The Scopolamine-Induced Impairment of Spatial Cognition Parallels the Acetylcholine Release in the Ventral Hippocampus in Rats

Mishima, Kenichi; Iwasaki, Katsunori; Tsukikawa, Hiroshi; Matsumoto, Yoshiaki; Egashira, Nobuaki; Abe, Kohji; Egawa, Takashi; Fujiwara, Michihiro

doi:10.1254/jjp.84.163

Cited by 60 publications

(38 citation statements)

References 29 publications

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“…in the scopolamine-induced impairment of spatial memory in the 8-arm radial maze, in agreement with our previous report (23). Moreover, we analyzed THC-and scopolamine-induced response patterns regarding arm choice by a CCD camera connected to a personal computer.…”

Section: Discussionsupporting

confidence: 90%

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Characteristics of Learning and Memory Impairment Induced by ⊿9-Tetrahydrocannabinol in Rats

Mishima

Egashira

Hirosawa

et al. 2001

Japanese Journal of Pharmacology

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ABSTRACT-We investigated the characteristics of D 9 -tetrahydrocannabinol (THC)-induced impairment of learning and memory using an 8-arm radial maze task, a water maze, a visual discrimination task with 2 figures and a passive avoidance test in rats. THC (6 mg /kg, i.p.) impaired spatial memory in the standard task of the 8-arm radial maze. THC (4 -6 mg /kg, i.p.) selectively impaired working memory in a reference and working memory task of the 8-arm radial maze. Even at a dose of 10 mg /kg, THC did not impair spatial memory in the water maze. In addition, THC at a dose of 6 mg /kg, which had inhibitory effects in the 8-arm radial maze, did not affect performance in the visual discrimination task. These results indicate that at low doses (2 -6 mg/kg), THC may not produce visual function abnormalities. THC impaired retrieval (6 mg /kg, i.p.) as well as acquisition (10 mg /kg, i.p.) in the passive avoidance test. The consolidation process was also impaired by i.c.v. injection (100 m g), but not i.p. injection (6 -10 mg /kg) of THC. These results suggest that THC-induced impairment of spatial memory is based on the selective impairment of working memory through its effects on acquisition and retrieval processes.

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Section: Discussionsupporting

confidence: 90%

“…We recently reported that the scopolamine-induced impairment of spatial memory in an 8-arm radial maze closely paralleled the change in acetylcholine release in the ventral hippocampus using microdialysis techniques (23). Therefore, scopolamine was used for comparison with the THC-induced impairment of working memory.…”

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confidence: 99%

Characteristics of Learning and Memory Impairment Induced by ⊿9-Tetrahydrocannabinol in Rats

Mishima

Egashira

Hirosawa

et al. 2001

Japanese Journal of Pharmacology

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“…In addition, we provide parallel evidence that fluoxetine's anxiolytic action may be mediated through a decrease of aversive stimulus-and aversive memory-evoked increases in cholinergic neurotransmission through M1 muscarinic receptors in the hippocampus, although this evidence is strictly circumstantial and needs to be further investigated in future studies. It seems unlikely that injections of pirenzepine induced an anxiolytic effect by reducing overall ACh efflux since previous studies have reported that pirenzepine either increases or does not affect ACh efflux (Douglas et al, 2001;Mishima et al, 2000). Therefore, the observed effect seems to be solely attributed to a blockade of the M1 receptors.…”

Section: Discussionmentioning

confidence: 87%

Fluoxetine Disrupts the Integration of Anxiety and Aversive Memories

Degroot

Nomikos

2004

Neuropsychopharmacol

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Anxiety disorders may result from an overexpression of aversive memories. Evidence suggests that the hippocampal cholinergic system could be the point of convergence of anxiety and memory. We propose that clinically effective anxiolytics may exert their effect by interfering with this integration mechanism. To assess anxiety and aversive memory, we used the shock-probe burying test. A reduction in anxiety in this test is indicated by decreased burying, whereas impaired cognition is reflected by an increased number of probe-contacts and/or reduced retention latency. Both an aversive stimulus and the memory of that stimulus significantly increased hippocampal acetylcholine (ACh) levels (Experiment 1). In fact, the memory of the event seemed to be more important than the event itself since the aversive memory induced a greater increase in hippocampal ACh. Injections (i.p.) of fluoxetine (Prozac s ) reduced burying behavior, while not affecting probe contacts or retention latency (Experiment 2). Although injections of fluoxetine did not affect basal hippocampal ACh efflux (Experiment 3), fluoxetine abolished the increase in ACh induced by the aversive stimulus and the memory of that stimulus (Experiment 4), emphasizing the significance of aversive memories in anxiety disorders. These actions may be mediated by a decrease in the event-related enhancement in cholinergic neurotransmission through M1 cholinergic receptors (Experiment 5). Therefore, anxiety disorders may stem from an unopposed formation of aversive memories and clinically effective anxiolytics hinder the association between emotional and cognitive processing. This reduces the emotional impact of aversive memories, thereby opposing consequent anxiety.

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“…This accumulation seemed to be due to a increase in the specific binding of The most important finding is that an increase in [ 3 H] QNB binding caused by irradiation can only be detected in the intact brain. In the cholinergic system, such as choline acethyltransferase and ACh receptor, it plays important roles in learning and spatial cognition (18)(19)(20). We indicated that a transitional increase of mACh receptor in vivo binding in the early phase at 24 hrs after irradiated with the proton beam at a dose of 30 Gy.…”

Section: Ach Receptor Binding Assaymentioning

confidence: 86%

The Focal Brain Proton Beam Irradiation Insult in Rats – Induced Memory Disturbance Related Change in Acetylcholine Receptor Binding

Takai¹,

Ohgami²,

Andō³

et al. 2017

RAD Conference Proceedings

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Abstract. Cerebral dysfunction is one of the major concerns associated with radiotherapy of brain tumours. However, little is known about the neurochemical basis of brain dysfunction induced by proton irradiation. We here investigated the early consequences of brain damages caused by a proton beam. Brains of male wistar rats were locally irradiated with a 70 MeV proton beam. The irradiation dose was set at level known to produce vascular change followed by necrosis, which appeared the late period after irradiation with 30 Gy. The eight-arm radial maze task in irradiated rats was used. In order to assess the preservation (recall) of memory, the rats that showed the spatial cognition were irradiated. The impairment of the preservation memory was not observed in the irradiated rats compared to the control ones 24 hrs after irradiation. Repeated measures of two-way ANOVA of correct choices and number of errors showed no differences between the control group and 30 Gy irradiated group. In order to assess the acquisition process of memory and working memory for the platform location in the water maze, the task was started on the 24 hrs after irradiation. In the learning task (the acquisition process of memory), there was no difference between the control group and irradiated group in the latency to platform. The rats that memorized the location of the standard position were irradiated, and the impairment of the long-term memory was not observed in the irradiated rats compared to the control ones 24 hrs after irradiation. However, the irradiated rats required a substantially longer time finding out the platform than the control rats when the platform was placed in a non-standard position. From this it follows that a proton dose of 30 Gy impaired the working memory of rats. The function of muscarinic acetylcholine receptors was analyzed by in vivo binding assay using radioligand quinuclidinyl benzilate ([ 3 H]QNB). The irradiated rats were intravenously injected with 5.5 MBq of [ 3 H]QNB on the 24 hrs after the irradiation. Autoradiographic studies showed a transitional increase of [ 3 H]QNB in-vivo binding in the early phase after proton irradiation. On the other hand, no change in in-vitro [ 3 H]QNB binding was seen in the autoradiogram of brain slices from the irradiated rats. The cerebral blood flow and the histopathological change in the brain appeared at 5 or 6 months after irradiation. These results indicate that the relation between behavioral impairment caused by radiation is closely related to the early change in the receptor function which could be detected in in-vivo conditions.

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The Scopolamine-Induced Impairment of Spatial Cognition Parallels the Acetylcholine Release in the Ventral Hippocampus in Rats

Cited by 60 publications

References 29 publications

Characteristics of Learning and Memory Impairment Induced by ⊿9-Tetrahydrocannabinol in Rats

Characteristics of Learning and Memory Impairment Induced by ⊿9-Tetrahydrocannabinol in Rats

Fluoxetine Disrupts the Integration of Anxiety and Aversive Memories

The Focal Brain Proton Beam Irradiation Insult in Rats – Induced Memory Disturbance Related Change in Acetylcholine Receptor Binding

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