Medullary monoamines and NMDA-receptor regulation of cardiovascular responses during peripheral nociceptive stimuli

Karlsson, Gudbjorn A.; Preuss, Charles; Chaitoff, Kevin A.; Maher, Timothy J.; Ally, Ahmmed

doi:10.1016/j.neures.2006.04.002

Cited by 16 publications

(9 citation statements)

References 65 publications

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“…injection of L-or D-Asp in chicks. On the other hand, several experiments have suggested that the stimulation of NMDA receptors is linked to the regulation of the monoaminergic system in the brain (Hanania and Zahniser, 2002;Karlsson et al, 2006;Hamasu et al, 2009). Thus, it remains unclear whether there is a relationship between L-or D-Asp and the monoaminergic system, because monoamine levels in the brain do not always reflect the activity of their neurons.…”

Section: Discussionmentioning

confidence: 99%

Oral Administration of D-aspartate, but not of L-aspartate, Reduces Food Intake in Chicks

et al. 2013

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Section: Discussionmentioning

confidence: 99%

Oral Administration of D-aspartate, but not of L-aspartate, Reduces Food Intake in Chicks

et al. 2013

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“…, 1997). These alterations in the catechol signal correlate with increased activity of catecholaminergic neurons in the RVLM and are abolished by blockade of postsynaptic activity in response to afferent activation (Karlsson et al. , 2006).…”

Section: Discussionmentioning

confidence: 99%

“…Similarly, a series of in vivo voltammetry studies show increased catechol signal measured within the C1 region during hypotension (Rentero et al, 1993(Rentero et al, , 2000, systemic acidosis (Rentero et al, 1998) and increased arterial partial CO 2 pressure (Rentero et al, 1997). These alterations in the catechol signal correlate with increased activity of catecholaminergic neurons in the RVLM and are abolished by blockade of postsynaptic activity in response to afferent activation (Karlsson et al, 2006). This strongly suggests that the catechol signal arises from somatodendritic release and supports our observation that a proportion of C1 cells express detectable levels of VMAT2 in their soma.…”

Section: Somatodendritic Catecholamine Release In the Rvlmmentioning

confidence: 91%

C1 neurons in the rat rostral ventrolateral medulla differentially express vesicular monoamine transporter 2 in soma and axonal compartments

Sevigny

Bassi

Teschemacher

et al. 2008

Eur J of Neuroscience

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Vesicular monoamine transporter 2 (VMAT2) packages biogenic amines into large dense core and synaptic vesicles for either somatodendritic or synaptic release from neurons of the CNS. Whilst the distribution of VMAT2 has been well characterized in many catecholaminergic cell groups, its localization amongst C1 adrenergic neurons in the medulla has not been examined in detail. Within the rostral ventrolateral medulla (RVLM), C1 neurons are a group of barosensitive, adrenergic neurons. Rostral C1 cells project to the thoracic spinal cord and are considered sympathetic premotor neurons. The majority of caudal C1 cells project rostrally to regions such as the hypothalamus. The present study sought to quantitate the somatodendritic expression of VMAT2 in C1 neurons, and to assess the subcellular distribution of the transporter. Immunoreactivity for VMAT2 occurred in 31% of C1 soma, with a high proportion of these in the caudal part of the RVLM. Retrograde tracing studies revealed that only two of 43 bulbospinal C1 neurons contained faint VMAT2-immunoreactivity, whilst 88 +/- 5% of rostrally projecting neurons were VMAT2-positive. A lentivirus, designed to express green fluorescent protein exclusively in noradrenergic and adrenergic neurons, was injected into the RVLM to label C1 neurons. Eighty-three percent of C1 efferents that occurred in close proximity to sympathetic preganglionic neurons within the T(3) intermediolateral cell column contained VMAT2-immunoreactivity. These data demonstrate differential distribution of VMAT2 within different subpopulations of C1 neurons and suggest that this might reflect differences in somatodendritic vs. synaptic release of catecholamines.

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“…Activation of specific neurons within the RVLM causes an increase in BP by increasing peripheral resistance and cardiac output via released catecholamines [94–97] . In addition to cardiovascular control, specific neurons within the RVLM are involved in nociception [98,99] and breathing [100] . Intracisternal (i.c) administration [101–103] or intra-RVLM microinjection [90,104] of cannabinoids such as WIN55,212-2 or CP-55940 elicited a pressor response and caused increases in sympathetic nerve activity, plasma norepinephrine and blood pressure, in conscious and anesthetized animals, and these responses were attenuated by pretreatment with the CB 1 R antagonists SR171416A or AM251.…”

Section: Cardiovascular Effects Of Cannabinoidsmentioning

confidence: 99%

Cannabinoid receptor 1 signaling in cardiovascular regulating nuclei in the brainstem: A review

Ibrahim

Abdel‐Rahman

2014

Journal of Advanced Research

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Cannabinoids elicit complex hemodynamic responses in experimental animals that involve both peripheral and central sites. Centrally administered cannabinoids have been shown to predominantly cause pressor response. However, very little is known about the mechanism of the cannabinoid receptor 1 (CB1R)-centrally evoked pressor response. In this review, we provided an overview of the contemporary knowledge regarding the cannabinoids centrally elicited cardiovascular responses and the possible underlying signaling mechanisms. The current review focuses on the rostral ventrolateral medulla (RVLM) as the primary brainstem nucleus implicated in CB1R-evoked pressor response.

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Medullary monoamines and NMDA-receptor regulation of cardiovascular responses during peripheral nociceptive stimuli

Cited by 16 publications

References 65 publications

Oral Administration of D-aspartate, but not of L-aspartate, Reduces Food Intake in Chicks

Oral Administration of D-aspartate, but not of L-aspartate, Reduces Food Intake in Chicks

C1 neurons in the rat rostral ventrolateral medulla differentially express vesicular monoamine transporter 2 in soma and axonal compartments

Cannabinoid receptor 1 signaling in cardiovascular regulating nuclei in the brainstem: A review

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