Asymmetry in behavioral responses to cholecystokinin microinjected into rat nucleus accumbens and amygdala

Belcheva, Iren; Belcheva, S.; Petkov, V.

doi:10.1016/0028-3908(94)90158-9

Cited by 53 publications

(27 citation statements)

References 33 publications

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“…Alternatively, since CB 1 receptors are located on CCKpositive interneurons within the BLA (McDonald and Mascagni, 2001), and activation of CB 1 receptors can inhibit CCK release from hippocampal slices (Beinfeld and Connolly, 2001), SR141716-induced blockade of eCB tone could result in increased CCK release within the BLA. Since intraamygdala injections of CCK can induce anxiety-like behaviors (Belcheva et al, 1994), and systemic administration of CCK increases Fos expression within the CeA (Day et al, 1994), a CCK-dependent mechanism could subserve the amygdala-activating effects of SR141716 in rodents.…”

Section: Discussionmentioning

confidence: 99%

Synergistic Interactions between Cannabinoids and Environmental Stress in the Activation of the Central Amygdala

Patel

Cravatt

Hillard

2004

Neuropsychopharmacol

147

100

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Anxiety and panic are the most common adverse effects of cannabis intoxication; reactions potentiated by stress. Data suggest that cannabinoid (CB 1 ) receptor modulation of amygdalar activity contributes to these phenomena. Using Fos as a marker, we tested the hypothesis that environmental stress and CB 1 cannabinoid receptor activity interact in the regulation of amygdalar activation in male mice. Both 30 min of restraint and CB 1 receptor agonist treatment (D 9 -tetrahydrocannabinol (2.5 mg/kg) or CP55940 (0.3 mg/kg); by i.p. injection) produced barely detectable increases in Fos expression within the central amygdala (CeA). However, the combination of restraint and CB 1 agonist administration produced robust Fos induction within the CeA, indicating a synergistic interaction between environmental stress and CB 1 receptor activation. An inhibitor of endocannabinoid transport, AM404 (10 mg/kg), produced an additive interaction with restraint within the CeA. In contrast, fatty acid amide hydrolase (FAAH) inhibitor-treated mice (URB597, 1 mg/kg) and FAAH À/À mice did not exhibit any differences in amygdalar activation in response to restraint compared to control mice. In the basolateral (BLA) and medial amygdala, restraint stress produced a low level of Fos induction, which was unaffected by cannabinoid treatment. Interestingly, the CB 1 receptor antagonist SR141716 dose-dependently increased Fos expression in the BLA and CeA. These data suggest the CeA is an important neural substrate subserving the interactions between cannabinoids and environmental stress, and could be relevant to understanding the context-dependent emotional and affective changes induced by marijuana intoxication and the role of endocannabinoid signaling in the modulation of amygdalar activity.

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Section: Discussionmentioning

confidence: 99%

Synergistic Interactions between Cannabinoids and Environmental Stress in the Activation of the Central Amygdala

Patel

Cravatt

Hillard

2004

Neuropsychopharmacol

147

100

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“…When injected into the amygdala, opioid antagonists enhance memory retention 38 , and the intra-amygdaloid administration of CCK agonists facilitates learning and memory 39,40 . Furthermore, CCK mRNA expression increases in the amygdala following repeated morphine administration, suggesting that the amygdala is a critical locus for a CCKmediated compensatory mechanism that contributes to opioid tolerance 41 .…”

Section: Discussionmentioning

confidence: 99%

A locus and mechanism of action for associative morphine tolerance

2000

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Repeated administration of an opioid in the presence of specific environmental cues can induce tolerance specific to that setting (associative tolerance). Prolonged or repeated administration of an opioid without consistent contextual pairing yields non-associative tolerance. Here we demonstrate that cholecystokinin acting at the cholecystokinin-B receptor is required for associative but not non-associative morphine tolerance. Morphine given in the morphineassociated context increased Fos-like immunoreactivity in the lateral amygdala and hippocampal area CA1. Microinjection of the cholecystokinin B antagonist L-365,260 into the amygdala blocked associative tolerance. These results indicate that cholecystokinin acting in the amygdala is necessary for associative tolerance to morphine's analgesic effect.The role of cholecystokinin (CCK) as an anti-opioid peptide is firmly established. CCK suppresses the analgesic effect of morphine and other μ-opioid receptor agonists 1,2 . CCK antagonists potentiate the analgesic effects of exogenous and endogenous μ-opioid receptor agonists 3-8 and enhance the inhibitory effect of morphine on nociceptive dorsal horn neurons 9,10 . Additionally, CCK antagonists impede the acquisition of morphine tolerance yet have no effect on morphine dependence or withdrawal 3,[11][12][13][14][15][16] . Although CCK antagonists potentiate the effects of opioids, they do not alter nociceptive threshold levels when administered independently 8,16 . There are two distinct CCK receptors (CCK-A and CCK-B) in the CNS [17][18][19][20] .Learning can contribute to drug tolerance [21][22][23][24][25][26][27] . When morphine administration is paired with specific environmental cues, these cues can act as conditioned stimuli that elicit a conditioned response opposing the agonist effect of morphine (associative tolerance). Although associative analgesic tolerance following repeated opioid administration is well established, the underlying neurobiological mechanisms are unknown.

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“…Also, thyrotropin-releasing hormone prevails in the left hypothalamus (Borson-Chazot et al 1986). Furthermore, cholecystokinin-8 or angiotensin II facilitate learning and memory when microinjected respectively into the left amygdala (Belcheva et al 1994) or hippocampus (Tashev and Stefanova 2015). Several angiotensinases also show signifi cant inter-hemispheric diff erences in amygdala, hippocampus, and prefrontal cortex (Banegas et al 2005).…”

Section: Brain Asymmetrymentioning

confidence: 99%

Bidirectional asymmetry in the neurovisceral communication for the cardiovascular control: New insights

Prieto

Segarra

Martı́nez-Cañamero

et al. 2017

Endocrine Regulations

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Th e cardiovascular control involves a bidirectional functional connection between the brain and heart. We hypothesize that this connection could be extended to other organs using endocrine and autonomic nervous systems (ANS) as communication pathways. Th is implies a neuroendocrine interaction controlling particularly the cardiovascular function where the enzymatic cascade of the renin-angiotensin system (RAS) plays an essential role. It acts not only through its classic endocrine connection but also the ANS. In addition, the brain is functionally, anatomically, and neurochemically asymmetric. Moreover, this asymmetry goes even beyond the brain and it includes both sides of the peripheral nervous and neuroendocrine systems. We revised the available information and analyze the asymmetrical neuroendocrine bidirectional interaction for the cardiovascular control. Negative and positive correlations involving the RAS have been observed between brain, heart, kidney, gut, and plasma in physiologic and pathologic conditions. Th e central role of the peptides and enzymes of the RAS within this neurovisceral communication, as well as the importance of the asymmetrical distribution of the various RAS components in the pathologies involving this connection, are particularly discussed. In conclusion, there are numerous evidences supporting the existence of a neurovisceral connection with multiorgan involvement that controls, among others, the cardiovascular function. Th is connection is asymmetrically organized.

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Asymmetry in behavioral responses to cholecystokinin microinjected into rat nucleus accumbens and amygdala

Cited by 53 publications

References 33 publications

Synergistic Interactions between Cannabinoids and Environmental Stress in the Activation of the Central Amygdala

Synergistic Interactions between Cannabinoids and Environmental Stress in the Activation of the Central Amygdala

A locus and mechanism of action for associative morphine tolerance

Bidirectional asymmetry in the neurovisceral communication for the cardiovascular control: New insights

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