scholarly journals Lateral Habenula Regulates Cardiovascular Autonomic Responses via the Serotonergic System in Rats

2021 ◽  
Vol 15 ◽  
Author(s):  
Tri Huu Doan ◽  
Yuma Sato ◽  
Masayuki Matsumoto ◽  
Tadachika Koganezawa
Keyword(s):  
Receptor Antagonist ◽  
Cardiovascular Responses ◽  
Sympathetic Nerves ◽  
Stressful Events ◽  
Serotonergic System ◽  
High Dose ◽  
Lateral Habenula ◽  
Autonomic Responses ◽  
Parasympathetic Nerves ◽  
Stimulation Of

The lateral habenula (LHb) plays essential roles in behavioral responses to stressful events. Stress is tightly linked to autonomic responses such as cardiovascular responses, yet how the LHb regulates these responses is not well understood. To address this issue, we electrically stimulated the LHb in rats, measured its effects on heart rate (HR) and mean arterial pressure (MAP), and investigated the neural circuits that mediate these LHb-induced cardiovascular responses via the autonomic nervous system. We observed that stimulation of the LHb induced bradycardia and pressor responses, whereas stimulation of the adjacent areas changed neither the HR nor the MAP. Bilateral vagotomy and administration of a muscarinic receptor antagonist suppressed the LHb stimulation effect on the HR but not on the MAP, whereas administration of a β-adrenoceptor antagonist partly attenuated the effect on the MAP but not on the HR. Thus, the LHb-induced cardiovascular responses of the HR and the MAP were likely caused by activations of the cardiac parasympathetic nerves and the cardiovascular sympathetic nerves, respectively. Furthermore, administration of a non-selective 5-HT receptor antagonist significantly attenuated the LHb stimulation effects on both the MAP and the HR. A 5-HT2 receptor antagonist also attenuated the LHb stimulation effects. A low dose of a 5-HT1A receptor antagonist enhanced the LHb stimulation effects, but a high dose of the drug attenuated them. 5-HT1B and 5-HT1D receptor antagonists as well as a 5-HT7 receptor antagonist did not affect the LHb stimulation effects. Taken together, our findings suggest that the LHb regulates autonomic cardiovascular responses at least partly through the serotonergic system, particularly via the 5-HT1A and 5-HT2 receptors.

Hepatic glucose balance in response to direct stimulation of sympathetic nerves in the intact liver of cats

1978 ◽  
Vol 56 (6) ◽  
pp. 1022-1028 ◽  
Author(s):  
W. Wayne Lautt ◽  
Chong Wong
Keyword(s):  
Sympathetic Nerves ◽  
Direct Stimulation ◽  
Blood Flows ◽  
Parasympathetic Nerves ◽  
Hepatic Glucose ◽  
Simultaneous Activation ◽  
Glucose Output ◽  
Hepatic Nerves ◽  
Mixed Nerve ◽  
Stimulation Of

Changes in hepatic glucose balance in response to direct stimulation of the hepatic nerves were measured in cats. Simultaneous measurements were made of glucose concentrations entering and leaving the intact liver; this, combined with measured blood flows, allows calculation of hepatic glucose balance. Stimulation of the hepatic sympathetic nerves (8 Hz, 15 V, 1 ms) produced a rapid increase in hepatic glucose output that was statistically significant after 1 min and reached a peak 3–5 min after onset of stimulation, after which time the output declined somewhat. The half time for deactivation of the response was 1.8–2 min. Variability in the responses was largely accounted for by the variable control base lines measured immediately prior to stimulation. Those animals showing the highest basal output showed the least increase in output in response to the nerves. The response to stimulation of the mixed nerve trunk in the presence and absence of atropine (1 mg/kg, intraportal) was similar. Simultaneous activation of hepatic sympathetic and parasympathetic nerves therefore produces a purely sympathetic type of effect on net glucose balance across the liver. It was also shown that changes in net splanchnic output or simply in arterial – hepatic venous glucose differences are an adequate reflection of liver glucose balance under the currently tested responses.

Visceral nociception: peripheral and central aspects of visceral nociceptive systems

1985 ◽  
Vol 308 (1136) ◽  
pp. 325-337 ◽  
Keyword(s):  
Central Nervous System ◽  
Intestinal Tract ◽  
Sympathetic Nerves ◽  
Noxious Stimulation ◽  
Visceral Sensation ◽  
Parasympathetic Nerves ◽  
The Central Nervous System ◽  
Specific Receptors ◽  
Gastro Intestinal Tract ◽  
Stimulation Of

Discomfort and pain are the sensations most commonly evoked from viscera. Most nociceptive signals that originate from visceral organs reach the central nervous system (c.n.s.) via afferent fibres in sympathetic nerves, whereas parasympathetic nerves contain mainly those visceral afferent fibres concerned with the non-sensory aspects of visceral afferent function. Noxious stimulation of viscera activates a variety of specific and non-specific receptors, the vast majority of which are connected to unmyelinated afferent fibres. Studies on the mechanisms of visceral sensation can thus provide information on the more general functions of unmyelinated afferent fibres. Specific visceral nociceptors have been found in the heart, lungs, testes and biliary system, whereas noxious stimulation of the gastro-intestinal tract appears to be detected mainly by non-specific visceral receptors that use an intensity-encoding mechanism.

scholarly journals Inhibition of Nitric Oxide Synthase Attenuates the Cerebral Blood Flow Response to Stimulation of Postganglionic Parasympathetic Nerves in the Rat

1993 ◽  
Vol 13 (6) ◽  
pp. 993-997 ◽  
Author(s):  
Yoko Morita-Tsuzuki ◽  
Jan Erik Hardebo ◽  
Eliete Bouskela
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Systemic Blood Pressure ◽  
High Dose ◽  
Parasympathetic Nerve ◽  
Doppler Flowmetry ◽  
Cortical Blood Flow ◽  
Parasympathetic Nerves ◽  
Flow Response ◽  
Stimulation Of

Stimulation of cerebrovascular parasympathetic nerves markedly increases cortical blood flow. Nitric oxide (NO) or a NO-containing compound is present in these nerves and may therefore, upon release, be partly responsible for the flow increase. In addition, transmitters released from the nerves may cause synthesis and release of this compound from the endothelium. The contribution of NO synthesis to the cortical blood flow (CoBF) increase during parasympathetic stimulation was elucidated in rat by laser–Doppler flowmetry. Thirty-minute exposure to circulating Nω-nitro-l-arginine methyl ester (l-NAME) 50 mg kg−1 eliminated most of the response (from 104 to 8% increase), whereas 10-min exposure to this dose or 30-min exposure to 5 mg kg−1 caused a less marked reduction. The reducing effect was particularly evident after elimination of the systemic blood pressure increase caused by l-NAME (only 3% increase after the high dose). Infusion of l-arginine restored the flow response. Resting CoBF was not substantially affected by blockade of NO formation. Thus, release of an NO-containing compound constitutes a major component of the increase in CoBF caused by parasympathetic nerve stimulation but does not seem to contribute to cortical flow regulation during resting conditions.

GABAergic effects on the depressor responses elicited by stimulation of central nucleus of the amygdala

1999 ◽  
Vol 276 (1) ◽  
pp. H242-H247 ◽  
Author(s):  
John Ciriello ◽  
Stefanie Roder
Keyword(s):  
Arterial Pressure ◽  
Receptor Antagonist ◽  
Wistar Rats ◽  
Cardiovascular Responses ◽  
Systemic Arterial Pressure ◽  
The Other ◽  
Central Nucleus ◽  
Male Wistar Rats ◽  
The Mean ◽  
Stimulation Of

GABAergic inputs have been demonstrated in the central nucleus of the amygdala (ACe). However, the contribution of these inhibitory inputs to the cardiovascular responses elicited from the ACe is not known. Experiments were done in chloralose-anesthetized, paralyzed, and artificially ventilated male Wistar rats to investigate the effects of microinjections of GABA, the selective GABAA-receptor antagonist bicuculline, or the GABAB-receptor antagonist phaclofen, in the ACe on the mean arterial pressure (MAP) and heart rate (HR) responses elicited byl-glutamate (Glu) stimulation of the ACe. Microinjections of Glu in the ACe elicited decreases in MAP (−13.7 ± 1.6 mmHg) and HR (−5.3 ± 1.9 beats/min). The MAP and HR responses elicited by Glu stimulation of the ACe were significantly reduced (89%) by the prior microinjection of GABA in the same ACe site. In addition, at some sites in the ACe at which microinjection of Glu did not elicit depressor responses, Glu injections in the presence of phaclofen elicited decreases in MAP (−9.5 ± 1.0 mmHg) and variable changes in HR. On the other hand, the magnitude of the depressor responses elicited during stimulation of the ACe site in the presence of bicuculline was significantly attenuated (60%), whereas phaclofen had no effect on the magnitude of the depressor responses elicited by Glu stimulation of the ACe. These data suggest that GABAergic mechanisms in the ACe alter the excitability of ACe neurons involved in mediating changes in systemic arterial pressure and HR.

scholarly journals Cardiovascular responses to electrical stimulation of sympathetic nerves in the pithed mouse

2008 ◽  
Vol 140 (1-2) ◽  
pp. 49-52
Author(s):  
Hamzeh H. Elayan ◽  
Ping Sun ◽  
Milos Milic ◽  
Fujun Liu ◽  
Xuping Bao ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Cardiovascular Responses ◽  
Sympathetic Nerves ◽  
Stimulation Of

Synergistic nonuniform shortening of atrial refractory period induced by autonomic stimulation

1991 ◽  
Vol 261 (6) ◽  
pp. H1988-H1993 ◽  
Author(s):  
M. Takei ◽  
Y. Furukawa ◽  
M. Narita ◽  
L. M. Ren ◽  
Y. Karasawa ◽  
...  
Keyword(s):  
Right Atrium ◽  
Refractory Period ◽  
Neural Control ◽  
Sympathetic Nerves ◽  
Autonomic Nerve ◽  
Parasympathetic Nerves ◽  
Nodal Region ◽  
The Individual ◽  
The Right ◽  
Stimulation Of

We investigated the nonuniform effects of autonomic nerve stimulation of the effective refractory period (ERP) of the right atrium in the anesthetized dog. Stimulation of the discrete intracardiac sympathetic nerves to the sinoatrial (SA) nodal region uniformly shortened ERPs at three sites in the right atrium after administration of atropine. Right ansa subclavia (RS) stimulation similarly shortened ERPs in the absence of atropine. Stimulation of the discrete intracardiac parasympathetic nerves to the SA nodal region (SAP stimulation) shortened ERPs of the right atrium in a nonuniform manner. Simultaneous RS and SAP stimulation additively shortened ERPs at each site and decreased sinus rate much more than SAP stimulation alone. Shortening of ERP induced by SAP stimulation was greater than that induced by RS stimulation at similar absolute changes in heart rate. These results suggest that simultaneous activation of sympathetic and parasympathetic nerves nonuniformly shortens the ERP in the right atrium as the algebraic sum of the individual responses to each stimulation. However, parasympathetics exert the principal neural control over atrial ERP.

Peripheral muscarinic control of norepinephrine release in the cardiovascular system

1980 ◽  
Vol 239 (6) ◽  
pp. H713-H720 ◽  
Author(s):  
E. Muscholl
Keyword(s):  
Physiological Role ◽  
Sympathetic Nerves ◽  
Adrenergic Nerve ◽  
Sequence Of Events ◽  
Adrenergic Response ◽  
Adrenergic Nerve Terminals ◽  
Muscarinic Cholinergic ◽  
Related Compounds ◽  
Stimulation Of

Activation of muscarinic cholinergic receptors located at the terminal adrenergic nerve fiber inhibits the process of exocytotic norepinephrine (NE) release. This neuromodulatory effect of acetylcholine and related compounds has been discovered as a pharmacological phenomenon. Subsequently, evidence for a physiological role of the presynaptic muscarinic inhibition was obtained on organs known to be innervated by the autonomic ground plexus (Hillarp, Acta. Physiol. Scand. 46, Suppl. 157: 1-68, 1959) in which terminal adrenergic and cholinergic axons run side by side. Thus, in the heart electrical vagal stimulation inhibits the release of NE evoked by stimulation of sympathetic nerves, and this is reflected by a corresponding decrease in the postsynaptic adrenergic response. On the other hand, muscarinic antagonists such as atropine enhance the NE release evoked by field stimulation of tissues innervated by the autonomic ground plexus. The presynaptic muscarine receptor of adrenergic nerve terminals probably restricts the influx of calcium ions that triggers the release of NE. However, the sequence of events between recognition of the muscarinic compound by the receptor and the process of exocytosis still remains to be clarified.

Role of paraventricular and supraoptic nuclei in central cardiovascular regulation in the cat

1980 ◽  
Vol 239 (1) ◽  
pp. R137-R142 ◽  
Author(s):  
J. Ciriello ◽  
F. R. Calaresu
Keyword(s):  
Heart Rate ◽  
Cardiovascular Responses ◽  
Inhibitory Influence ◽  
Sympathetic Nervous Systems ◽  
Aortic Depressor Nerve ◽  
Bilateral Lesions ◽  
Alpha Chloralose ◽  
Supraoptic Nuclei ◽  
Stimulation Of

To investigate the role of the paraventricular (PAH) and supraoptic (SON) nuclei in regulation of the cardiovascular system experiments were done in 26 cats anesthetized with alpha-chloralose, paralyzed, and artificially ventilated. Electrical stimulation of histologically verified sites in the region of the PAH and SON elicited increases in arterial pressure in bilaterally vagotomized animals and increases in heart rate both in spinal (C2) animals and in animals bilaterally vagotomized, In addition, stimulation of either the PAH or SON inhibited the reflex vagal bradycardia elicited by stimulation of the carotid sinus nerve (CSN) and bilateral lesions of these areas increased the magnitude of the response. On the other hand, stimulation and lesions of these hypothalamic regions did not alter the magnitude of the cardiovascular responses to stimulation of the aortic depressor nerve. These results demonstrate that stimulation of the PAH and SON elicit cardiovascular responses due to reciprocal changes in activity of the parasympathetic and sympathetic nervous systems and that these structures maintain a tonic inhibitory influence on the heart rate component of the CSN reflex.

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