation of the MLF revealed a modest temporal facilitation of the short-latency excitatory postsynaptic potential (EPSP) at short interstimulus intervals (20–200 ms). Trains of stimulation at longer interstimulus intervals (1–30 s) resulted in a depression of EPSP amplitude. The time course of the synaptic depression was compared with that found in EPSPs resulting from paired-pulse stimulation of the dorsal root and found to be comparable. 5. The short-latency MLF EPSP was reversibly blocked by 6-cyano-7-nitroquinoxaline (CNQX), an antagonist of non-N-methyl-D-aspartate glutamate receptors, with a small CNQX-resistant component. Longer-latency components of the MLF EPSP were also blocked by CNQX, and some late components of the PSP were sensitive to strychnine. MLF activation of multiple polysynaptic pathways in the spinal cord is discussed.

Sign in / Sign up

Export Citation Format

Share Document