Conditioned fear-induced tachycardia in the rat; vagal involvement

Nijsen, Marjoleen; Croiset, Gerda; Diamant, Michaëla; Stam, Rianne; Delsing, Dianne J.; Wied, D. de; Wiegant, V.M.

doi:10.1016/s0014-2999(98)00261-1

Cited by 83 publications

(64 citation statements)

References 42 publications

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“…Thus, the observed tachycardia does not necessarily reflect increased anxiety. Although the majority of animal studies focuses on the effects of aversive situations on autonomic responses, e.g., foot-shock in mice (Gross et al 2000), fear-conditioning in rats and mice (Marchand and Kamper 2000;Nijsen et al 1998b;Stiedl and Spiess 1997;Stiedl et al 1999), novelty in rats (Nijsen et al 1998a), increased tachycardia after appetitive situations has also been reported, e.g., after feeding in pigs (Schouten et al 1991), and reinforcing intracranial brain stimulation in rats (Burgess et al 1993).…”

Section: Discussionmentioning

confidence: 99%

“…In animals, experimentally induced stress elicits tachycardia (Bouwknecht et al 2000;Nijsen et al 1998a) and increases body temperature (Borsini et al 1989;Bouwknecht et al 2000;Olivier et al 1998). Moreover, conditioned fear also elicits tachycardia in freely moving rats (Nijsen et al 1998b) and mice (Stiedl and Spiess 1997;Stiedl et al 1999). Interestingly, a preliminary study indicated that 5-HT 1A receptor KO mice showed increased tachycardia compared with wild type (WT) mice in response to footshock also accompanied by increased freezing (Gross et al 2000).…”

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confidence: 99%

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Autonomic Changes Associated with Enhanced Anxiety in 5-HT1A Receptor Knockout Mice

Pattij

Groenink

Hijzen

et al. 2002

Neuropsychopharmacology

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Autonomic Changes Associated with Enhanced Anxiety in 5-HT1A Receptor Knockout Mice

Pattij

Groenink

Hijzen

et al. 2002

Neuropsychopharmacology

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“…In contrast, the P component of the PQRST waveform had amplitudes of 20 to 40 V. One implication of this lower signal-to-noise ratio for the P component was that although the peak amplitude could be resolved routinely, the exact onset could not. The PQ interval was most reliably measured by a peak detection algorithm (Origin Software, Northampton, MA) as the distance between the peaks of the P and Q components of the 4,000-ms ECG recording -a measure that has been used previously in the analysis of animal ECG data (Hayes, Pugsley, Penz, Adaikan, & Walker, 1994;Nijsen et al, 1998;. The PQ interval was measured in the present experiment as an index of central nervous system parasympathetic control of HR because the PQ interval is modulated in large part by inputs from the motor nucleus of the vagus that receive inputs from the amygdala (Nijsen et al, 1998;.…”

Section: Data Collectionmentioning

confidence: 99%

Cholesterol enhances classical conditioning of the rabbit heart rate response

Schreurs

Smith-Bell

Darwish

et al. 2007

Behavioural Brain Research

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The cholesterol-fed rabbit is a model of atherosclerosis and has been proposed as an animal model of Alzheimer's disease. Feeding rabbits cholesterol has been shown to increase the number of beta amyloid immunoreactive neurons in the cortex. Addition of copper to the drinking water of cholesterol-fed rabbits can increase this number still further and may lead to plaque-like structures. Classical conditioning of the nictitating membrane response in cholesterol-fed rabbits is retarded in the presence of these plaque-like structures but may be facilitated in their absence. In a factorial design, rabbits fed 2% cholesterol or a normal diet (0% cholesterol) for 8 weeks with or without copper added to the drinking water were given trace classical conditioning using a tone and periorbital electrodermal stimulation to study the effects of cholesterol and copper on classical conditioning of heart rate and the nictitating membrane response. Cholesterol-fed rabbits showed significant facilitation of heart rate conditioning and conditioning-specific modification of heart rate relative to normal diet controls. Consistent with previous research, cholesterol had minimal effects on classical conditioning of the nictitating membrane response when periorbital electrodermal stimulation was used as the unconditioned stimulus. Immunohistochemical analysis showed a significant increase in the number of beta amyloid positive neurons in the cortex, hippocampus and amygdala of the cholesterol-fed rabbits. Supplementation of drinking water with copper increased the number of beta amyloid positive neurons in the cortex of cholesterol-fed rabbits but did not produce plaque-like structures or have a significant effect on heart rate conditioning. The data provide additional support for our finding that, in the absence of plaques, dietary cholesterol may facilitate learning and memory. Cholesterol enhances rabbit heart rate conditioningThe cholesterol-fed rabbit has been used as an animal model of atherosclerosis since 1913 when Anitchkow first demonstrated that a cholesterol diet induced vascular lesions (Bocan, 1998;Fan & Watanabe, 2000;Finking & Hanke, 1997;Moghadasian, 2002). More recently, the cholesterol-fed rabbit has been proposed as an animal model of Alzheimer's disease (Ghribi, Larsen, Schrag, & Herman, 2006;Sjogren, Mielke, Gustafson, Zandi, & Skoog, 2006 Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Sparks, 1997;Sparks, Martin, Gross, & Hunsaker III, 2000;Zatta, Zambenedetti, Stella, & Licastro, 2002). Based on the observation that patients with heart disease had beta amyloid st...

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“…A telemetric transmitter to record gross activity, HR, and PQ interval was implanted in the abdominal cavity according to the procedure described by Nijsen et al (1998b). Briefly, a small longitudinal incision was made on the linea alba at the anterior of the abdomen.…”

Section: Surgerymentioning

confidence: 99%

CRH Signalling in the Bed Nucleus of the Stria Terminalis is Involved in Stress-Induced Cardiac Vagal Activation in Conscious Rats

Nijsen

Croiset

Diamant

et al. 2001

Neuropsychopharmacology

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The bed nucleus of the stria terminalis (BNST) is involved in autonomic and behavioral reactions to fearful stimuli and contains corticotropin-releasing hormone (CRH) fibers and terminals. The role of CRH in the medial part of the BNST in the regulation of heart rate (HR) and PQ interval of theThe bed nucleus of the stria terminalis (BNST) is a rostral forebrain structure that is enclosed by the lateral ventricle, lateral septum, fornix, nucleus accumbens, preoptic area and hypothalamus. The BNST has been recognized as an important relay station which links the amygdala and hippocampus with the paraventricular hypothalamic nucleus (PVN) and brain stem regions (Herman et al. 1994;Pacak et al. 1995;Davis et al. 1997). Projections have been found from the BNST to autonomic regulatory brain stem areas: the nucleus tractus solitarius (NTS) (Holstege et al. 1985;Gray and Magnuson 1987), caudal ventrolateral medulla (CVLM) (Giancola et al. 1993), and dorsal nucleus of the vagus (DMV) (Gray and Magnuson 1987;Hopkins 1987), supporting the role of the BNST in the regulation of autonomic responses.Its rich connections with the amygdala and PVN sug-

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Conditioned fear-induced tachycardia in the rat; vagal involvement

Cited by 83 publications

References 42 publications

Autonomic Changes Associated with Enhanced Anxiety in 5-HT1A Receptor Knockout Mice

Autonomic Changes Associated with Enhanced Anxiety in 5-HT1A Receptor Knockout Mice

Cholesterol enhances classical conditioning of the rabbit heart rate response

CRH Signalling in the Bed Nucleus of the Stria Terminalis is Involved in Stress-Induced Cardiac Vagal Activation in Conscious Rats

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