Opioid modulation of calcium current in cultured  sensory neurons: μ-modulation of baroreceptor input

Hamra, Mary; McNeil, Robert S.; Runciman, Martin; Kunze, Diana L.

doi:10.1152/ajpheart.1999.277.2.h705

Cited by 12 publications

(10 citation statements)

References 32 publications

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“…1995), activation of pre‐synaptic metabotropic glutamate receptors (Liu et al. 1998), activation of mu‐opiate receptors (Hamra et al. 1999), and frequency‐dependent depression of endocytosis (Pamidimukkala and Hay 2001).…”

Section: Discussionmentioning

confidence: 99%

Brain‐derived neurotrophic factor in arterial baroreceptor pathways: implications for activity‐dependent plasticity at baroafferent synapses

Martin

Jenkins

Hsieh

et al. 2008

Journal of Neurochemistry

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Abbreviations used: ABC, avidin-biotin reagent; ADN, aortic depressor nerve; BDNF, brain-derived neurotrophic factor; DAB, diaminobenzidine; DB, dilution buffer; FDD, frequency-dependent depression; HCN1, hyperpolarization-activated cyclic nucleotide-gated ion channel protein 1; HRP, horseradish peroxidase; IR, immunoreactive or immunoreactivity; NG, nodose ganglion; NPG, nodose-petrosal ganglion complex; NTS, nucleus tractus solitarius; P, postnatal day; PBS, phosphate-buffered saline; SDS, sodium dodecyl sulfate; TRPV1, transient receptor potential vanilloid type 1. AbstractFunctional characteristics of the arterial baroreceptor reflex change throughout ontogenesis, including perinatal adjustments of the reflex gain and adult resetting during hypertension. However, the cellular mechanisms that underlie these functional changes are not completely understood. Here, we provide evidence that brain-derived neurotrophic factor (BDNF), a neurotrophin with a well-established role in activitydependent neuronal plasticity, is abundantly expressed in vivo by a large subset of developing and adult rat baroreceptor afferents. Immunoreactivity to BDNF is present in the cell bodies of baroafferent neurons in the nodose ganglion, their central projections in the solitary tract, and terminal-like structures in the lower brainstem nucleus tractus solitarius. Using ELISA in situ combined with electrical field stimulation, we show that native BDNF is released from cultured newborn nodose ganglion neurons in response to patterns that mimic the in vivo activity of baroreceptor afferents. In particular, highfrequency bursting patterns of baroreceptor firing, which are known to evoke plastic changes at baroreceptor synapses, are significantly more effective at releasing BDNF than tonic patterns of the same average frequency. Together, our study indicates that BDNF expressed by first-order baroreceptor neurons is a likely mediator of both developmental and postdevelopmental modifications at first-order synapses in arterial baroreceptor pathways. Keywords: calcium channels, electrical field stimulation, frequency-dependent depression, nodose ganglion, nucleus tractus solitarius. (Scheuer et al. 1996;Liu et al. 1998Liu et al. , 2000Chen et al. 1999;Doyle and Andresen 2001), a form of synaptic plasticity that may influence baroreflex function (Liu et al. 2000). However, the exact molecular mechanisms underlying changes in either the perinatal or adult system are not well understood.In recent years, brain-derived neurotrophic factor (BDNF), a member of the neurotrophin family of growth factors, has emerged as a key mediator of mechanisms regulating activity-dependent synaptic maturation and plasticity (Huang and Reichardt 2001;Poo 2001), including sensory plasticity (Malcangio and Lessmann 2003). During embryonic development, BDNF is required for the survival of a large subset of NPG neurons, including cardio-respiratory control neurons (Erickson et al. 1996), and specifically arterial baroreceptors (Brady et al. 1999). Namely, BDNF is e...

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Section: Discussionmentioning

confidence: 99%

Brain‐derived neurotrophic factor in arterial baroreceptor pathways: implications for activity‐dependent plasticity at baroafferent synapses

Martin

Jenkins

Hsieh

et al. 2008

Journal of Neurochemistry

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“…Morphine modified the response to haemorrhage after blast so that the compensatory phase was apparent, with an initial maintenance of arterial blood pressure and tachycardia, while the bradycardia associated with severe haemorrhage was abolished. It is unlikely that morphine achieved this effect by increasing the sensitivity of the baroreflex since it is known that m opioid receptor agonists, in the absence of blast, reduce baroreflex sensitivity (Gordon, 1990;Hamra et al 1999). …”

Section: Discussionmentioning

confidence: 99%

The Effects of Primary Thoracic Blast Injury and Morphine on the Response to Haemorrhage in the Anaesthetised Rat

Sawdon

Ohnishi

Watkins

et al. 2002

Experimental Physiology

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Primary thoracic blast injury causes a triad of bradycardia, hypotension and apnoea mediated in part via a vagal reflex. Blast casualties may also suffer blood loss, and the response to progressive simple haemorrhage is biphasic: an initial tachycardia followed by a vagally mediated reflex bradycardia which can be attenuated by μ opioid agonists. The aims of this study were to determine the effects of thoracic blast injury on the response to subsequent haemorrhage, and the effects of morphine, administered after blast, on the response to blood loss. Male Wistar rats, terminally anaesthetised with alphadolone‐alphaxolone (19‐21 mg kg−1 h−1 I.V.), were allocated randomly to one of three groups: Group I, sham blast; Group II, thoracic blast; Group III, thoracic blast plus morphine (0.5 mg kg−1 I.V. given 5 min after blast). Blast (Groups II and III) resulted in significant (P < 0.05, ANOVA) bradycardia, hypotension and apnoea. Sham blast (Group I) had no effect. Ten minutes later, haemorrhage (40% of the estimated total blood volume (BV)) in Group I produced a biphasic response comprising a tachycardia followed by a peak bradycardia after the loss of 33% BV. Arterial blood pressure did not fall significantly until the loss of 13.3% BV. In Group II the haemorrhage‐induced tachycardia was absent and the bradycardia was augmented: peak bradycardia was seen after the loss of 23% BV. Mean arterial blood pressure (MBP) began to fall as soon as haemorrhage commenced and was significant after the loss of 10% BV. Morphine (Group III) prevented the haemorrhage‐induced bradycardia and delayed the significant fall in MBP until the loss of 30% BV. It is concluded that the response to thoracic blast injury augments the depressor response to haemorrhage while morphine attenuates this response.

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“…Recent work with both opioid and metabotropic glutamate receptor agonists support this conclusion. -Opioid agonists inhibit voltage-gated calcium currents in the soma of baroreceptor neurons (20). Consistent with this inhibition at the soma, -opioid agonists depress glutamate-mediated excitatory postsynaptic potentials in NTS neurons evoked by stimulation of the solitary tract (38).…”

Section: Does Modulation Of Ionic Channels In Nodose Cell Body Correlmentioning

confidence: 87%

II. Integration of afferent signaling from the viscera by the nodose ganglia

Browning

Mendelowitz

2003

American Journal of Physiology-Gastrointestinal and Liver Physi

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To understand vago-vagal reflexes, one must have an appreciation of the events surrounding the encoding, integration, and central transfer of peripheral sensations by vagal afferent neurons. A large body of work has shown that vagal afferent neurons have nonuniform properties and that distinct subpopulations of neurons exist within the nodose ganglia. These sensory neurons display a considerable degree of plasticity; electrophysiological, pharmacological, and neurochemical properties have all been shown to alter after peripheral tissue injury. The validity of claims of selective recordings from populations of neurons activated by peripheral stimuli may be diminished, however, by the recent demonstration that stimulation of a subpopulation of nodose neurons can enhance the activity of unstimulated neuronal neighbors. To better understand the neurophysiological processes occurring after vagal afferent stimulation, it is essential that the electrophysiological, pharmacological, and neurochemical properties of nodose neurons are correlated with their sensory function or, at the very least, with their specific innervation target.

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Opioid modulation of calcium current in cultured sensory neurons: μ-modulation of baroreceptor input

Cited by 12 publications

References 32 publications

Brain‐derived neurotrophic factor in arterial baroreceptor pathways: implications for activity‐dependent plasticity at baroafferent synapses

Brain‐derived neurotrophic factor in arterial baroreceptor pathways: implications for activity‐dependent plasticity at baroafferent synapses

The Effects of Primary Thoracic Blast Injury and Morphine on the Response to Haemorrhage in the Anaesthetised Rat

II. Integration of afferent signaling from the viscera by the nodose ganglia

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