Taste Responses of Neurons in the Hamster Solitary Nucleus Are Modulated by the Central Nucleus of the Amygdala

2002 ◽  
Vol 88 (6) ◽  
pp. 2979-2992 ◽  
Author(s):  
Cheng-Shu Li ◽  
Young K. Cho ◽  
David V. Smith
Keyword(s):  
Electrical Stimulation ◽  
Signal To Noise Ratio ◽  
Central Nucleus ◽  
Homocysteic Acid ◽  
Excitatory Response ◽  
Afferent Information ◽  
Parabrachial Nuclei ◽  
Evoked Activity ◽  
Stimulation Of

Previous studies have shown a modulatory influence of forebrain gustatory areas, such as the gustatory cortex and lateral hypothalamus, on the activity of taste-responsive cells in the nucleus of the solitary tract (NST). The central nucleus of the amygdala (CeA), which receives gustatory afferent information, also exerts descending control over taste neurons in the parabrachial nuclei (PbN) of the pons. The present studies were designed to investigate the role of descending amgydaloid projections to the NST in the modulation of gustatory activity. Extracellular action potentials were recorded from 109 taste-responsive cells in the NST of urethan-anesthetized hamsters and analyzed for a change in excitability following electrical and chemical stimulation of the CeA. Electrical stimulation of the CeA orthodromically modulated 36 of 109 (33.0%) taste-responsive NST cells. An excitatory response was observed in 33 (30.28%) cells. An initial decrease in excitability to electrical stimulation of the CeA, suggestive of postsynaptic inhibition, was observed in three (2.75%) NST taste cells. NST cells modulated by the CeA were significantly less responsive to taste stimuli than cells that were not. Many of these cells were under the modulatory influence of the contralateral CeA (28/36 = 77.8%) as well as the ipsilateral (22/36 = 61.1%); 14 (38.9%) were excited bilaterally. Latencies for excitation were longer after ipsilateral than after contralateral CeA stimulation. Microinjection of dl-homocysteic acid (DLH) into the CeA mimicked the effect of electrical stimulation on each of the nine cells tested: DLH excited eight and inhibited one of these electrically activated NST cells. Application of subthreshold electrical stimulation to the CeA during taste trials increased the taste responses of every CeA-responsive NST cell ( n = 7) tested with this protocol. These effects would enhance taste discriminability by increasing the signal-to-noise ratio of taste-evoked activity.

Modulation of Parabrachial Taste Neurons by Electrical and Chemical Stimulation of the Lateral Hypothalamus and Amygdala

2005 ◽  
Vol 93 (3) ◽  
pp. 1183-1196 ◽  
Author(s):  
Cheng-Shu Li ◽  
Young K. Cho ◽  
David V. Smith
Keyword(s):  
Citric Acid ◽  
Lateral Hypothalamus ◽  
Ingestive Behavior ◽  
Central Nucleus ◽  
Homocysteic Acid ◽  
Quinine Hydrochloride ◽  
Neural Substrate ◽  
Parabrachial Nuclei ◽  
Gustatory Neurons ◽  
Stimulation Of

The lateral hypothalamus (LH) and the central nucleus of the amygdala (CeA) exert an influence on ingestive behavior and are reciprocally connected to gustatory and viscerosensory areas, including the nucleus of the solitary tract (NST) and the parabrachial nuclei (PbN). We investigated the effects of LH and CeA stimulation on the activity of 101 taste-responsive neurons in the hamster PbN. Eighty three of these neurons were antidromically activated by stimulation of these sites; 57 were antidromically driven by both. Of these 83 neurons, 21 were also orthodromically activated—8 by the CeA and 3 by the LH. Additional neurons were excited ( n = 5) or inhibited ( n = 8) by these forebrain nuclei but not antidromically activated. Taste stimuli were: 0.032 M sucrose, 0.032 M sodium chloride (NaCl), 0.032 M quinine hydrochloride (QHCl), and 0.0032 M citric acid. Among the 34 orthodromically activated neurons, more sucrose-best neurons were excited than inhibited, whereas the opposite occurred for citric-acid- and QHCl-best cells. Neurons inhibited by the forebrain responded significantly more strongly to citric acid and QHCl than cells excited by these sites. The effects of electrical stimulation were mimicked by microinjection of dl-homocysteic acid, indicating that cells at these forebrain sites were responsible for these effects. These data demonstrate that many individual PbN gustatory neurons project to both the LH and CeA and that these areas modulate the gustatory activity of a subset of PbN neurons. This neural substrate is likely involved in the modulation of taste activity by physiological and experiential factors.

Protein kinase Cε and the antiadrenergic action of adenosine in rat ventricular myocytes

2004 ◽  
Vol 287 (4) ◽  
pp. H1721-H1729 ◽  
Author(s):  
Koji Miyazaki ◽  
Satoshi Komatsu ◽  
Mitsuo Ikebe ◽  
Richard A. Fenton ◽  
James G. Dobson
Keyword(s):  
Electrical Stimulation ◽  
Protein Kinase ◽  
Ventricular Myocytes ◽  
Adrenergic Agonist ◽  
Inhibitory Peptide ◽  
Rat Ventricular Myocytes ◽  
Adult Rat ◽  
Tubular System ◽  
Stimulation Of

Adenosine-induced antiadrenergic effects in the heart are mediated by adenosine A1 receptors (A1R). The role of PKCε in the antiadrenergic action of adenosine was explored with adult rat ventricular myocytes in which PKCε was overexpressed. Myocytes were transfected with a pEGFP-N1 vector in the presence or absence of a PKCε construct and compared with normal myocytes. The extent of myocyte shortening elicited by electrical stimulation of quiescent normal and transfected myocytes was recorded with video imaging. PKCε was found localized primarily in transverse tubules. The A1R agonist chlorocyclopentyladenosine (CCPA) at 1 μM rendered an enhanced localization of PKCε in the t-tubular system. The β-adrenergic agonist isoproterenol (Iso; 0.4 μM) elicited a 29–36% increase in myocyte shortening in all three groups. Although CCPA significantly reduced the Iso-produced increase in shortening in all three groups, the reduction caused by CCPA was greatest with PKCε overexpression. The CCPA reduction of the Iso-elicited shortening was eliminated in the presence of a PKCε inhibitory peptide. These results suggest that the translocation of PKCε to the t-tubular system plays an important role in A1R-mediated antiadrenergic actions in the heart.

Parabrachial units responding to stimulation of buffer nerves and forebrain in the cat

1983 ◽  
Vol 245 (6) ◽  
pp. R811-R819 ◽  
Author(s):  
D. F. Cechetto ◽  
F. R. Calaresu
Keyword(s):  
Nerve Stimulation ◽  
Carotid Sinus ◽  
Respiratory Control ◽  
Firing Frequency ◽  
Central Nucleus ◽  
Paraventricular Nuclei ◽  
Control Signals ◽  
Parabrachial Nuclei ◽  
Excitatory Responses ◽  
Stimulation Of

Spontaneously firing units in the region of parabrachial nuclei (PB) and Kolliker-Fuse nuclei (KF) of 19 chloralose-anesthetized cats were monitored for changes in firing frequency during electrical stimulation of carotid sinus (CSN) and aortic depressor (ADN) nerves, of central nucleus of the amygdala (ACE), and of paraventricular nuclei of the hypothalamus (PVH). In the ipsilateral PB 64 of 189 and in the contralateral PB 9 of 103 units responded to CSN stimulation; 18 of 185 ipsilaterally and 7 of 97 contralaterally responded to ADN stimulation. Responses were primarily excitatory, and units were located primarily in the ventrolateral portion of the PB. Only 9 of 267 units responded to stimulation of both CSN and ADN. Stimulation of the ACE and PVH antidromically activated 9 and 7 units, respectively, in PB and approximately half of these also responded to buffer nerve stimulation. In the ipsilateral PB 56 of 207 and in the contralateral PB 11 of 103 units responded orthodromically to ACE stimulation, and 23 of 177 ipsilaterally and 2 of 103 contralaterally responded orthodromically to PVH stimulation with primarily excitatory responses and were located primarily in the ventrolateral portion of the PB and KF. Of these units approximately half also responded to buffer nerve stimulation. These results suggest an important role for PB-KF in mediating ascending and descending cardiovascular and respiratory control signals.

Norepinephrine uptake as an indicator of cardiac reinnervation in dogs

1978 ◽  
Vol 235 (3) ◽  
pp. H289-H294 ◽  
Author(s):  
M. P. Kaye ◽  
G. M. Tyce
Keyword(s):  
Electrical Stimulation ◽  
Sympathetic Nerves ◽  
Progressive Increase ◽  
Canine Heart ◽  
Storage Mechanism ◽  
Specific Membrane ◽  
Heart Uptake ◽  
Membrane Mechanism ◽  
Stimulation Of

To study the possible role of uptake of [3H]norepinephrine ([3H]NE) as an indicator of sympathetic reinnervation of the surgically denervated canine heart, uptake was determined from multiple areas of hearts at various stages of reinnervation (1--6 mo), and these data were correlated with myocardial catecholamine content and functional response of the heart to electrical stimulation of the sympathetic nerves. Our experiments confirm that NE content correlates poorly with the degree of reinnervation of the previously denervated canine heart. There is, however, a progressive increase of [3H]NE uptake from 1 mo to 6 mo, at which time uptake has returned to approximately 57% of control values in the left atrium. The development of the storage mechanism lags far behind the specific-membrane mechanism for uptake in the reinnervating surgically denervated canine heart.

scholarly journals Responses of Neurons in the Insular Cortex to Gustatory, Visceral, and Nociceptive Stimuli in Rats

1998 ◽  
Vol 79 (5) ◽  
pp. 2535-2545 ◽  
Author(s):  
Takamitsu Hanamori ◽  
Takato Kunitake ◽  
Kazuo Kato ◽  
Hiroshi Kannan
Keyword(s):  
Electrical Stimulation ◽  
Intravenous Injection ◽  
Anterior Commissure ◽  
Insular Cortex ◽  
Inhibitory Response ◽  
Inhibitory Neurons ◽  
Excitatory Response ◽  
Tail Pinch ◽  
Posterior Tongue ◽  
Stimulation Of

Hanamori, Takamitsu, Takato Kunitake, Kazuo Kato, and Hiroshi Kannan. Responses of neurons in the insular cortex to gustatory, visceral, and nociceptive stimuli in rats. J. Neurophysiol. 79: 2535–2545, 1998. Extracellular unit responses to baroreceptor and chemoreceptor stimulation, gustatory stimulation of the posterior tongue, electrical stimulation of the superior laryngeal (SL) nerve, and tail pinch were recorded from the insular cortex of anesthetized and paralyzed rats. Forty-three neurons identified responded to stimulation by at least one of the stimuli used in the present study. Of the 43 neurons, 33 responded to tail pinch, and the remaining 10 had no response; 18 showed an excitatory response, and 15 showed an inhibitory response. Of the 43 neurons, 35 responded to electrical stimulation of the SL nerve; 27 showed an excitatory response, and 8 showed an inhibitory response. Of the 20 neurons that responded to baroreceptor stimulation by an intravenous injection of methoxamine hydrochloride (Mex), 11 were excitatory and 9 were inhibitory. Twenty-seven neurons were responsive to an intravenous injection of sodium nitroprusside (SNP); 10 were excitatory and 17 were inhibitory. Ten neurons were excited and 16 neurons were inhibited by arterial chemoreceptor stimulation by an intravenous injection of sodium cyanide (NaCN). Twenty-six neurons were responsive to at least one of the gustatory stimuli (1.0 M NaCl, 30 mM HCl, 30 mM quinine HCl, and 1.0 M sucrose): four to six excitatory neurons and three to nine inhibitory neurons for each stimulus. A large number of the neurons (42/43) received convergent inputs from more than one stimulus among the nine stimuli used in the present study. Most neurons (38/43) were responsive to two or more stimulus groups when the natural stimuli used in the present study are grouped into three, gustatory, visceral, and nociceptive stimuli. The neurons recorded were located in the insular cortex between 2.8 mm anterior and 1.1 mm posterior to the anterior edge of the joining of the anterior commissure (AC); the mean location was 1.0 mm ( n = 43) anterior to the AC. This indicates that most of the neurons identified in the present study were located in the region posterior to the taste area and anterior to the visceral area in the insular cortex. These results indicate that the insular cortex neurons distributing between the taste area and the visceral area receive convergent inputs from baroreceptor, chemoreceptor, gustatory, and nociceptive organs and may have roles in taste aversion or in regulation of visceral responses.

Stimulation of the caudal ventrolateral medulla decreases total lung resistance in dogs

1987 ◽  
Vol 63 (3) ◽  
pp. 912-917 ◽  
Author(s):  
J. C. Connelly ◽  
L. W. McCallister ◽  
M. P. Kaufman
Keyword(s):  
Electrical Stimulation ◽  
Nucleus Ambiguus ◽  
Ventrolateral Medulla ◽  
Adrenergic Blockade ◽  
Homocysteic Acid ◽  
Caudal Ventrolateral Medulla ◽  
Airway Caliber ◽  
Lung Resistance ◽  
Total Lung Resistance ◽  
Stimulation Of

Although the role played by the caudal ventrolateral medulla in the regulation of the cardiovascular system has been extensively investigated, little is known about the role played by this area in the regulation of airway caliber. Therefore, in alpha-chloralose-anesthetized dogs, we used both electrical and chemical means to stimulate the caudal ventrolateral medulla while we monitored changes in total lung resistance breath by breath. We found that electrical stimulation (25 microA) of 26 sites in this area significantly decreased total lung resistance from 7.1 +/- 0.4 to 5.7 +/- 0.3 cmH2O.1'1.s (P less than 0.001). The bronchodilation evoked by electrical stimulation was unaffected by beta-adrenergic blockade but was abolished by cholinergic blockade. In addition, chemical stimulation of seven sites in the caudal ventrolateral medulla with microinjections of DL-homocysteic acid (0.2 M; 66 nl), which stimulates cell bodies but not fibers of passage, also decreased total lung resistance from 8.3 +/- 1.1 to 6.5 +/- 0.8 cmH2O.l'1.s (P less than 0.01). In contrast, microinjections of DL-homocysteic acid into the nucleus ambiguus (n = 6) increased total lung resistance from 7.5 +/- 0.5 to 9.2 +/- 0.4 cmH2O.l'1.s (P less than 0.05). We conclude that the caudal ventrolateral medulla contains a pool of cell bodies whose excitation causes bronchodilation by withdrawing cholinergic input to airway smooth muscle.

Efferent-mediated protection from acoustic overexposure: relation to slow effects of olivocochlear stimulation

1995 ◽  
Vol 73 (2) ◽  
pp. 506-514 ◽  
Author(s):  
E. R. Reiter ◽  
M. C. Liberman
Keyword(s):  
Electrical Stimulation ◽  
Inner Ear ◽  
Guinea Pigs ◽  
Threshold Shift ◽  
Exposure Condition ◽  
Protective Effects ◽  
Acoustic Overstimulation ◽  
Different Levels ◽  
Stimulation Of

1. The present study attempts to resolve discrepancies in the reported role of olivocochlear (OC) efferent activation in protecting the inner ear from acoustic overstimulation: in previous studies, activating the OC system in guinea pigs reduced the threshold shift caused by 1 min monaural exposure to a 10-kHz tone; whereas unilateral OC activation in cats had no effect on threshold shifts following binaural exposure to a 10 min 6-kHz tone. 2. In this study, anesthetized and curarized guinea pigs were exposed either monaurally or binaurally to tones of different duration (1-5 min), frequency (6 to 10 kHz) and intensity (105-118 dB SPL). For each exposure condition, threshold shifts were compared among ears with different levels of OC activation: in some cases, the OC bundle (OCB) was electrically stimulated during (and/or before) the acoustic overexposure; in others, the OCB was cut before the exposure; in control cases, the OCB was neither cut nor electrically stimulated. 3. Electrical stimulation of the OCB delivered simultaneously with acoustic overstimulation produced significant reductions in threshold shift only for acoustic exposures at higher frequencies (8 and 10 kHz) and shorter durations (1 and 2 min). The protective effects on 1-min exposures could be extinguished by prior stimulation of the OCB, i.e., if the OC stimulation was turned on 4 min before the acoustic overexposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of periaqueductal gray in the pressor response produced by central injections of angiotensin II

1993 ◽  
Vol 265 (5) ◽  
pp. R1052-R1059
Author(s):  
L. R. Portis ◽  
S. J. Lewis ◽  
M. J. Brody
Keyword(s):  
Electrical Stimulation ◽  
Angiotensin Ii ◽  
Fluorescent Dyes ◽  
Pressor Response ◽  
Periaqueductal Gray ◽  
Ang Ii ◽  
Hemodynamic Responses ◽  
Anesthetized Rats ◽  
Stimulation Of

The present studies were undertaken to determine the role of rostral periaqueductal gray (PAG) in mediating the pressor effect produced by intracerebroventricular (icv) injection of angiotensin II (ANG II, 200 ng). Two functionally and anatomically distinct sites were identified in rostral PAG: a dorsomedial site involved in the hemodynamic responses produced by electrical stimulation of the anteroventral third ventricle (AV3V) region and a ventromedial site required for the pressor response elicited by icv administration of ANG II. In Saffan-anesthetized rats, injection of lidocaine (LIDO, 4%) in dorsomedial PAG, but not in ventromedial PAG, significantly attenuated the decrease in hindquarter resistance (HQR) produced by electrical stimulation of the AV3V region, and the poststimulatory increase in mean arterial pressure (MAP) and HQR. The injection of LIDO in ventromedial PAG had no effect on the hemodynamic responses produced by electrical stimulation of the AV3V region in anesthetized rats but significantly attenuated the pressor response produced by icv administration of ANG II in conscious rats. The hypothesis that these two sites receive separate projections was addressed by microinjecting two retrogradely transported fluorescent dyes, Fluoro-Gold and Fast Blue. The anatomic findings suggest that separation of the pathways activated by electrical and chemical stimulation of the AV3V region occurs at the level of rostral PAG.

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