Psychomotor behaviour and cardiovascular patterns during stimulation of the amygdala

Stock, Günter; Schlör, K. H.; Heidt, Hartmut; Buss, J

doi:10.1007/bf00581581

Cited by 85 publications

(31 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…A possible role for drinking behavior is discussed for the septal area, 31 32 and limbic structures may be implicated in cardiovascular adaptations to emotional stimuli. 33 Moreover, the development of DOCA-salt hypertension was recently reported to be prevented in rats with lesions of the lateral septal area. 34 Thus, these and our results suggest that brain septum could take part in blood pressure regulation.…”

Section: Discussionmentioning

confidence: 99%

Influence of captopril treatment on angiotensin II receptors and angiotensinogen in the brain of spontaneously hypertensive rats.

Schelling¹,

Felix²

1983

Hypertension

View full text Add to dashboard Cite

SUMMARY The brain renin-angiotensin system (RAS) has been suggested as contributing to the pathogenesis of spontaneous hypertension in rats. Brain angiotensinogen-and angiotensin II (AII)-sensitive neurons were therefore investigated in stroke-prone spontaneously hypertensive rats (SHRsp) and in Wistar-Kyoto (WKY) rats with and without treatment by captopril (CAP). Angiotensinogen was decreased in the anterior hypothalamus but increased in the cortex, the hippocampus, and cerebellum of SHR-sp. There were no differences between SHR-sp and WKY rats concerning the angiotensinogen content of posterior hypothalamus, brain stem, and septum. The sensitivity of the septal neurons to microiontophoretically applied AH was elevated, however, in SHR-sp as compared to WKY rats with regard to threshold and maximal response for All-evoked neuronal discharges. The excitation characteristics did not change with the age of animals in both WKY rats and SHR-sp. The treatment of SHR-sp with CAP (50 mg/kg/day per os) starting in weanlings kept animals normotensive and reduced the high sensitivity of septal neurons to AH. Simultaneously angiotensinogen content was increased in the anterior hypothalamus and suppressed in the hippocampus. The same treatment of WKY rats reduced blood pressure somewhat and increased the angiotensinogen content in the anterior hypothalamus without affecting the neuronal sensitivity to AH. Thus, malfunction of the brain RAS may participate in the hypertension of SHR-sp, since converting enzyme blockade with CAP inhibited the blood pressure rise, augmented the angiotensinogen content of the anterior hypothalamus, and decreased the sensitivity of AH receptors in the brains of these rats. (Hypertension 5: 935-942, 1983) KEY WORDS • brain renin angiotensin system • chronic captopril treatment • microiontophoresis • septal area • stroke-prone spontaneously hypertensive rats • Wistar-Kyoto rats T HE spontaneously hypertensive rat (SHR) 1 has been used as a model for human essential hypertension, and several hypotheses have been formulated about the pathogenesis of the high blood pressure in these rats. Recently, Ganten and colleagues 2 have applied the term "peptidergic stimulation syndrome" to the observation that rats of the stroke-prone substrain of SHR (SHR-sp) 3 demonstrate an exaggerated response, e.g., of blood pressure, to several peptide hormones after their intracerebral application. Much interest was addressed to the brain renin-angiotensin system (RAS) in this respect, since all components needed for a functional system, includ-

show abstract

Section: Discussionmentioning

confidence: 99%

Influence of captopril treatment on angiotensin II receptors and angiotensinogen in the brain of spontaneously hypertensive rats.

Schelling¹,

Felix²

1983

Hypertension

View full text Add to dashboard Cite

show abstract

“…Although reciprocal connexions from the n.t.s. to the central nucleus have been demonstrated anatomically (Ricardo & Koh, 1978;Ottersen, 1981;our (Bonvallet & Gary Bobo, 1972;Heinemann, Stock & Schaefer, 1973;Hilton & Zbrozyna, 1963;Stock et al 1978) whilst both excitation and inhibition of n.t.s. neurones has been observed in the cat following amygdala stimulation (Jordan, In addition, in the present study we have shown that a small group of neurones having properties consistent with a cardioinhibitory function were also excited by central nucleus stimulation.…”

Section: Discussionmentioning

confidence: 99%

“…Our findings, however, are consistent with related anatomical data showing a direct pathway from the central nucleus to the n.t.s. in cats (Hopkins & Holstege, 1978), monkeys (Hopkins, McLean & Takeuchi, 1981;Price & Amaral, 1981) and rabbits (Schwaber et al 1980;Higgins & Schwaber, 1981;Schwaber et al 1982) and with an extensive physiological literature demonstrating cardiovascular effects elicited from the central nucleus of the cat (Hilton & Zbrozyna, 1963;Stock et al 1978;Timms, 1981) and rabbit Applegate, Kapp, Underwood & McNall, 1983). The strength of the excitatory response elicited in n.t.s.…”

Section: Discussionmentioning

confidence: 99%

“…The central nucleus has been considered to have a role in the generation of affective behaviour and, in particular, the cardiovascular and other visceral components of such behaviour (Hilton & Zbrozyna, 1963;Stock, Schlor, Heidt & Buss, 1978;Timms, 1981). Furthermore, in the anaesthetized rabbit electrical stimulation of the central nucleus produces a profound, short latency, vagally mediated bradyeardia (Fredericks, Moore, Metcalf, Schwaber & Schneiderman, 1974;Kapp, Gallagher, Underwood, McNall & Whitehorn, 1982).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Amygdaloid influences on brain‐stem neurones in the rabbit.

Cox¹,

Jordan²,

Moruzzi³

et al. 1986

The Journal of Physiology

View full text Add to dashboard Cite

SUMMARY1. Electrical stimulation of the central nucleus of the amygdala in the urethane or a-chloralose anaesthetized rabbit evokes a bradyeardia with a rapid onset and a concomitant fall in arterial blood pressure.2. Extracellular neuronal activity was recorded in the ipsilateral nucleus tractus solitarius and dorsal vagal nucleus whilst stimulating the ipsilateral central nucleus of the amygdala, the aortic and vagus nerves.3. A total of 213 neurones were activated by stimulation of at least one of these inputs. 93 of these neurones received a marked excitatory input from the central nucleus with a wide range of latencies (2-100 ms). 50 of these cells also received inputs from either the aortic or vagus nerves, or both.4. The activity of42 vagal preganglionic neurones was recorded in the dorsal vagal nucleus of which 22 had properties typical of cardioinhibitory neurones. 9 of these vagal motoneurones received inputs from the central nucleus with latencies between 2 and 100 ms. Of these, 5 had physiological properties indicating they were cardioinhibitory neurones.5. We conclude that neurones in the nucleus tractus solitarius and dorsal vagal nucleus can be influenced by descending inputs arising from the central nucleus of the amygdala. Some of these neurones are also likely to be influenced by afferents innervating the thoracic viscera and arterial baroreceptors. The implications of these observations on the role of forebrain-brain-stem interactions in cardiovascular control are discussed.

show abstract

“…Electrical or chemical stimulation of the ACE mimics stress-like responses such as increases in arterial blood pressure, heart rate and respiratory rate [39,40], and it induces ulcer formation [41]. Furthermore, lesions of the ACE attenuate or abolish the autonomic or behavioral changes produced by a variety of stresses [4,5].…”

Section: Discussionmentioning

confidence: 99%

Effects of Conditioning Stimulation of the Central Amygdaloid Nucleus on Tooth Pulp-Driven Neurons in the Cat Somatosensory Cortex(SI).

Kawarada

Kamata²,

Matsumoto³

1999

JJP

View full text Add to dashboard Cite

The sensation we call pain, like other sensations, can be modulated by exposure to a stressful situation such as a fight or athletic competition. It has been suggested that stress is a physiologic trigger of the intrinsic pain inhibitory system. This phenomenon has been termed as stress-induced analgesia (SIA) (see Amit and Galina [1] for review) or fear-induced analgesia [2]. Actually, acupuncture and transcutaneous electrical nerve stimulation, which might be considered stressful, have been used for analgesia as a clinical procedure [1]. However, the neuronal mechanism and anatomical substrates involved in SIA have remained unclear.It has been demonstrated that the central amygdaloid nucleus (ACE) has an integrative role for coordinating an organism's autonomic, endocrine, and behavioral responses to various stressful stimuli, and that electrical stimulation of the ACE can mimic several of the stress-like responses (see Glavin et al. [3] for review). Lesions of the ACE have been found to block cardiovascular, respiratory, and behavioral parameters of responses to stressors [4,5]. Intracere- Japanese Journal of Physiology, 49, 485-497, 1999 Key words: central amygdaloid nucleus, stress-induced antinociception, somatosensory cortex, tooth pulp-driven neuron, H 1 receptor. Abstract:To study the limbic control of nociception, we examined the effect of conditioning stimulation of the central amygdaloid nucleus (ACE) on tooth pulp-driven (TPD) neurons in the first somatosensory cortex (SI). Cats were anesthetized with N 2 O-O 2 (2 : 1) and 0.5% halothane, and immobilized with tubocurarine chloride. The tooth pulp test stimulus was applied by a single rectangular pulse (0.5 ms in duration and 3-5 times the threshold intensity for the jaw-opening reflex). Conditioning stimuli to the ACE consisted of trains of 33 pulses (300 A) delivered at 330 Hz at intervals of 8-10 s. In 35 out of 61 of the slow (S)-type TPD neurons with latencies of more than 20 ms, conditioning stimulation in the ACE, especially in the medial division, markedly reduced the firing response to the pulpal stimulation. The inhibition of the firing rate in the S-type neurons was 74% of the control. In these S-type neurons, the neurons that were inhibited had significantly longer latencies compared to the noninhibited neurons (45.0Ϯ17.6 ms, nϭ32 vs. 34.8Ϯ10.5 ms, nϭ26). In contrast, the ACE conditioning stimulation affected only one out of 18 fast-type TPD neurons with latencies of less than 20 ms. In addition, ACE stimulation had no effect on the spontaneous discharges of either S-type or F-type neurons. The ACE inhibitory effect on S-type neurons was not diminished by naloxone administration (1 mg/kg, I.V.), while the blockade of histamine H 1 -receptor by diphenhydramine hydrochloride (0.5 mg/kg, I.V.) partially reversed the inhibitory effect. These results suggest that the ACE inhibits ascending nociceptive information to the SI and that this inhibition is mediated in part by histamine (H 1 ) receptors. It seems likely that the antinociceptive ...

show abstract

Psychomotor behaviour and cardiovascular patterns during stimulation of the amygdala

Cited by 85 publications

References 20 publications

Influence of captopril treatment on angiotensin II receptors and angiotensinogen in the brain of spontaneously hypertensive rats.

Influence of captopril treatment on angiotensin II receptors and angiotensinogen in the brain of spontaneously hypertensive rats.

Amygdaloid influences on brain‐stem neurones in the rabbit.

Effects of Conditioning Stimulation of the Central Amygdaloid Nucleus on Tooth Pulp-Driven Neurons in the Cat Somatosensory Cortex(SI).

Contact Info

Product

Resources

About