Excitatory amino acid‐mediated chemoreflex excitation of respiratory neurones in rostral ventrolateral medulla in rats.

Sun, Miao Kun; Reis, Donald J.

doi:10.1113/jphysiol.1996.sp021329

Cited by 25 publications

(20 citation statements)

References 35 publications

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“…Examples of Nissl-stained coronal sections of the dorsal CA1 field, revealing densely packed pyramidal cells with well-defined nuclei in control rats (a) and rats subjected to 8 episodes of brief hypoxia (b). Reis, 1994Reis, , 1996 that control cardiovascular and respiratory systems, brain circulation, and other functions are also rapidly and powerfully affected. Hypoxia, depending on intensity and duration, modulates Ca 2ϩ , K ϩ , Na ϩ channel activity and the expression of various genes and induces cellular injury, necrosis, and/or apoptosis (Lopez-Barneo et al, 1988;Sun and Reis, 1994;Hammarström and Gage, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…Control rats were placed in the same jar for the same period of blowing in air. The intensity of hypoxia was chosen for its sufficiency to produce a brief hypoxic functional interruption, synaptic arrest, of the hippocampal CA1 network, with full recovery immediately after oxygenation in vitro and a brief period of gasping (indicating an activation of respiratory chemoreflex; Sun and Reis, 1996) in vivo, in our preliminary experiments. The neuronal responses to 90% N 2 /5% O 2 /5% CO 2 for 3 min or 95% N 2 /5% CO 2 for 100 s at 31°C were also found to be identical in preliminary experiments.…”

Section: Downloaded Frommentioning

confidence: 99%

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Pharmacological Protection of Synaptic Function, Spatial Learning, and Memory from Transient Hypoxia in Rats

Sun

Xu²,

Alkon³

2002

J Pharmacol Exp Ther

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Hypoxia significantly reduced cholinergic activity in rat CA1 field and intracellular in the CA1 pyramidal cells, recorded in hippocampal slices. The hypoxic responses of the hippocampal CA1 pyramidal cells to a brief hypoxia consisted of a short period of "synaptic arrest", observed as an elimination of excitatory postsynaptic current under voltage clamp and recovered immediately as oxygenation was reinitiated. The hypoxic synaptic arrest was not associated with reduced postsynaptic responses of the pyramidal cells to externally applied L-glutamate, suggesting that the synaptic arrest might result from a presynaptic mechanism. The hypoxic synaptic arrest was abolished in the presence of 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), a specific adenosine A 1 receptor antagonist. Blocking adenosine A 1 receptors also eliminated effects of hypoxia on the hippocampal CA1 field activity and intracellular of the CA1 pyramidal cells. In behaving rats, brief hypoxia impaired their water maze performance in both the escape latency and probe tests. The impairment was prevented by intralateral cerebroventricular injections of DPCPX. These results suggest that hypoxia releases adenosine and produces an inhibition of synaptic transmission and intracellular signal cascade(s) involved in generation/maintenance of hippocampal CA1 activity. This protection of synaptic efficacy and spatial learning through adenosine A 1 receptor antagonism may represent an effective therapeutic strategy to eliminate functional interruption due to transient hypoxic episodes and/or chronic hypoxia secondary to compromise of respiratory function.

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Section: Discussionmentioning

confidence: 99%

Section: Downloaded Frommentioning

confidence: 99%

Pharmacological Protection of Synaptic Function, Spatial Learning, and Memory from Transient Hypoxia in Rats

Sun

Xu²,

Alkon³

2002

J Pharmacol Exp Ther

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“…Data from the present study found that a heterogeneous population of E neurons, including E DEC and E AUG neurons, was excited by exogenous SP. This suggests that endogenous SP and NK1-R may be involved in modulating the excitability of E DEC and E AUG neurons, and these neurons are involved in modulating respiratory rhythm in response to activation of a variety of afferents, including arterial chemoreceptors (Sun and Reis 1996), pulmonary stretch receptors (Hayashi et al 1996), and somatic afferents (Potts et al 2005). It has previously been shown that activation of the slowly adapting pulmonary stretch receptors (SARs) by the HeringBreuer reflex (HB-reflex) excites E DEC neurons in the VRG (Hayashi et al 1996).…”

Section: Reflex Activation Of Nk1-r On Expiratory Neurons Modulates Rmentioning

confidence: 99%

Neurokinin-1 Receptors Modulate the Excitability of Expiratory Neurons in the Ventral Respiratory Group

Fong

Potts

2008

Journal of Neurophysiology

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We studied the role of neurokinin-1 receptors (NK1-R) on the excitability of expiratory (E) neurons (tonic discharge, E TONIC ; augmenting, E AUG ; decrementing, E DEC ) throughout the ventral respiratory group, including Bötzinger Complex (BötC) using extracellular single-unit recording combined with pressurized picoejection in decerebrate, arterially perfused juvenile rats. Responses evoked by picoejection of the NK1-R agonist, [Sar 9 -Met (O 2 ) 11 ]-substance P (SSP) were determined before and after the selective NK1-R antagonist, CP99,994. SSP excited 20 of 35 expiratory neurons by increasing the number of action potentials per burst (ϩ33.7 Ϯ 6.5% of control), burst duration (ϩ20.6 Ϯ 7.9% of control), and peak firing frequency (ϩ16.2 Ϯ 4.8% of control; means Ϯ SE). Pretreatment with CP99,994 completely blocked SSP-evoked excitation in a subset of neurons tested, supporting the notion that SSP excitation was mediated through NK1-R activation. Because we had previously shown that E AUG neurons were crucial to locomotorrespiratory coupling (LRC), we reasoned that blockade of NK1-R would alter LRC by preventing somatic-evoked excitation of E AUG neurons. Blockade of NK1-Rs by CP99,994 in the BötC severely disrupted LRC and prevented somatic-evoked excitation of E AUG neurons. These findings demonstrate that LRC is dependent on endogenous SP release acting via NK1-Rs on E AUG neurons of the BötC. Taken together with our earlier finding that inspiratory offswitching by the Hering-Breuer Reflex requires endogenous activation of NK1-Rs through activation of NK1-Rs on E DEC neurons, we suggest that endogenous release of substance P in the BötC provides a reflex pathway-dependent mechanism to selectively modulate respiratory rhythm.

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“…These neurons are directly, selectively, rapidly, and reversibly excited in vitro or in vivo by hypoxia Sun and Reis, 1993). Although the elevations in sympathetic, cardiovagal, or respiratory nerve activities are mediated over spinal or intramedullary pathways (Sun and Reis, 1999), hypoxic activation of RVLM neurons elevates rCBF and synchronizes the EEG, and this is not fully understood. Most likely, it is multisynaptic because the RVLM does not innervate the cerebral cortex (Ruggiero et al, 1989).…”

mentioning

confidence: 99%

Neurons of a Limited Subthalamic Area Mediate Elevations in Cortical Cerebral Blood Flow Evoked by Hypoxia and Excitation of Neurons of the Rostral Ventrolateral Medulla

2001

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Sympathoexcitatory reticulospinal neurons of the rostral ventrolateral medulla (RVLM) are oxygen detectors excited by hypoxia to globally elevate regional cerebral blood flow (rCBF). The projection, which accounts for Ͼ50% of hypoxic cerebral vasodilation, relays through the medullary vasodilator area (MCVA). However, there are no direct cortical projections from the RVLM/MCVA, suggesting a relay that diffusely innervates cortex and possibly originates in thalamic nuclei. Systematic mapping by electrical microstimulation of the thalamus and subthalamus revealed that elevations in rCBF were elicited only from a limited area, which encompassed medial pole of zona incerta, Forel's field, and prerubral zone. Stimulation (10 sec train) at an active site increased rCBF by 25 Ϯ 6%. Excitation of local neurons with kainic acid mimicked effects of electrical stimulation by increasing rCBF. Stimulation of the subthalamic cerebrovasodilator area (SVA) with single pulses (0.5 msec; 80 A) triggered cortical EEG burst-CBF wave complexes with latency 24 Ϯ 5 msec, which were similar in shape to complexes evoked from the MCVA. Selective bilateral lesioning of the SVA neurons (ibotenic acid, 2 g, 200 nl) blocked the vasodilation elicited from the MCVA and attenuated hypoxic cerebrovasodilation by 52 Ϯ 12% ( p Ͻ 0.05), whereas hypercarbic vasodilation remained preserved. Lesioning of the vasodilator site in the basal forebrain failed to modify SVA-evoked rCBF increase. We conclude that (1) excitation of intrinsic neurons of functionally restricted region of subthalamus elevates rCBF, (2) these neurons relay signals from the MCVA, which elevate rCBF in response to hypoxia, and (3) the SVA is a functionally important site conveying vasodilator signal from the medulla to the telencephalon.

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Excitatory amino acid‐mediated chemoreflex excitation of respiratory neurones in rostral ventrolateral medulla in rats.

Cited by 25 publications

References 35 publications

Pharmacological Protection of Synaptic Function, Spatial Learning, and Memory from Transient Hypoxia in Rats

Pharmacological Protection of Synaptic Function, Spatial Learning, and Memory from Transient Hypoxia in Rats

Neurokinin-1 Receptors Modulate the Excitability of Expiratory Neurons in the Ventral Respiratory Group

Neurons of a Limited Subthalamic Area Mediate Elevations in Cortical Cerebral Blood Flow Evoked by Hypoxia and Excitation of Neurons of the Rostral Ventrolateral Medulla

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