Nerve growth factor increases extracellular acetylcholine levels in the parietal cortex and hippocampus of aged rats and restores object recognition

Scali, Carla; Casamenti, Fiorella; Pazzagli, Marta; Bartolini, L.; Pepeu, Giancarlo

doi:10.1016/0304-3940(94)90253-4

Cited by 75 publications

(33 citation statements)

References 27 publications

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“…For instance, aged rats that display memory deficits often display correlated decreases in hippocampal ACh markers (Lippa et al 1980(Lippa et al , 1985Sherman et al 1981;Ikegami 1994;Scali et al 1994;Aubert et al 1995;Baxter et al 1999b). Chronic dietary restriction of choline (Nakamura et al 2001) or vitamin A (Cocco et al 2002), and chronic alcohol consumption (Arendt et al 1990;Melis et al 1996) produce correlated deficits in memory and hippocampal ACh.…”

Section: Hippocampal Ach Activity Is Correlated With Memorymentioning

confidence: 99%

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Septohippocampal Acetylcholine: Involved in but not Necessary for Learning and Memory?

Parent¹,

Baxter²

2004

Learn. Mem.

175

132

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The neurotransmitter acetylcholine (ACh) has been accorded an important role in supporting learning and memory processes in the hippocampus. Cholinergic activity in the hippocampus is correlated with memory, and restoration of ACh in the hippocampus after disruption of the septohippocampal pathway is sufficient to rescue memory. However, selective ablation of cholinergic septohippocampal projections is largely without effect on hippocampal-dependent learning and memory processes. We consider the evidence underlying each of these statements, and the contradictions they pose for understanding the functional role of hippocampal ACh in memory. We suggest that although hippocampal ACh is involved in memory in the intact brain, it is not necessary for many aspects of hippocampal memory function.The goal of this review is to consider the role of septohippocampal acetylcholine (ACh) in learning and memory processes. The evidence in this regard falls broadly into two different classes. On the one hand, considerable data implicate septohippocampal ACh in memory function. This system is engaged during memory processing, indexed by ACh release or by modification of cholinergic markers, and manipulations that affect memory produce parallel changes in hippocampal cholinergic activity. Furthermore, agents that increase hippocampal cholinergic function are sufficient to reverse memory impairments caused by disruption of the septohippocampal system. However, data from studies of selective lesions of septohippocampal cholinergic neurons with the immunotoxin 192 IgG-saporin call into question the essential role of this system in learning and memory, because these studies generally failed to find severe impairments in memory function. Our goal in this article is to review the data underlying each of these lines of evidence, and to attempt to reconcile these apparently disparate observations.The discrepancy between these lines of evidence might imply that septohippocampal ACh is involved in memory processing, but is not necessary for it to occur. This viewpoint would allow for correlated changes in ACh release and memory, and for the ability of cholinergic agents to reverse memory impairments caused by disruption of septohippocampal function. However, it also would permit memory to proceed relatively normally in the absence of septohippocampal cholinergic input. By describing this viewpoint and its implications for the functional role of hippocampal ACh in memory, we seek to promote the idea that data from lesions are compatible with data from other experimental approaches. Furthermore, we suggest that a convergent approach that incorporates observations from different experimental methods will reveal functional characteristics of hippocampal ACh that would not be apparent from studies using a single strategy.Before discussing the role of this system in cognition, a brief review of its anatomical and neurochemical organization is warranted. The septum is connected to the hippocampus via the fimbria-fornix, which carries projections ...

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Section: Hippocampal Ach Activity Is Correlated With Memorymentioning

confidence: 99%

“…Similar correlations are observed with intracerebroventricular (i.c.v.) manipulations (Scali et al 1994;Hiramatsu et al 1996;Choi et al 2001;Olariu et al 2001).…”

Section: Hippocampal Ach Activity Is Correlated With Memorymentioning

confidence: 99%

Septohippocampal Acetylcholine: Involved in but not Necessary for Learning and Memory?

Parent¹,

Baxter²

2004

Learn. Mem.

175

132

View full text Add to dashboard Cite

show abstract

“…More specifically, prefrontal ACh has been implicated in working memory processes as demonstrated by behavioral tasks including delayed nonmatching to sample (Broersen et al, 1995) and object recognition tests (Aigner et al, 1987;Giovannini et al, 1998;Scali et al, 1994). Furthermore, cognitive-enhancing drugs can increase ACh release in the prefrontal cortex (Scali et al, 1994;Yamamoto et al, 1994) whereas direct application of the muscarinic cholinergic receptor antagonist scopolamine into the frontal cortex (Mouton et al, 1988) or the hippocampus (Messer et al, 1991) impairs working memory. Consistent with these findings, increased ACh release has been demonstrated in the prefrontal cortex during and after performance in a delayed alternation task (Hironaka et al, 2001).…”

Section: A Potential Role Of Da D 3 Receptors In the Effect Of Apds Omentioning

confidence: 99%

Selective Antagonism at Dopamine D3 Receptors Enhances Monoaminergic and Cholinergic Neurotransmission in the Rat Anterior Cingulate Cortex

Lacroix

Hows

Shah

et al. 2002

Neuropsychopharmacol

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Recent neuroanatomical and functional investigations focusing on dopamine (DA) D 3 receptors have suggested a potential role of this receptor in psychiatric diseases such as schizophrenia and drug dependence. In line with the key role of the prefrontal cortex in psychiatric disorders, the present study aimed at assessing the effects of the acute systemic administration of the selective DA D 3 receptor antagonist SB-277011-A on the in vivo extracellular levels of monoamines (DA, norepinephrine (NE), and serotonin (5-HT)) and acetylcholine (ACh) in the anterior cingulate subregion of the medial prefrontal cortex. The in vivo neurochemical profile of SB-277011-A (10 mg/kg, i.p.) in the anterior cingulate cortex was compared with both typical and atypical antipsychotics including clozapine (10 mg/kg, s.c.), olanzapine (10 mg/kg, s.c.), sulpiride (10 mg/kg, s.c.), and haloperidol (0.5 mg/kg, s.c.). The acute administration of SB-277011-A, clozapine, and olanzapine produced a significant increase in extracellular levels of DA, NE, and ACh without affecting levels of 5-HT. Sulpiride also significantly increased extracellular DA, but with a delayed onset over SB-277011-A, clozapine, and olanzapine. In contrast, haloperidol failed to alter any of the three monoamines and ACh in the anterior cingulate cortex. These findings add to a growing body of evidence suggesting a differentiation between typical and atypical antipsychotic drugs (APDs) in the anterior cingulate cortex and a role of DA D 3 receptors in desired antipsychotic drug profile. Similar to their effects on DA and NE, SB-277011-A, clozapine, and olanzapine increased extracellular levels of ACh, whereas haloperidol and sulpiride did not alter ACh. The results obtained in the present study provide evidence of the important role of DA D 3 receptors in the effect of pharmacotherapeutic agents that are used for the treatment of psychiatric disorders such as schizophrenia and drug dependence.

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“…Recently it has been shown that intraventricular infusion of NGF can reduce cholinergic neuron atrophy and improve spatial learning or memory retention in aged rats (Fischer et al, 1987(Fischer et al, , 1991(Fischer et al, , 1994Markowska et al, 1994;Scali et al, 1994). The expression of the low-affinity p75 NGF receptors seems to be intimately linked with these processes, because the immunoreactivity for this receptor is decreased in the basal forebrain of aged rodents (Koh and Loy, 1988;Koh et al, 1989;Markram andSegal, 1990, Fischer et al, 1992).…”

Section: Abstract: Septal Nucleus; Basal Forebrain; Neurotrophic Facmentioning

confidence: 99%

Systemic Administration of a Nerve Growth Factor Conjugate Reverses Age-Related Cognitive Dysfunction and Prevents Cholinergic Neuron Atrophy

et al. 1996

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Intraventricular administration of nerve growth factor (NGF) in rats has been shown to reduce age-related atrophy of central cholinergic neurons and the accompanying memory impairment. Intraventricular administration of NGF is necessary because NGF will not cross the blood-brain barrier (BBB). Here we have used a novel carrier system, consisting of NGF covalently linked to an anti-transferrin receptor antibody (OX-26), to transport biologically active NGF across the BBB. In our experiment, aged (24 months old) Fischer 344 rats received intravenous injections of the OX-26-NGF conjugate or a control solution (a mixture of unconjugated OX-26 and NGF) twice weekly for 6 weeks. The OX-26-NGF injections resulted in a significant improvement in spatial learning in previously impaired rats but disrupted the learning ability of previously unimpaired rats. Neuroanatomical analyses showed that OX-26-NGF conjugate treatment resulted in a significant increase in cholinergic cell size in the medial septal region of rats initially impaired in spatial learning. These results indicate the potential use of the transferrin receptor antibody delivery system for treatment of CNS disorders with neurotrophic proteins.

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Nerve growth factor increases extracellular acetylcholine levels in the parietal cortex and hippocampus of aged rats and restores object recognition

Cited by 75 publications

References 27 publications

Septohippocampal Acetylcholine: Involved in but not Necessary for Learning and Memory?

Septohippocampal Acetylcholine: Involved in but not Necessary for Learning and Memory?

Selective Antagonism at Dopamine D3 Receptors Enhances Monoaminergic and Cholinergic Neurotransmission in the Rat Anterior Cingulate Cortex

Systemic Administration of a Nerve Growth Factor Conjugate Reverses Age-Related Cognitive Dysfunction and Prevents Cholinergic Neuron Atrophy

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