Temporal correlation of responses in blood pressure and motor reaction under electrical stimulation of limbic structures in unanaesthetized, unrestrained cats

Heinemann, H.; Stock, Günter; Schaefer, H.

doi:10.1007/bf00586572

Cited by 30 publications

(5 citation statements)

References 27 publications

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“…Studies in rats, cats, and rabbits have shown that electrical stimulation of the CeA causes anxiety-like responses (Kaada et al, 1954; Hilton and Zbrozyna, 1963; Heinemann et al, 1973; Mogenson and Calaresu, 1973) and conversely, lesions of the CeA attenuate anxiety-like responses (Moller et al, 1997; Kalin et al, 2004). The primate amygdala plays a role in certain anxiety-like behaviors such as anxiety-related defensive responses, which may have a conditioned fear component (Kalin et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of corticotropin releasing factor expression in the central nucleus of the amygdala attenuates stress-induced behavioral and endocrine responses

2013

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Corticotropin releasing factor (CRF) is a primary mediator of endocrine, autonomic and behavioral stress responses. Studies in both humans and animal models have implicated CRF in a wide-variety of psychiatric conditions including anxiety disorders such as post-traumatic stress disorder (PTSD), depression, sleep disorders and addiction among others. The central nucleus of the amygdala (CeA), a key limbic structure with one of the highest concentrations of CRF-producing cells outside of the hypothalamus, has been implicated in anxiety-like behavior and a number of stress-induced disorders. This study investigated the specific role of CRF in the CeA on both endocrine and behavioral responses to stress. We used RNA Interference (RNAi) techniques to locally and specifically knockdown CRF expression in CeA. Behavior was assessed using the elevated plus maze (EPM) and open field test (OF). Knocking down CRF expression in the CeA had no significant effect on measures of anxiety-like behavior in these tests. However, it did have an effect on grooming behavior, a CRF-induced behavior. Prior exposure to a stressor sensitized an amygdalar CRF effect on stress-induced HPA activation. In these stress-challenged animals silencing CRF in the CeA significantly attenuated corticosterone responses to a subsequent behavioral stressor. Thus, it appears that while CRF projecting from the CeA does not play a significant role in the expression stress-induced anxiety-like behaviors on the EPM and OF it does play a critical role in stress-induced HPA activation.

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Section: Discussionmentioning

confidence: 99%

Inhibition of corticotropin releasing factor expression in the central nucleus of the amygdala attenuates stress-induced behavioral and endocrine responses

2013

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“…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%

“…responses would be produced if different cardiovascular responses were evoked by the amygdala stimulus. In the cat, for example, tachycardia and pressor responses are obtained by stimulation of the central nucleus (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, 1.…”

Section: Discussionmentioning

confidence: 99%

Amygdaloid influences on brain‐stem neurones in the rabbit.

Cox¹,

Jordan²,

Moruzzi³

et al. 1986

The Journal of Physiology

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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.

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“…31, No. 5,1990 cardiovascular changes were characterized by a decrease in BP with no significant change or an increase in HR (Heinemann et al, 1973; Stock et al, 1978) or a bradycardia followed by an increase in BP (Reis and Oliphant, 1964). One possible explanation for the difference in results between these past studies and ours may be the use of different stimulus parameters, specifically stimulus frequency and duration.…”

Section: )mentioning

confidence: 99%

Kindled Seizures Elevate Blood Pressure and Induce Cardiac Arrhythmias

1990

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The effect of kindled seizures on the cardiovascular system was examined in amygdaloid kindled rats. The most prominent cardiovascular response during a generalized kindled seizure was an abrupt 50% increase in mean arterial pressure (MAP) lasting 20-30 s after initiation of the seizure. Superimposed on this change in blood pressure (BP) was a profound bradycardia characterized by a rate about half that recorded before stimulation. Changes in heart rate (HR) and BP observed during amygdaloid kindled seizures were similar to those observed during secondary spontaneous seizures. These effects apparently are independent of the kindling stimulus because stimulus-induced cardiovascular changes were not present at the beginning of the kindling process. These results suggest that the kindling seizure model is useful to study the underlying mechanisms of seizure-induced cardiac arrhythmias and possibly the clinical phenomenon of sudden unexplained death in epileptic patients.

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Temporal correlation of responses in blood pressure and motor reaction under electrical stimulation of limbic structures in unanaesthetized, unrestrained cats

Cited by 30 publications

References 27 publications

Inhibition of corticotropin releasing factor expression in the central nucleus of the amygdala attenuates stress-induced behavioral and endocrine responses

Inhibition of corticotropin releasing factor expression in the central nucleus of the amygdala attenuates stress-induced behavioral and endocrine responses

Amygdaloid influences on brain‐stem neurones in the rabbit.

Kindled Seizures Elevate Blood Pressure and Induce Cardiac Arrhythmias

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