Vagally evoked synaptic currents in the immature rat nucleus tractus solitarii in an intact <i>in vitro</i> preparation

Smith, Bret N.; Dou, Ping; Barber, William J.; Dudek, F. Edward

doi:10.1111/j.1469-7793.1998.149bf.x

Cited by 87 publications

(99 citation statements)

References 46 publications

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“…This occurred in ϳ50% of the neurons that initially displayed constant-latency EPSCs in response to vagal afferent stimulation. All IPSCs were blocked by bicuculline, indicating that vagal nerve stimulation had activated a local NTS GABAergic circuit (33). The data of Bailey et al (3) confirm these results with the finding that solitary tract stimulation activates GABAergic inputs to GABA neurons in the NTS.…”

Section: Discussionsupporting

confidence: 81%

GABA signaling in the nucleus tractus solitarius sets the level of activity in dorsal motor nucleus of the vagus cholinergic neurons in the vagovagal circuit

Herman

Cruz²,

Sahibzada³

et al. 2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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It has been proposed that there is an "apparent monosynaptic" connection between gastric vagal afferent nerve terminals and inhibitory projection neurons in the nucleus tractus solitarius (NTS) and that two efferent parallel pathways from the dorsal motor nucleus of the vagus (DMV) influence peripheral organs associated with these reflexes (6). The purpose of our study was to verify the validity of these views as they relate to basal control of gastric motility. To test the validity of a direct connection of vagal afferent terminals (known to release L-glutamate) directly impacting second-order projection neurons, we evaluated the effect of GABA A receptor blockade in the area of the medial subnucleus of the tractus solitarius (mNTS) on gastric motility. Microinjection of bicuculline methiodide into the mNTS produced robust decreases in gastric motility (Ϫ1.6 Ϯ 0.2 mmHg, P Ͻ 0.05, n ϭ 23), which were prevented by cervical vagotomy and by pretreatment with kynurenic acid microinjected into the mNTS. Kynurenic acid per se had no effect on gastric motility. However, after GABA A receptor blockade in the mNTS, kynurenic acid produced a robust increase in gastric motility. To test for the contribution of two parallel efferent DMV pathways, we assessed the effect of either intravenous atropine methylbromide or N G -nitro-L-arginine methyl ester on baseline motility and on decreases in gastric motility induced by GABA A receptor blockade in the mNTS. Only atropine methylbromide altered baseline motility and prevented the effects of GABA A receptor blockade on gastric motility. Our data demonstrate the presence of intra-NTS GABAergic signaling between the vagal afferent nerve terminals and inhibitory projection neurons in the NTS and that the cholinergic-cholinergic excitatory pathway comprises the functionally relevant efferent arm of the vagovagal circuit. gastric; vagus; afferent; inhibition; rat THE IMPORTANCE OF THE VAGOVAGAL reflexes in the regulation of gastrointestinal (GI) function has been highlighted in a recent series of articles published under the theme "Musings on the Wanderer: What's New in Our Understanding of Vagovagal Reflexes?" (6, 37). The central nervous system component of this reflex circuit is located in the hindbrain and consists of a sensory nucleus, the nucleus tractus solitarius (NTS), and a motor nucleus, the dorsal motor nucleus of the vagus (DMV). Currently it is thought that signals from sensory receptors in the GI tract are received in the NTS and conveyed to DMV preganglionic vagal nerves (28, 36). These impulses produce functional changes in thoracic and abdominal viscera (28, 36). Critical to conveying sensory signals to vagal efferent impulses are synaptic connections between NTS and DMV neurons. There is considerable evidence that GABAergic neurons are responsible for a significant part of this communication (9, 35). There is also evidence that noradrenergic neurons take part in this communication process (10,11,18,26,29). Both the GABAergic and noradrenergic neurons are considered...

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Section: Discussionsupporting

confidence: 81%

GABA signaling in the nucleus tractus solitarius sets the level of activity in dorsal motor nucleus of the vagus cholinergic neurons in the vagovagal circuit

Herman

Cruz²,

Sahibzada³

et al. 2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…This interpretation is based on to the relatively larger probability of evoking IPSCs compared with EPSCs. There are possibly additional excitatory inputs to the DMV originating from NTS neurons that are tonically inhibited by GABAergic inputs [27]. Evidence for this is that an increase in eEPSC responses was seen in the presence of the GABA A antagonist, picrotoxin.…”

Section: Discussionmentioning

confidence: 99%

Excitatory and inhibitory local circuit input to the rat dorsal motor nucleus of the vagus originating from the nucleus tractus solitarius

et al. 2004

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The nucleus tractus solitarius (NTS) and dorsal motor nucleus of the vagus nerve (DMV) constitute sensory and motor nuclei of the dorsal vagal complex, respectively. We used whole-cell patch-clamp recordings from DMV neurons in rat brain slices and three methods of stimulation (electrical, glutamate microdrop, glutamate photostimulation) to test the hypothesis that convergent excitatory and inhibitory inputs to DMV neurons originate from intact neurons in multiple NTS areas. Electrical stimulation of the NTS resulted in evoked excitatory and inhibitory postsynaptic currents (eEPSCs and eIPSCs) in DMV neurons. Stimulation of the dorsal NTS with glutamate microdrops, which selectively stimulates the soma and dendrites of intact neurons, resulted in 31% of DMV neurons receiving eEPSCs, 44% receiving eIPSCs, and 6% receiving convergent excitatory and inhibitory inputs. Glutamate photostimulation allowed selective activation of intact neurons in multiple, discrete areas of the NTS and resulted in 36% of DMV neurons receiving eEPSCs, 65% receiving eIPSCs and 20% receiving both inputs. Data obtained by stimulation of multiple NTS areas support the hypothesis that there are anatomically convergent inputs to DMV neurons originating from intact neurons within the NTS. These data support the hypothesis that there is transfer of convergent information from the NTS to the DMV, implying that significant sensory-motor processing occurs within the brainstem.

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“…Propofol likely enhances solitary tract driven GABAergic inputs as well as other major sources of inhibitory input to NTS from the forebrain (Saha, 2005). Thus propofol enhancement of IPSCs may greatly disrupt the widespread EPSC-IPSC temporal sequence triggered by afferent activation (Andresen & Yang, 1995;Mifflin & Felder, 1988;Smith et al, 1998).…”

Section: Propofol Actions In Nts In Vitro and Autonomic Controlmentioning

confidence: 99%

Propofol enhances both tonic and phasic inhibitory currents in second-order neurons of the solitary tract nucleus (NTS)

et al. 2008

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The anesthetic propofol is thought to induce rapid hypnotic sedation by facilitating a GABAergic tonic current in forebrain neurons. The depression of cardiovascular and respiratory regulation often observed during propofol suggests potential additional actions within the brainstem. Here we determined the impacts of propofol on both GABAergic and glutamatergic synaptic mechanisms in a class of solitary tract nucleus (NTS) neurons common to brainstem reflex pathways. In horizontal brainstem slices, we recorded from NTS neurons directly activated by solitary tract (ST) axons. We identified these second-order NTS neurons by time-invariant ("jitter" <200 µs), "all-or-none" glutamatergic excitatory postsynaptic currents (EPSCs) in response to shocks to the ST. In order to assess propofol actions, we measured ST-evoked, spontaneous and miniature EPSCs and inhibitory postsynaptic currents (IPSCs) during propofol exposure. Propofol prolonged miniature IPSC decay time constants by 50% above control at 1.8 µM. Low concentrations of gabazine (SR-95531) blocked phasic GABA currents. At higher concentrations, propofol (30 µM) induced a gabazine-insensitive tonic current that was blocked by picrotoxin or bicuculline. In contrast, total propofol concentrations up to 30 µM had no effect on EPSCs. Thus, propofol enhanced phasic GABA events in NTS at lower concentrations than tonic current induction, opposite to the relative sensitivity observed in forebrain regions. These data suggest that therapeutic levels of propofol facilitate phasic (synaptic) inhibitory transmission in second order NTS neurons which likely inhibits autonomic reflex pathways during anesthesia.

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Vagally evoked synaptic currents in the immature rat nucleus tractus solitarii in an intact in vitro preparation

Cited by 87 publications

References 46 publications

GABA signaling in the nucleus tractus solitarius sets the level of activity in dorsal motor nucleus of the vagus cholinergic neurons in the vagovagal circuit

GABA signaling in the nucleus tractus solitarius sets the level of activity in dorsal motor nucleus of the vagus cholinergic neurons in the vagovagal circuit

Excitatory and inhibitory local circuit input to the rat dorsal motor nucleus of the vagus originating from the nucleus tractus solitarius

Propofol enhances both tonic and phasic inhibitory currents in second-order neurons of the solitary tract nucleus (NTS)

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