The comparison of effects of various anesthetics on expression of Fos protein in the rat brain

Takayama, Kiyoshige; Suzuki, Takashi; Miura, Mitsuhiko

doi:10.1016/0304-3940(94)90871-0

Cited by 139 publications

(70 citation statements)

References 10 publications

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“…FOS expression was substantially increased during systemic pentobarbital anesthesia compared with the wake group ( p Ͻ 0.01), consistent with earlier reports (Krukoff et al, 1992;Takayama et al, 1994;Ryabinin et al, 2000;Lu et al, 2008). However, no such increase occurred in the anesthesia-like state induced by intracerebral pentobarbital (MPTA group, p Ͼ 0.2 compared with awake, p Ͻ 0.01 compared with IP) (Figs.…”

Section: Lhbsupporting

confidence: 91%

“…During normal wakefulness, FOS, the protein product of c-fos expression, is present at relatively high levels in most cortical areas (Pompeiano et al, 1994;Cirelli and Tononi, 2000). Systemic pentobarbital causes widespread suppression of cortical FOS (Takayama et al, 1994;Lu et al, 2008). We have now evaluated cortical and subcortical changes in FOS expression following intracerebral microinjection in the MPTA.…”

Section: Introductionmentioning

confidence: 99%

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Cerebral Activity during the Anesthesia-Like State Induced by Mesopontine Microinjection of Pentobarbital

Abulafia¹,

Zalkind²,

Devor³

2009

J. Neurosci.

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Microinjection of pentobarbital into a restricted region of rat brainstem, the mesopontine tegmental anesthesia area (MPTA), induces a reversible anesthesia-like state characterized by loss of the righting reflex, atonia, antinociception, and loss of consciousness as assessed by electroencephalogram synchronization. We examined cerebral activity during this state using FOS expression as a marker. Animals were anesthetized for 50 min with a series of intracerebral microinjections of pentobarbital or with systemic pentobarbital and intracerebral microinjections of vehicle. FOS expression was compared with that in awake animals microinjected with vehicle. Neural activity was suppressed throughout the cortex whether anesthesia was induced by systemic or MPTA routes. Changes were less consistent subcortically. In the zona incerta and the nucleus raphe pallidus, expression was strongly suppressed during systemic anesthesia, but only mildly during MPTA-induced anesthesia. Dissociation was seen in the tuberomammillary nucleus where suppression occurred during systemic-induced anesthesia only, and in the lateral habenular nucleus where activity was markedly increased during systemicinduced anesthesia but not following intracerebral microinjection. Several subcortical nuclei previously associated with cerebral arousal werenotaffected.IntheMPTAitselfFOSexpressionwassuppressedduringsystemicanesthesia.Differencesinthepatternofbrainactivityinthe two modes of anesthesia are consistent with the possibility that anesthetic endpoints might be achieved by alternative mechanisms: direct drug action for systemic anesthesia or via ascending pathways for MPTA-induced anesthesia. However, it is also possible that systemically administered agents induce anesthesia, at least in part, by a primary action in the MPTA with cortical inhibition occurring secondarily.

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Section: Lhbsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Cerebral Activity during the Anesthesia-Like State Induced by Mesopontine Microinjection of Pentobarbital

Abulafia¹,

Zalkind²,

Devor³

2009

J. Neurosci.

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“…Although there is evidence that nodose ganglion cardiac afferent neurons also transmit ischemic signals, only ϳ10% of these neurons are sensitive to the mechanical and chemical stimuli associated with cardiac ischemia (2). The very low levels of Fos in the cervical and thoracic spinal segments, even with the use of urethane, an anesthetic noted to result in high background levels of Fos in the brain stem and other higher centers (36), indicate that the differences in Fos expression were clearly a function of the experimental interventions and not the anesthetic.…”

Section: Discussionmentioning

confidence: 99%

“…Cardiac chemosensitive fibers transmit signals through the dorsal laminae and a number of spinoanterolateral ascending tracts, including the STT, primarily in spinal segments C 1 -C 3 and T 2 -T 6 , and then to a number of higher sites (13,15,23). Some of these higher sites project to the caudal NTS (36), the dorsal motor nucleus of the vagus, and sympathetic thoracic intermediolateral cell columns (17) as part of the circuitry processing this noxious cardiac visceral information.…”

mentioning

confidence: 99%

c-Fos expression in rat brain stem and spinal cord in response to activation of cardiac ischemia-sensitive afferent neurons and electrostimulatory modulation

Fang

Harrison²,

Qin³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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-Fos expression in rat brain stem and spinal cord in response to activation of cardiac ischemia-sensitive afferent neurons and electrostimulatory modulation. Am J Physiol Heart Circ Physiol 287: H2728 -H2738, 2004. First published July 29, 2004 doi:10.1152/ajpheart.00180. 2004.-The purpose of this study was to identify central neuronal sites activated by stimulation of cardiac ischemia-sensitive afferent neurons and determine whether electrical stimulation of left vagal afferent fibers modified the pattern of neuronal activation. Fos-like immunoreactivity (Fos-LI) was used as an index of neuronal activation in selected levels of cervical and thoracic spinal cord and brain stem. Adult Sprague-Dawley rats were anesthetized with urethane and underwent intrapericardial infusion of an "inflammatory exudate solution" (IES) containing algogenic substances that are released during ischemia (10 mM adenosine, bradykinin, prostaglandin E2, and 5-hydroxytryptamine) or occlusion of the left anterior descending coronary artery (CoAO) to activate cardiac ischemia-sensitive (nociceptive) afferent fibers. IES and CoAO increased Fos-LI above resting levels in dorsal horns in laminae I-V at C2 and T4 and in the caudal nucleus tractus solitarius. Dorsal rhizotomy virtually eliminated Fos-LI in the spinal cord as well as the brain stem. Neuromodulation of the ischemic signal by electrical stimulation of the central end of the left thoracic vagus excited neurons at the cervical and brain stem level but inhibited neurons at the thoracic spinal cord during IES or CoAO. These results suggest that stimulation of the left thoracic vagus excites descending inhibitory pathways. Inhibition at the thoracic spinal level that suppresses the ischemic (nociceptive) input signal may occur by a short-loop descending pathway via signals from cervical propriospinal circuits and/or a longer-loop descending pathway via signals from the nucleus tractus solitarius. neuronal activation; coronary artery occlusion; intrapericardial algogenic solution; thoracic spinal cord; nucleus tractus solitarius; central nervous system MYOCARDIAL CHEMOSENSITIVE afferent neurons in nodose and dorsal root ganglia transduce the signals associated with regional ischemia to induce symptoms of angina (12, 13). The afferent pathways conducting the nociceptive signals from these cardiac ischemic sympathetic and vagal afferent fibers are well documented by electrophysiological studies using two models of cardiac "ischemia": intrapericardial infusion of algogenic substances and temporary occlusion of the left anterior descending artery.Several substances activate these cardiac chemosensitive neurons: bradykinin, substance P, prostaglandins, leukotrienes, lactate, potassium, and adenosine. It has been shown that the concentration of all these substances increases in the exudate solution of various animal models of ischemia (3-5, 13, 19, 25, 35, 40, 41). Models using occlusion of the left anterior descending coronary artery result in activation of cardiac sympathetic afferent fi...

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“…In all but one study (Gieroba and Blessing, 1994), stimulation was carried out in anesthetized animals. Anesthesia can increase Fos protein throughout brain (Takayama et al, 1994), which could mask effects of vagal stimulation. Anesthesia can also change the threshold for activation of different types of fibers in the vagal bundle (Woodbury and Woodbury, 1990).…”

Section: Introductionmentioning

confidence: 99%

Induction of c-Fos and ΔFosB Immunoreactivity in Rat Brain by Vagal Nerve Stimulation

Cunningham

Mifflin

Gould

et al. 2007

Neuropsychopharmacol

149

123

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Vagus nerve stimulation (VNS) is used as therapy for treatment-resistant depression or epilepsy. This study used immunohistochemistry for biomarkers of short-term (c-Fos) and long-term (DFosB) neuronal activation to map regions in brain that are activated by acute (2 h) or chronic (3 weeks) VNS in conscious Sprague-Dawley rats. Electrodes (Cyberonics Inc.) were implanted on the left vagus nerve and 1 week after surgery, stimulation began using parameters employed clinically (one burst of 20 Hz, 250 ms pulse width, 0.25 mA stimulation for 30 s every 5 min). Radio telemetry transmitters were used for monitoring blood pressure, heart rate, activity, and respiratory rate during VNS; neither acute nor chronic VNS significantly affected these parameters. Acute VNS significantly increased c-Fos staining in the nucleus of the solitary tract, paraventricular nucleus of the hypothalamus, parabrachial nucleus, ventral bed nucleus of the stria terminalis, and locus coeruleus but not in the cingulate cortex or dorsal raphe nucleus (DRN). Acute VNS did not affect DFosB staining in any region. Chronic VNS significantly increased DFosB and c-Fos staining bilaterally in each region affected by acute VNS as well as in the cingulate cortex and DRN. Using these stimulation parameters, VNS was tested for antidepressant-like activity using the forced swim test (FST). Both VNS and desipramine significantly decreased immobility in the FST; whereas desipramine decreased immobility by increasing climbing behavior, VNS did so by increasing swimming behavior. This study, then, identified potential sites in brain where VNS may produce its clinical effects.

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The comparison of effects of various anesthetics on expression of Fos protein in the rat brain

Cited by 139 publications

References 10 publications

Cerebral Activity during the Anesthesia-Like State Induced by Mesopontine Microinjection of Pentobarbital

Cerebral Activity during the Anesthesia-Like State Induced by Mesopontine Microinjection of Pentobarbital

c-Fos expression in rat brain stem and spinal cord in response to activation of cardiac ischemia-sensitive afferent neurons and electrostimulatory modulation

Induction of c-Fos and ΔFosB Immunoreactivity in Rat Brain by Vagal Nerve Stimulation

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