Innervation of the amygdaloid complex by catecholaminergic cell groups of the ventrolateral medulla

1993 ◽  
Vol 332 (1) ◽  
pp. 105-122 ◽  
Author(s):  
Stefanie Roder ◽  
John Ciriello
2008 ◽  
Vol 93 (4-5) ◽  
pp. 870-876 ◽  
Author(s):  
Kathleen S. Lynch ◽  
Bettina Diekamp ◽  
Gregory F. Ball

2005 ◽  
Vol 289 (4) ◽  
pp. R1107-R1115 ◽  
Author(s):  
Y. Ootsuka ◽  
R. M. McAllen

Anatomical studies indicate that sympathetic preganglionic neurons receive inputs from several brain stem cell groups, but the functional significance of this organization for vasomotor control is not known. We studied the roles of two brain stem premotor cell groups, the medullary raphé and the rostral ventrolateral medulla (RVLM), in determining the activity of sympathetic vasomotor supply to the tail of urethane-anesthetized, artificially ventilated rats. Chemical inactivation of either RVLM (bilaterally) or raphé cells by microinjecting glycine (120–200 nl, 0.5 M) or muscimol (40–160 nl, 2.1–8 mM) was sufficient to inhibit ongoing tail sympathetic fiber activity and to block its normally strong response to mild cooling via the trunk skin (reducing rectal temperature from 38.5 to 37°C). After bilateral RVLM inactivation, tail sympathetic fibers could still be excited by chemical stimulation of raphé neurons (l-glutamate, 120 nl, 50 mM), and strong cooling (rectal temperature ∼33°C) caused a low level of ongoing activity. After chemical inhibition of raphé neurons, however, neither strong cooling nor chemical stimulation of RVLM neurons activated tail sympathetic fibers. Electrical stimulation of the RVLM elicited tail sympathetic fiber volleys before and after local anesthesia of the raphé (150–500 nl of 5% tetracaine), demonstrating the existence of an independent descending excitatory pathway from the RVLM. The data show that neurons in both the medullary raphé and the RVLM, acting together, provide the essential drive to support vasomotor tone to the tail. Inputs from these two premotor nuclei interact in a mutually facilitatory manner to determine tonic, and cold-induced, tail sympathetic activity.


1993 ◽  
Vol 264 (5) ◽  
pp. R891-R902 ◽  
Author(s):  
D. Saphier

Responses of electrophysiologically identified tuberohypophysial paraventricular nucleus (PVN) neurons were examined following electrical stimulation of the A1, A2, A6, and C2 catecholaminergic cell groups and of the ventral noradrenergic ascending bundle (VNAB). A1, A2, and A6 stimulation evoked primarily excitatory responses from the cells recorded, but C2 stimulation yielded a greater proportion of inhibitory responses. VNAB stimulation at low frequencies (0.5/5 Hz) excited the majority of cells tested, but high-frequency (50 Hz) trains of stimulation reversed the direction of response to inhibition for approximately half of the cells excited by single-shock stimulation. Only 5-Hz stimulation had any affect on blood pressure, causing a slight increase. Treatment with alpha-methylparatyrosine, to inhibit (nor) epinephrine synthesis, reduced the proportion of excitatory responses and prevented the response reversals following 50-Hz VNAB stimulation. Treatment with 6-hydroxydopamine also reduced the proportion of cells excited by VNAB stimulation. Iontophoresis of either norepinephrine or the alpha 1-adrenoceptor agonist l-phenylephrine increased the activity of most cells tested whilst the alpha 1-antagonist ergotamine reduced the activity of most cells tested and prevented excitation elicited by VNAB stimulation. The alpha 2-agonist clonidine excited all cells tested. The beta-antagonist propranolol increased the activity of the majority of cells and prevented inhibitory responses following 50-Hz VNAB stimulation. The results confirm a role for brain stem projections in regulating PVN neuronal activity and demonstrate for the first time that the VNAB provides excitatory input to the PVN, primarily regulated by alpha 1-adrenoceptors. The effects of propranolol on spontaneous activity, and on the inhibitory responses following high-frequency VNAB stimulation, indicate the presence of an inhibitory counterbalancing beta-adrenoceptor mechanism.


2007 ◽  
Vol 1171 ◽  
pp. 93-103 ◽  
Author(s):  
Meredith M. LeBlanc ◽  
Christopher T. Goode ◽  
Elizabeth A. MacDougall-Shackleton ◽  
Donna L. Maney

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