Activation of cannabinoid CB1 receptors in the ventral hippocampus improved stress-induced amnesia in rat

Mohammadmirzaei, Negin; Rezayof, Ameneh; Ghasemzadeh, Zahra

doi:10.1016/j.brainres.2016.06.008

Cited by 11 publications

(5 citation statements)

References 67 publications

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“…Bilateral BLA inactivation impaired consolidation of IA memory, which was similar to previous studies on amnesia effects of post-training BLA optogenetic modulation or inactivation by lidocaine or muscimol, infusion of glutamate receptor antagonists or inhibition of the protein kinase C in the BLA (Liang et al 1994;Parent and McGaugh 1994;Roesler et al 2000;Wilensky et al 2000;Rossato et al 2004;Bonini et al 2005;Lalumiere and McGaugh 2005;McIntyre et al 2005;Huff et al 2013;Nazari-Serenjeh and Rezayof 2013). And other researchers have reported that inactivation of the VH, or changes of the cannabinoid CB1 receptor and histamine receptor in it, could impair or modulate IA memory consolidation (Ambrogi Lorenzini et al 1997;Alvarez and Banzan 2008;Wang and Cai 2008;Mohammadmirzaei et al 2016). The data in this study, in combination with that of previous studies, supports that BLA and VH are key anatomical structures in IA memory consolidation.…”

supporting

confidence: 86%

Post-training reversible disconnection of the ventral hippocampal–basolateral amygdaloid circuits impairs consolidation of inhibitory avoidance memory in rats

2017

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The ventral hippocampus (VH) and the basolateral amygdala (BLA) are both crucial in inhibitory avoidance (IA) memory. However, the exact role of the VH-BLA circuit in IA memory consolidation is unclear. This study investigated the effect of post-training reversible disconnection of the VH-BLA circuit in IA memory consolidation. Male Wistar rats with implanted guide cannulae were trained with a one-trial IA task, then received immediate intracerebral injections of muscimol or saline, and were tested 24 h later. Muscimol injection into the bilateral BLA, or the unilateral VH and contralateral BLA, but not the unilateral VH and ipsilateral BLA, significantly decreased the retention latencies (versus saline treatment). The results suggest that the VH-BLA circuit could be an important circuit to modulate consolidation of IA memory in rats.

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supporting

confidence: 86%

Post-training reversible disconnection of the ventral hippocampal–basolateral amygdaloid circuits impairs consolidation of inhibitory avoidance memory in rats

2017

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“…In a study conducted by Sardari et al [32], it has been shown that exposure to inescapable stress before the retention trial of a passive avoidance task induces memory retrieval impairment. Furthermore, post-training exposure to stress also decreased memory retrieval on the test day [34,41]. Interestingly, before being exposed to the retention stage, the same stressful situation completely reversed stress-induced memory impairment and showed a typical memory performance [34].…”

Section: Stress Impairs Memory Formationmentioning

confidence: 92%

Cellular and molecular mechanisms of stress-induced memory impairment

2022

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Exposure to stressful conditions plays a critical role in brain processes, including neural plasticity, synaptic transmission, and cognitive functions. Since memory-related brain regions, the hippocampus (Hip), the amygdala, and the prefrontal cortex, express high glucocorticoid receptors (GRs), these areas are the potential targets of stress hormones. Stress affects memory encoding, consolidation, and retrieval, which may depend on many factors such as the type, duration, the intensity of the stressor or the brain region. Here, this review mainly focused on the mechanisms involved in stress-induced memory impairment. Acute/chronic stress induces structural and functional changes in neurons and glial cells. Dendritic arborization, reduction of dendritic spine density, and alteration in glutamatergic-mediated synaptic transmission via N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors are mechanisms that stress affect long-term memory formation. Exposure to acute or chronic stress could interplay with multiple neurotransmitter signaling, modulating the neuronal circuits involved in memory impairment or state-dependent learning. Stress hormones also modulate the expression of microRNAs in the specific brain regions responsible for stress-induced behaviors. Because of expressing GRs in astrocytes and microglial cells, stress could affect the morphology, structure, and functions of these glial cells in memory-related brain regions. Astrocytes play a crucial role in stress-induced aversive or fear memory formation. Over-activation of the microglial cells enhances the release of inflammatory cytokines, which results in neuronal injury. Stress has a prominent role in cognitive decline to induces memory problems, particularly in older adults. Due to the issue’s importance, here the provided overview attempted to address the question of how stress alters neuronal epigenetic regulators, synaptic transmissions, and glial activity in the brain.

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“…In the striatum, 100 ng of ACPA improves movement activity in a Parkinson's rat model (Moghaddam, Khodayar, Abarghouei, & Ardestani, 2010). Moreover, 0.125–5 ng of ACPA in the amygdala (Zarrindast et al., 2008) and 5–7.5 ng of ACPA in the ventral hippocampus (Mohammadmirzaei, Rezayof, & Ghasemzadeh, 2016) result in some cognitive effects. Therefore, we choose the 3.125 ng/μl (low dose; prepared from stock solution of 5 mg/ml; 5/(16 × 10 5 ) dilution) and 25 ng/μl (high dose; 5/(2 × 10 5 ) dilution) doses.…”

Section: Methodsmentioning

confidence: 99%

Activation of cannabinoid type 1 receptors decreases the synchronization of local field potential oscillations in the hippocampus and entorhinal cortex and prolongs the interresponse time during a differential‐reinforcement‐of‐low‐rate task

Liao

Chang

Hsiao

2020

Eur J of Neuroscience

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Marijuana intoxication impairs neurocognitive functions. Common side effects of consuming cannabis include time distortion and memory loss. However, the underlying neurophysiological mechanisms involved in these effects remain unclear. We hypothesized that communication between the hippocampal CA1 region and medial entorhinal cortex (MEC) is essential for the transmission of temporal‐associated information. We used a differential‐reinforcement‐of‐low‐rate (DRL) task, which requires subjects to press a lever at an optimal time point, to correlate the distributions of interresponse time (IRT) with local field potentials (LFPs) recorded in the CA1 and MEC under the effects of a cannabinoid type 1 (CB1) receptor agonist. We used a DRL 10‐s schedule and trained the rats to withhold for 10 s before pressing a lever. Our data showed that the percentage of 12.4‐ to 14‐s IRT events rose after activation of CB1 receptors in the MEC. In addition, gamma amplitude synchronization and CA1 theta phase–MEC gamma amplitude coupling decreased during the 6‐ to 14‐s IRT events. These results suggest that activation of CB1 receptors in the MEC disrupt the functional connectivity between the CA1 and the MEC. This inefficient communication may result in increased IRT during a DRL schedule. Overall, we postulate that marijuana intoxication impairs the communication between the CA1 and MEC and influences behavioral performances that require precise timing ability.

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Activation of cannabinoid CB1 receptors in the ventral hippocampus improved stress-induced amnesia in rat

Cited by 11 publications

References 67 publications

Post-training reversible disconnection of the ventral hippocampal–basolateral amygdaloid circuits impairs consolidation of inhibitory avoidance memory in rats

Post-training reversible disconnection of the ventral hippocampal–basolateral amygdaloid circuits impairs consolidation of inhibitory avoidance memory in rats

Cellular and molecular mechanisms of stress-induced memory impairment

Activation of cannabinoid type 1 receptors decreases the synchronization of local field potential oscillations in the hippocampus and entorhinal cortex and prolongs the interresponse time during a differential‐reinforcement‐of‐low‐rate task

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