Sentences with phrase «receptor changing in function»

«The bottom line is we don't know which variation leads to the dopamine receptor changing in function,» says Susan Smalley of UCLA.

Not exact matches

In animal models, exposure to cigarette smoke or nicotine during fetal development alters the expression of the nicotinic acetylcholine receptor in areas of the brainstem important for autonomic function, 28 alters the neuronal excitability of neurons in the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and alters fetal autonomic activity and medullary neurotransmitter receptors.30 In human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDIn animal models, exposure to cigarette smoke or nicotine during fetal development alters the expression of the nicotinic acetylcholine receptor in areas of the brainstem important for autonomic function, 28 alters the neuronal excitability of neurons in the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and alters fetal autonomic activity and medullary neurotransmitter receptors.30 In human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin areas of the brainstem important for autonomic function, 28 alters the neuronal excitability of neurons in the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and alters fetal autonomic activity and medullary neurotransmitter receptors.30 In human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and alters fetal autonomic activity and medullary neurotransmitter receptors.30 In human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDIn human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDS.

The acetylation changes were observed at genes that mediate glutamatergic function, specifically the glutamate receptor gene GRIA1, which has previously been implicated in drug use.

As they studied brain activity in the knockout mice, the researchers also found prominent changes in a receptor in the brain known as mGluR5 and other proteins that support the function of neurons and synapses, said co-lead author Xiaoming Wang, M.D., Ph.D., senior research associate in Duke's department of pediatrics.

To further explore the therapeutic potential of these receptors, Kalbe says his team are planning to obtain tissue from people with chronic airway diseases to compare them to healthy tissue, to observe if the receptors change in abundance or function in disease states.

The bile acids accumulate in the blood and interact with the TGR5 receptor on white fat cells to change their metabolic function.

It has been known for some time that dopamine and NMDA receptor function are altered in schizophrenic patients - our data mirror the direction of these changes and therefore might give insight into how these changes come about mechanistically.»

A dopamine - receptor gene variation is linked to changes in brain function, possibly neurotransmitter signaling

Angiotensin II receptor type 1 (Agtr1a): Lowering Agtr1a protein levels protects mitochondrial function and modestly extends life in mice, though as for many of these methods of somewhat slowing aging there are probably many other changes to the operation of metabolism that are as yet unexplored.

In Emory's Department of Pharmacology, the Traynelis and Yuan labs have been harvesting the vast amounts of information now available from public genome databases, to better understand how changes in the NMDA receptor genes relate to functioIn Emory's Department of Pharmacology, the Traynelis and Yuan labs have been harvesting the vast amounts of information now available from public genome databases, to better understand how changes in the NMDA receptor genes relate to functioin the NMDA receptor genes relate to function.

Phospholipase C is required for changes in postsynaptic structure and function associated with NMDA receptor - dependent long - term depression.

We hypothesize that loss of MLL3 / KMT2C function leads to a shift in the enhancer landscape, altering the sites available for estrogen receptor binding and thus changing gene transcription in breast cancer.

A recent paper in the Journal of Lipid Research proposes that anesthetics indirectly affect receptors by changing membrane dipole potential, acting like a car fob signal and causing an indirect change in receptor function.