Ventral hippocampal ibotenic acid lesions block chronic nicotine-induced spatial working memory improvement in rats

Levin, Edward D.; Christopher, N. Channelle; Weaver, T; Moore, Julie; Brucato, Frederic H.

doi:10.1016/s0926-6410(98)00044-5

Cited by 49 publications

(29 citation statements)

References 28 publications

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“…We have found the hippocampus to be important for chronic nicotine effects on memory function. Small hippocampal ibotenic acid lesions, which did not significantly impair working memory performance, blocked the chronic nicotine-induced memory improvement (Levin et al, 1999b). The critical site of action for chronic nicotine in the hippocampus appears to be postsynaptic to the septohippocampal projection.…”

Section: Hippocampal Involvement In Nicotinic Actions On Memorymentioning

confidence: 82%

Nicotinic receptor subtypes and cognitive function

2002

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ABSTRACT:Nicotinic receptor systems are involved in a wide variety of behavioral functions including cognitive function. Nicotinic medications may provide beneficial treatment for cognitive dysfunction such as Alzheimer's disease, schizophrenia, and attention deficit hyperactivity disorder (ADHD). Nicotine has been shown to improve attentional performance in all of these disorders. Better efficacy with fewer side effects might be achieved with novel nicotinic ligands selective for particular nicotinic subtypes. To develop these novel selective nicotinic ligands it is important to use animal models to determine the critical neurobehavioral bases for nicotinic involvement in cognitive function. Nicotineinduced cognitive improvement in rats is most consistently seen in working memory tasks. We have found that both acute and chronic nicotine administration significantly improves working memory performance of rats in the radial-arm maze. The pharmacologic and anatomic mechanisms for this effect have been examined in our laboratory in a series of local drug infusion studies. Both ␣4␤2 and ␣7 nicotinic receptors in the ventral hippocampus and basolateral amygdala are involved in working memory function. Working memory impairments were caused by local infusion of either ␣4␤2 or ␣7 antagonists. Ventral hippocampal ␣4␤2 blockade-induced working memory deficits are reversed by chronic systemic nicotine treatment, while ventral hippocampal ␣7 blockade-induced working memory deficits were not found to be reversed by the same nicotine regimen. Interestingly, ␣4␤2 and ␣7 induced deficits were not found to be additive in either the ventral hippocampus or the basolateral amygdala. In fact, in the amygdala, ␣7 antagonist cotreatment actually reversed the working memory impairment caused by ␣4␤2 antagonist administration. These studies of the neural nicotinic mechanisms underlying cognitive function are key for opening avenues for development of safe and effective nicotinic treatments for cognitive dysfunction.

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Section: Hippocampal Involvement In Nicotinic Actions On Memorymentioning

confidence: 82%

Nicotinic receptor subtypes and cognitive function

2002

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“…This may have been related to the modest damage to the hippocampus from the local infusion cannulae. Our previous work has shown that even mild damage to the ventral hippocampus that does not in itself cause memory impairment does block the memory improvement seen with chronic systemic nicotine infusion (Levin et al 1999). Even so, there was a modest improvement in the nicotine-treated rats when no other drug treatment was given.…”

Section: Discussionmentioning

confidence: 95%

Ventral hippocampal α7 and α4β2 nicotinic receptor blockade and clozapine effects on memory in female rats

2006

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Rationale-Nicotinic systems in the hippocampus play important roles in memory function. Decreased hippocampal nicotinic receptor concentration is associated with cognitive impairment in schizophrenia and Alzheimer's disease.Methods-We modeled in rats the cognitive effects of chronic decrease in hippocampal α7 or α4β2 receptors with 4-week continuous bilateral local infusions of the α7 nicotinic antagonist methyllycaconitine (MLA) or the α4β2 antagonist dihydro-β-erythroidine (DHβE). The working memory effects of these infusions were assessed by performance on the radial-arm maze. To test the effect of antipsychotic medication, we gave acute injections of clozapine and to determine the impact of nicotine, which is widely used by people with schizophrenia approximately half of the rats received chronic systemic infusions of nicotine.Results-Chronic ventral hippocampal DHβE infusion caused a significant (p<0.001) working memory impairment. Acute systemic clozapine (2.5 mg/kg) caused a significant (p<0.005) working memory impairment in rats given control aCSF hippocampal infusions. Clozapine significantly (p<0.025) attenuated the memory deficit caused by chronic hippocampal DHβE infusions. Chronic ventral hippocampal infusions with MLA did not significantly affect the working memory performance in the radial-arm maze, but it did significantly (p<0.05) potentiate the memory impairment caused by 1.25 mg/kg of clozapine. Chronic systemic nicotine did not significantly interact with these effects. Conclusions-The state of nicotinic receptor activation in the ventral hippocampus significantly affected the impact of clozapine on working memory with blockade of α7 nicotinic receptors potentiating clozapine-induced memory impairment and blockade of α4β2 receptors reversing the clozapine effect from impairing to improving memory.

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“…While there is debate on assigning function to each of these hippocampal sub-regions, the DHPC is considered by some to be necessary for learning and memory processes that involve the utilization of spatial information, whereas the VHPC is linked with learning processes that involve an emotional or motivational component (de Hoz et al, 2003;Bannerman et al, 2004;Fanselow and Dong, 2010). This differentiation of function, however, is complicated by several findings showing that VHPC lesions or inactivation interferes with spatial memory processing (eg Ogren et al, 1996;Schott et al, 1998;Wilkerson and Levin, 1999;Levin et al, 1999;Ferbinteanu and McDonald, 2001;de Hoz et al, 2003). Here we show that VHPC leptin signaling modulates the consolidation of memory for the spatial location of food, which further challenges the belief that hippocampal spatial memory processing is mediated exclusively by the dorsal region.…”

Section: Discussionmentioning

confidence: 99%

Hippocampal Leptin Signaling Reduces Food Intake and Modulates Food-Related Memory Processing

Kanoski

Hayes

Greenwald

et al. 2011

Neuropsychopharmacol

133

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The increase in obesity prevalence highlights the need for a more comprehensive understanding of the neural systems controlling food intake; one that extends beyond food intake driven by metabolic need and considers that driven by higher-order cognitive factors. The hippocampus, a brain structure involved in learning and memory function, has recently been linked with food intake control. Here we examine whether administration of the adiposity hormone leptin to the dorsal and ventral sub-regions of the hippocampus influences food intake and memory for food. Leptin (0.1 mg) delivered bilaterally to the ventral hippocampus suppressed food intake and body weight measured 24 h after administration; a higher dose (0.4 mg) was needed to suppress intake following dorsal hippocampal delivery. Leptin administration to the ventral but not dorsal hippocampus blocked the expression of a conditioned place preference for food and increased the latency to run for food in an operant runway paradigm. Additionally, ventral but not dorsal hippocampal leptin delivery suppressed memory consolidation for the spatial location of food, whereas hippocampal leptin delivery had no effect on memory consolidation in a non-spatial appetitive response paradigm. Collectively these findings indicate that ventral hippocampal leptin signaling contributes to the inhibition of food-related memories elicited by contextual stimuli. To conclude, the results support a role for hippocampal leptin signaling in the control of food intake and food-related memory processing.

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Ventral hippocampal ibotenic acid lesions block chronic nicotine-induced spatial working memory improvement in rats

Cited by 49 publications

References 28 publications

Nicotinic receptor subtypes and cognitive function

Nicotinic receptor subtypes and cognitive function

Ventral hippocampal α7 and α4β2 nicotinic receptor blockade and clozapine effects on memory in female rats

Hippocampal Leptin Signaling Reduces Food Intake and Modulates Food-Related Memory Processing

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