Purinergic and Vanilloid Receptor Activation Releases Glutamate from Separate Cranial Afferent Terminals in Nucleus Tractus Solitarius

Jin, Young Ho; Bailey, Timothy W.; Li, Bai Yan; Schild, John H.; Andresen, Michael

doi:10.1523/jneurosci.0753-04.2004

Cited by 168 publications

(183 citation statements)

References 59 publications

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“…Propofol did not alter the shape of EPSC events whether evoked or spontaneous, a result consistent with cortical neurons (Kitamura et al, 2003). The latency of ST triggered events is a sensitive, integrated index of axon conduction and terminal excitation that includes voltage dependent channel function such as sodium channels (Jin et al, 2004b;Bailey et al, 2006b). Latency of ST-EPSCs was unaffected by 30 µM propofol.…”

Section: Propofol Does Not Affect Glutamatergic Transmission In Seconsupporting

confidence: 70%

“…Cranial visceral afferent excitation of second-order NTS neurons relies on non-NMDA receptor mediated glutamatergic transmission (Jin et al, 2004a;Jin et al, 2004b). Propofol did not alter the shape of EPSC events whether evoked or spontaneous, a result consistent with cortical neurons (Kitamura et al, 2003).…”

Section: Propofol Does Not Affect Glutamatergic Transmission In Seconsupporting

confidence: 57%

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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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Section: Propofol Does Not Affect Glutamatergic Transmission In Seconsupporting

confidence: 70%

Section: Propofol Does Not Affect Glutamatergic Transmission In Seconsupporting

confidence: 57%

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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“…Although submaximal electrical stimulation of the tractus solitarius was used, the anatomical organization of the coronally sectioned caudal brainstem makes it likely that multiple fibers were recruited, unlike the horizontal brainstem preparation that restricts the stimulation to solitary fibers (Doyle and Andresen, 2001;Bailey et al, 2002Bailey et al, , 2006aJin et al, 2004). Nonvagal fibers of passage may also be stimulated during our paradigm, because several CNS areas that project to the NTS use glutamate as a neurotransmitter (Blessing, 1997;Schaffar et al, 1997;Lin et al, 2000) MC4R expressed on nonvagal inputs to NTS neurons enhance glutamatergic currents exclusively The MC4R activated in our experimental conditions appear to be located principally, but not exclusively, on vagal afferent fibers.…”

Section: Mc4r Expressed On Central Terminals Of Vagal Afferent Fibersmentioning

confidence: 99%

Presynaptic Melanocortin-4 Receptors on Vagal Afferent Fibers Modulate the Excitability of Rat Nucleus Tractus Solitarius Neurons

Wan¹,

Browning²,

Coleman³

et al. 2008

J. Neurosci.

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“…ST afferents can be divided into C-fibers and A-fibers by their sensitivity or resistance to CAP, respectively Jin et al, 2004). In five of nine AVP-sensitive, non-failure-type NTS neurons, CAP (200 nM) blocked ST-EPSCs and the remainder were CAP resistant.…”

Section: Avp-sensitive St Afferents Include Both a And C Fibersmentioning

confidence: 99%

Vasopressin Inhibits Glutamate Release via Two Distinct Modes in the Brainstem

Bailey

Jin

Doyle

et al. 2006

Journal of Neuroscience

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103

140

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Purinergic and Vanilloid Receptor Activation Releases Glutamate from Separate Cranial Afferent Terminals in Nucleus Tractus Solitarius

Cited by 168 publications

References 59 publications

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

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

Presynaptic Melanocortin-4 Receptors on Vagal Afferent Fibers Modulate the Excitability of Rat Nucleus Tractus Solitarius Neurons

Vasopressin Inhibits Glutamate Release via Two Distinct Modes in the Brainstem

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