Brain function, carbon dioxide, anticonvulsants, and tranquilizers. Spinal fluid PH in brain diseases.
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Anticonvulsants↗
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Results for “brain function”
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Hypotensive anesthesia for total hip arthroplasty: a study of blood loss and organ function (brain, heart, liver, and kidney).
The authors attempted to determine whether hypotensive anesthesia or the method of inducing hypotension has any effect on postoperative brain, liver, or kidney function and myocardial status following total hip arthroplasty. Thirty patients were anesthestized with halothane-nitrous oxide for total hip arthroplasty and randomly assigned to one of three groups. In two groups mean arterial blood pressure was decreased to 50 torr by high inspired concentrations of halothane (n = 90) or sodium nitroprusside (n = 12). In the third group (n = 9) mean blood pressure was maintained within 20% of control. Intraoperative blood losses decreased from 1,183 +/- 172 ml in the normotensive group to 406 +/- 102 ml and 326 +/- 41 ml in the halothane and nitroprusside hypotensive groups, respectively. Neither method of inducing hypotension nor hypertensive technique affected the results of postoperative tests of cerebral, hepatic, or renal function and myocardial status. These tests were performed before anesthesia and operation and at intervals in the postoperative course. In this small group of patients, deliberate hypotension for total hip arthroplasty added no morbidity and significantly shortened operating time, decreased blood loss, and decreased the number of blood transfusions needed.
Aged↗
Long term effects of high altitude on brain function.
Absence of oxygen to the brain for even a very few minutes results in loss of consciousness and can cause permanent injury. Can the wanderer to the limits of earth-bound hypoxia suffer similar harm from more prolonged exposure to milder hypoxia that does not cause loss of consciousness? I shall review the results from studies where neurobehavioral function has been compared in mountaineers before and after return from great heights and in individuals with chronic pulmonary disease before and after prolonged, continuous oxygen therapy. Many (although not all) of these studies report mild impairment of neurobehavioral function after fairly prolonged hypoxic exposure. Impairment was manifest by deficits in memory storage and recall, aphasia, concentration, and finger tapping speed; the last deficit was still detectable a year later in one group of mountaineers. Limited evidence suggests that climbers with a high ventilatory response to hypoxia (HVR) may be more susceptible to impairment than those with a lower HVR.
Altitude Sickness↗
[Neurogenesis in the adult brain. Functional consequences].
In the adult mammalian brain, neuroblasts are continuously produced within the subgranular zone of the hippocampus and the subventricular zone (SVZ) of the forebrain. In this review we describe how some physiological and environmental factors play important roles in regulating neurogenesis in the hippocampus. Neuroblasts in the SVZ network migrate rostrally into the olfactory bulb where they differentiate into local interneurons. We focus on the production, survival and functional consequences of these newly generated interneurons. We show that enriched odor-exposure enhances the number of newborn neurons in the adult olfactory bulb but not in the hippocampus. This effect did not result from changes in cell proliferation but rather was due to greater neuronal survival. Furthermore, the enriched condition was found to dramatically extend the olfactory memory. By maintaining a constitutive turnover of interneurons subjected to regulation by bulbar activity, ongoing neurogenesis plays a key role in olfactory memory.
Adult↗
The development and evaluation of a low-cost microdensitometer for use with the 2-deoxy-D-glucose method of functional brain mapping.
The conversion of a standard laboratory compound microscope into a microdensitometer for use in the 2-deoxy-D-glucose autoradiographic method of functional mapping in the brain is described. A solid-state detector was attached to the camera port of a Zeiss Universal Microscope and minor modifications to the microscope optics were made to produce a microdensitometer with a field of view 0.15 mm in diameter. Details are presented showing the modifications to the microscope which do not permanently destroy its functional ability to perform as a viewing microscope. A simple electronic circuit is presented to digitally display the output of the photo detector. Calibration of the instrument in terms of optical density or 2-deoxy-D-glucose activity is also described. The primary design goal was the construction of a simple, reliable, inexpensive microdensitometer that could be assembled by laboratory personnel. This densitometer should allow laboratories on modest budgets to have access to quantitative methods for the study of brain functional activity at a cost considerably less than the price of a commercial microdensitometer.
Animals↗
Effects of the diet on brain function.
The rates of synthesis by brain neurons of the neurotransmitters serotonin, acetylcholine, and the catecholamines depend on the brain levels of the respective precursor molecules. Brain levels of each precursor are influenced by their blood concentration, and for the amino acid precursors, by the blood levels of other amino acids as well. Since diet readily alters blood concentrations of each of these precursors, it thereby also influences the brain formation of their neurotransmitter products.
Acetylcholine↗
An outline of brain function.
An outline of how the brain may compute is proposed. In the cerebral cortex memories are stored through long-term potentiation at synapses from layer 1 cortical inputs (representing contexts) on layer 2/3 pyramidal cells linked with the thalamus in a cortico-thalamic (CT) unit. The signals which are memorized are the layer 3 inputs from the thalamus or other cortical areas. Signals are memorized (and later recalled) at the gamma frequency. A conscious thought comprises the outputs of layer 5 cells in CT units in different cortical regions firing in synchrony through the contribution of oscillatory thalamic and cortical inputs. This cortical output influences sub-cortical areas to cause or participate in a movement. Cerebral cortical outputs may be stored in the cerebellum and generated later in a particular context by the basal ganglia and cerebellum. Thus the brain may either generate 'conscious' outputs using the cerebral cortex or 'automatic' outputs using the basal ganglia and cerebellum. When contexts are recognized by the basal ganglia it permits outputs stored in the cerebellum to commence and in this way the basal ganglia can control complex sequences of outputs or movements. Working memory involves the prefrontal cortex using similarly the basal ganglia and cerebellum. The hippocampus has a role in the storage and recall of cortical outputs by providing unique layer 1 contexts to all the CT loops in different cortical areas in a conscious thought. With further recall of the thought new layer 1 contexts may become associated with the CT loops enabling recall without the hippocampal input.
Animals↗
Correlation of brain function with emotional behavior.
Identification of brain sites where physiologic activity was correlated with subjective emotional experiences in patients undergoing treatment was the starting point for our investigations of the neural basis for emotion and related clinically documented behavioral phenomena. By use of anatomic and physiologic techniques, the neural substrate has been shown to be notably different from that which continues to be described in textbooks, that is, the limbic system. Establishing the neurophysiologic basis for emotion has led to effective treatment for some neurologic and psychiatric disorders. Further, it has provided a basis for defining the origin of certain clinical disorders that are still obscure, the first step toward development of their specific treatment.
Animals↗
Mouse Dach2 mutants do not exhibit gross defects in eye development or brain function.
Drosophila dachshund is a critical regulator of eye, brain, and limb formation. Vertebrate homologs, Dach1 and Dach2, are expressed in the developing retina, brain, and limbs, suggesting functional conservation of the dachshund/Dach gene family. Dach1 mutants die postnatally, but exhibit grossly normal development. Here we report the generation of Dach2 mutant mice. Although deletion of Dach2 exon 1 results in abrogation of RNA expression, Dach2 mutants are viable and fertile. Histochemical analysis reveals grossly normal Dach2 mutant eye development. In addition, a battery of neurological assays failed to yield significant differences in behavior between Dach2 mutants and controls. We discuss these findings in the light of published observations of DACH2 mutations in the human population. Finally, to test the functional conservation hypothesis, we generated Dach2; Dach1 double mutant mice. Dach double mutants die after birth, similar to Dach1 homozygotes. However, unlike Drosophila dachshund mutants that lack eyes and exhibit leg truncations, the eyes and limbs of Dach double mutants are present, suggesting differences between Dach and dachshund gene function during embryonic eye and limb formation.
Animals↗
Sequential effects of propofol on functional brain activation induced by auditory language processing: an event-related functional magnetic resonance imaging study.
BACKGROUND: We have investigated the effect of propofol on language processing using event-related functional magnetic resonance imaging (MRI). METHODS: Twelve healthy male volunteers underwent MRI scanning at a magnetic field strength of 3 Tesla while performing an auditory language processing task. Functional images were acquired from the perisylvian cortical regions that are associated with auditory and language processing. The experiment consisted of three blocks: awake state (block 1), induction of anaesthesia with 3 mg kg(-1) propofol (block 2), and maintenance of anaesthesia with 3 mg kg(-1) h(-1) propofol (block 3). During each block normal sentences and pseudo-word sentences were presented in random order. The subjects were instructed to press a button to indicate whether a sentence was made up of pseudo-words or not. All subjects stopped responding during block two. The data collected before and after the subjects stopped responding during this block were analyzed separately. In addition, propofol plasma concentrations were measured and the effect-site concentrations of propofol were calculated. RESULTS: During wakefulness, language processing induced brain activation in a widely distributed temporofrontal network. Immediately after unresponsiveness, activation disappeared in frontal areas but persisted in both temporal lobes (block 2 second half, propofol effect-site concentration: 1.51 microg ml(-1)). No activation differences related to the task were observed during block 3 (propofol effect-site concentration: 4.35 microg ml(-1)). CONCLUSION: Our findings suggest sequential effects of propofol on auditory language processing networks. Brain activation firstly declines in the frontal lobe before it disappears in the temporal lobe.
Acoustic Stimulation↗
Unsupervised learning and mapping of active brain functional MRI signals based on hidden semi-Markov event sequence models.
In this paper, a novel functional magnetic resonance imaging (fMRI) brain mapping method is presented within the statistical modeling framework of hidden semi-Markov event sequence models (HSMESMs). Neural activation detection is formulated at the voxel level in terms of time coupling between the sequence of hemodynamic response onsets (HROs) observed in the fMRI signal, and an HSMESM of the hidden sequence of task-induced neural activations. The sequence of HRO events is derived from a continuous wavelet transform (CWT) of the fMRI signal. The brain activation HSMESM is built from the timing information of the input stimulation protocol. The rich mathematical framework of HSMESMs makes these models an effective and versatile approach for fMRI data analysis. Solving for the HSMESM Evaluation and Learning problems enables the model to automatically detect neural activation embedded in a given set of fMRI signals, without requiring any template basis function or prior shape assumption for the fMRI response. Solving for the HSMESM Decoding problem allows to enrich brain mapping with activation lag mapping, activation mode visualizing, and hemodynamic response function analysis. Activation detection results obtained on synthetic and real epoch-related fMRI data demonstrate the superiority of the HSMESM mapping method with respect to a real application case of the statistical parametric mapping (SPM) approach. In addition, the HSMESM mapping method appears clearly insensitive to timing variations of the hemodynamic response, and exhibits low sensitivity to fluctuations of its shape.
Algorithms↗
HBNF and MK, members of a novel gene family of heparin-binding proteins with potential roles in embryogenesis and brain function.
HBNF (heparin-binding neurite-promoting factor) is a heparin-binding protein which is found primarily in the brain and stimulates neurite outgrowth in cultured perinatal neurons. It was also reported to be mitogenic for fibroblasts and endothelial cells but this activity is still controversial. The sequence of HBNF is highly conserved in diverse species suggesting important function. Expression of the HBNF gene in brain tissue appears to be developmentally regulated, increasing during gestation to highest levels around the time of birth. The HBNF gene shows high sequence homology to another gene, MK (midkine). Like HBNF, the MK gene is developmentally regulated, however, high expression occurs in most fetal tissues during mid-gestation. The biological properties of the MK protein are remarkably similar to those of HBNF. The available evidence suggests that HBNF and MK are members of a new family of genes with potential roles in fetal development and in brain function or maintenance.
Amino Acid Sequence↗
Inflammation and brain function under basal conditions and during long-term elevation of brain corticotropin-releasing hormone levels.
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Animals↗
Brain function and macromolecules. I. Incorporation of uridine into RNA of mouse brain during short-term training experience.
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Animals↗
Brain function and macromolecules. II. Site of increased labeling of RNA in brains of mice during a short-term training experience.
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Animals↗
[Functional brain lateralization in children: developmental theories and implication for developmental diseases].
The functional specialization of each hemisphere in adults is now well accepted. Neuropsychology of hemispheric functioning in young children is a more debatable issue and must take into account additional factors such as development and maturation, characterized by complex changes in anatomy and organization. The first part of this review describes the theory behind the development of the functional organization of the brain. Second, we discuss data regarding brain lesions in children with brain damage and with normal development. We comment on the concept of plasticity and the critical period. We also discuss the neurobiological processes underlying the functional organization of the brain in the model of developmental disorders in children. We chose three disorders involving the left hemisphere (developmental dysphasia), both hemispheres (benign rolandic epilepsy) or the right hemisphere (congenital hydrocephalus) in order to examine their relationship to a specific hemispheric functional organization. We used classic neuropsychological tests such as the dichotic listening task, the dichaptic palpation and the time-sharing paradigm. The patterns observed in each pathology are discussed in light of data obtained in children with brain lesions.
Child Development↗
Thyroid physiology and brain function.
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Brain↗
Cholinesterases: new roles in brain function and in Alzheimer's disease.
The most important therapeutic effect of cholinesterase inhibitors (ChEI) on approximately 50% of Alzheimer's disease (AD) patients is to stabilize cognitive function at a steady level during a 1-year period of treatment as compared to placebo. Recent studies show that in a certain percentage (approximately 20%) of patients this cognitive stabilizing effect can be prolonged up to 24 months. This long-lasting effect suggests a mechanism of action other than symptomatic and cholinergic. In vitro and in vivo studies have consistently demonstrated a link between cholinergic activation and APP metabolism. Lesions of cholinergic nuclei cause a rapid increase in cortical APP and CSF. The effect of such lesions can be reversed by ChEI treatment. Reduction in cholinergic neurotransmission--experimental or pathological, such as in AD--leads to amyloidogenic metabolism and contributes to the neuropathology and cognitive dysfunction. To explain the long-term effect of ChEI, mechanisms based on beta-amyloid metabolism are postulated. Recent data show that this mechanism may not necessarily be related to cholinesterase inhibition. A second important aspect of brain cholinesterase function is related to enzymatic differences. The brain of mammals contains two major forms of cholinesterases: acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE). The two forms differ genetically, structurally, and for their kinetics. Butyrylcholine is not a physiological substrate in mammalian brain, which makes the function of BuChE of difficult interpretation. In human brain, BuChE is found in neurons and glial cells, as well as in neuritic plaques and tangles in AD patients. Whereas, AChE activity decreases progressively in the brain of AD patients, BuChE activity shows some increase. To study the function of BuChE, we perfused intracortically the rat brain with a selective BuChE inhibitor and found that extracellular acetylcholine increased 15-fold from 5 nM to 75 nM concentrations with little cholinergic side effect in the animal. Based on these data and on clinical data showing a relation between cerebrospinal fluid (CSF) BuChE inhibition and cognitive function in AD patients, we postulated that two pools of cholinesterases may be present in brain, the first mainly neuronal and AChE dependent and the second mainly glial and BuChE dependent. The two pools show different kinetic properties with regard to regulation of ACh concentration in brain and can be separated with selective inhibitors. Within particular conditions, such as in mice nullizygote for AChE or in AD patients at advanced stages of the disease, BuChE may replace AChE in hydrolizing brain acetylcholine.
Alzheimer Disease↗