2009
DOI: 10.1101/lm.1513109
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Abstract: Exposure to novel contexts produce heightened states of arousal and biochemical changes in the brain to consolidate memory. However, processes permitting simple exposure to unfamiliar contexts to elevate sympathetic output and to improve memory are poorly understood. This shortcoming was addressed by examining how novelty-induced changes in peripheral and/or central arousal modulates memory for Pavlovian fear conditioning. Male rats were either exposed to the conditioning chamber for 5-min or given no exposure… Show more

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Cited by 35 publications
(27 citation statements)
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References 89 publications
(106 reference statements)
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“…After determining that peripheral β-adrenergic signaling mediates the acute hypophagic effect of rimonabant, we wondered whether such a mechanism might also underpin other behavioral effects of CB 1 antagonism. Indeed, brain functions, like fear and anxiety responses, are regulated by interactions between the SNS and brainstem glutamatergic activity (13), and alterations in these functions represent the main side-effects of rimonabant use in humans (14). For example, the increase in SNS activity induced by rimonabant may be partly responsible of the drug's effect on conditioned freezing in fear-conditioning experiments (15).…”
Section: Glutamatergic Transmission In the Nucleus Tractus Solitarii mentioning
confidence: 99%
See 1 more Smart Citation
“…After determining that peripheral β-adrenergic signaling mediates the acute hypophagic effect of rimonabant, we wondered whether such a mechanism might also underpin other behavioral effects of CB 1 antagonism. Indeed, brain functions, like fear and anxiety responses, are regulated by interactions between the SNS and brainstem glutamatergic activity (13), and alterations in these functions represent the main side-effects of rimonabant use in humans (14). For example, the increase in SNS activity induced by rimonabant may be partly responsible of the drug's effect on conditioned freezing in fear-conditioning experiments (15).…”
Section: Glutamatergic Transmission In the Nucleus Tractus Solitarii mentioning
confidence: 99%
“…Finally, visceral afferents also play an important role in transmitting nutrient-derived intestinal signals to the brainstem, where glutamate and NMDA receptors modulate visceral sensory signaling pathways, ultimately regulating food intake (12). Interestingly, the interplay between SNS and brainstem glutamatergic activity also regulates other brain functions, such as fear and anxiety responses (13), and alterations in these functions represent the main sideeffects of rimonabant use in humans (14).…”
mentioning
confidence: 99%
“…Moreover, stress-induced activation of the HPA axis involves the synthesis and secretion of glucocorticoids (cortisol in humans and corticosterone in most rodents) from the adrenal cortex (8). Both animal and human studies have shown that these stress hormones have profound effects on cognition by acting on specific brain regions involved in the processing of emotional stimuli (1,(9)(10)(11)(12).…”
mentioning
confidence: 99%
“…These limbic inputs are complemented by norepinephrine containing axons supplied by the A2 class of noradrenergic neurons housed in the brainstem region of the nucleus of the solitary tract (NTS) (Delfs et al 1998). Norepinephrine release from A2 NTS neurons play an important role in conveying information regarding experience-induced changes in the physiological state of the organism.The A2 neurons are activated during times of heightened arousal by the release of glutamate from vagal nerve fibers that ascend from the periphery to the brainstem (Allchin et al 1994;King and Williams 2009). Highly arousing events increase epinephrine secretion from the adrenals and facilitate binding to b-adrenergic receptors along the vagus nerve (Lawrence et al 1995) that in turn, increase impulse flow to brainstem neurons in the NTS (Lawrence et al 1995;Miyashita and Williams 2006).…”
mentioning
confidence: 99%
“…The A2 neurons are activated during times of heightened arousal by the release of glutamate from vagal nerve fibers that ascend from the periphery to the brainstem (Allchin et al 1994;King and Williams 2009). Highly arousing events increase epinephrine secretion from the adrenals and facilitate binding to b-adrenergic receptors along the vagus nerve (Lawrence et al 1995) that in turn, increase impulse flow to brainstem neurons in the NTS (Lawrence et al 1995;Miyashita and Williams 2006).…”
mentioning
confidence: 99%