Faculty Opinions recommendation of Gamma-aminobutyric acid-mediated neurotransmission in the pontine reticular formation modulates hypnosis, immobility, and breathing during isoflurane anesthesia.

2008 ◽  
Author(s):  
Stuart Forman
Keyword(s):  
Reticular Formation ◽  
Aminobutyric Acid ◽  
Pontine Reticular Formation ◽  
Gamma Aminobutyric Acid ◽  
Isoflurane Anesthesia

scholarly journals γ-Aminobutyric Acid–mediated Neurotransmission in the Pontine Reticular Formation Modulates Hypnosis, Immobility, and Breathing during Isoflurane Anesthesia

2008 ◽  
Vol 109 (6) ◽  
pp. 978-988 ◽  
Author(s):  
Giancarlo Vanini ◽  
Christopher J. Watson ◽  
Ralph Lydic ◽  
Helen A. Baghdoyan
Keyword(s):  
Reticular Formation ◽  
Induction Time ◽  
Aminobutyric Acid ◽  
Gaba Uptake ◽  
Breathing Rate ◽  
Pontine Reticular Formation ◽  
General Anesthetics ◽  
Nipecotic Acid ◽  
Mercaptopropionic Acid ◽  
Isoflurane Anesthesia

Background Many general anesthetics are thought to produce a loss of wakefulness, in part, by enhancing gamma-aminobutyric acid (GABA) neurotransmission. However, GABAergic neurotransmission in the pontine reticular formation promotes wakefulness. This study tested the hypotheses that (1) relative to wakefulness, isoflurane decreases GABA levels in the pontine reticular formation; and (2) pontine reticular formation administration of drugs that increase or decrease GABA levels increases or decreases, respectively, isoflurane induction time. Methods To test hypothesis 1, cats (n = 5) received a craniotomy and permanent electrodes for recording the electroencephalogram and electromyogram. Dialysis samples were collected from the pontine reticular formation during isoflurane anesthesia and wakefulness. GABA levels were quantified using high-performance liquid chromatography. For hypothesis 2, rats (n = 10) were implanted with a guide cannula aimed for the pontine reticular formation. Each rat received microinjections of Ringer's (vehicle control), the GABA uptake inhibitor nipecotic acid, and the GABA synthesis inhibitor 3-mercaptopropionic acid. Rats were then anesthetized with isoflurane, and induction time was quantified as loss of righting reflex. Breathing rate was also measured. Results Relative to wakefulness, GABA levels were significantly decreased by isoflurane. Increased power in the electroencephalogram and decreased activity in the electromyogram caused by isoflurane covaried with pontine reticular formation GABA levels. Nipecotic acid and 3-mercaptopropionic acid significantly increased and decreased, respectively, isoflurane induction time. Nipecotic acid also increased breathing rate. Conclusion Decreasing pontine reticular formation GABA levels comprises one mechanism by which isoflurane causes loss of consciousness, altered cortical excitability, muscular hypotonia, and decreased respiratory rate.

GABAA Receptors Inhibit Acetylcholine Release in Cat Pontine Reticular Formation: Implications for REM Sleep Regulation

2004 ◽  
Vol 92 (4) ◽  
pp. 2198-2206 ◽  
Author(s):  
Jacqueline Vazquez ◽  
Helen A. Baghdoyan
Keyword(s):  
Reticular Formation ◽  
Rem Sleep ◽  
In Vivo Microdialysis ◽  
Pontine Reticular Formation ◽  
Gamma Aminobutyric Acid ◽  
Ach Release ◽  
Sleep Regulation ◽  
Maximal Increase ◽  
Series Of Experiments

This study used in vivo microdialysis in cat ( n = 12) to test the hypothesis that gamma aminobutyric acid A (GABAA) receptors in the pontine reticular formation (PRF) inhibit acetylcholine (ACh) release. Animals were anesthetized with halothane to hold arousal state constant. Six concentrations of the GABAA receptor antagonist bicuculline (0.03, 0.1, 0.3, 1, 3, and 10 mM) were delivered to a dialysis probe in the PRF, and endogenously released ACh was collected simultaneously. Bicuculline caused a concentration dependent increase in ACh release (maximal increase = 345%; EC50 = 1.3 mM; r2 = 0.997). Co-administration of the GABAA receptor agonist muscimol prevented the bicuculline-induced increase in ACh release. In a second series of experiments, the effects of bicuculline (0.1, 0.3, 1, and 3 mM) on ACh release were examined without the use of general anesthesia. States of wakefulness, rapid-eye-movement (REM) sleep, and non-REM sleep were identified polygraphically before and during dialysis delivery of bicuculline. Higher concentrations of bicuculline (1 and 3 mM) significantly increased ACh release during wakefulness (36%), completely suppressed non-REM sleep, and increased ACh release during REM sleep (143%). The finding that ACh release in the PRF is modulated by GABAA receptors is consistent with the interpretation that inhibition of GABAergic transmission in the PRF contributes to the generation of REM sleep, in part, by increasing pontine ACh release.

Actions of neurotransmitters on pontine medical reticular formation neurons of the cat

1985 ◽  
Vol 54 (3) ◽  
pp. 520-531 ◽  
Author(s):  
R. W. Greene ◽  
D. O. Carpenter
Keyword(s):  
Reticular Formation ◽  
High Frequency ◽  
Spatial Separation ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Inhibitory Receptors ◽  
Reticulospinal Neurons ◽  
Frequency Responses ◽  
Pressure Injection ◽  
Anesthetized Cat

The actions of several neurotransmitters were determined on 43 antidromically identified reticulospinal neurons and 72 unidentified neurons in the paraabducens reticular formation of the anesthetized cat. All neurons were excited by glutamate and aspartate, both of which caused brief, high-frequency responses. In 80% of the reticulospinal neurons glutamate was more potent than aspartate, whereas in 61% of the unidentified neurons aspartate was more potent. Glutamate responses were reversibly antagonized by curare applied by pressure injection. Fast inhibitory responses were obtained on all neurons tested to gamma-aminobutyric acid, glycine, and norepinephrine. Some neurons showed similarly fast inhibitory responses to acetylcholine and serotonin. Acetylcholine and serotonin both acted on most neurons, but approximately equal numbers of neurons showed a relatively fast inhibition, a relatively slow and long-lasting excitation, and a biphasic combination of inhibition and slow-excitation responses. The pattern of responses to acetylcholine and serotonin is consistent with a spatial separation of excitatory and inhibitory receptors on different portions of the cell, possibly reflecting different inputs that use the same transmitter but have effects of opposite electrical and functional polarity. Although complicated by the phenomenon of excitatory and inhibitory responses to the same transmitter, these results are compatible with the Hobson-McCarley model of generation of desynchronized sleep.

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