Deficit in Selective and Divided Attention Associated with Cholinergic Basal Forebrain Immunotoxic Lesion Produced by 192-Saporin; Motoric/Sensory Deficit Associated with Purkinje Cell Immunotoxic Lesion Produced by OX7-Saporin

Waite, Jerene J.; Wardlow, M.L.; Power, Ann E.

doi:10.1006/nlme.1998.3884

Cited by 76 publications

(46 citation statements)

References 61 publications

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“…Similarly, McGaughey et al (2002, Exp. 2) found that bilateral infusion of relatively low levels (0.075 μg/hemisphere) of 192IgG-saporin into nBM impaired attention in the 5CSRT, as indicated by reduced accuracy when the density of trials was increased, and Waite et al (1999) found that intraventricular administration of 192IgG-saporin exacerbated the detrimental effects of a number of manipulations thought to affect attention in the 5CSRT task, including reductions in event rate, introduction of distractors, and increasing the array size (number of cue ports).…”

Section: Discussionmentioning

confidence: 99%

Disconnection of the amygdala central nucleus and the substantia innominata/nucleus basalis magnocellularis disrupts performance in a sustained attention task.

Holland

2007

Behavioral Neuroscience

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The basal forebrain cholinergic system is broadly implicated in the regulation of attention. Disruptions in the function of this system produce impairments in many attentional functions, including the performance of well-learned responses under increased attentional load, and the surprise-induced enhancement of learning rate. Similarly, lesions of the amygdala central nucleus (CeA) have been found to impair attentional function in some circumstances. Here we examined the effects of lesions that disconnected CeA from the cholinergic substantia innominata/nucleus basalis magnocellularis (SI/nBM) on performance in a modified five-choice serial reaction time (5CSRT) task, thought to assess selective or sustained attention. The lesions impaired performance under conditions of increased attentional load, suggesting that a circuit that includes CeA and SI/nBM regulates these aspects of attention.

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Section: Discussionmentioning

confidence: 99%

Disconnection of the amygdala central nucleus and the substantia innominata/nucleus basalis magnocellularis disrupts performance in a sustained attention task.

Holland

2007

Behavioral Neuroscience

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“…As one drawback of i.c.v. administration of 192 IgG-saporin is the damage of Purkinje cells in the cerebellum (eg Heckers et al, 1994;Waite et al, 1995) and possible accompanying alterations in sensory-motor function (eg Gandhi et al, 2000, Waite et al, 1999, additional groups with selective lesions of Purkinje cells in the cerebellum were included as controls.…”

Section: Surgerymentioning

confidence: 99%

Combined Damage to Entorhinal Cortex and Cholinergic Basal Forebrain Neurons, Two Early Neurodegenerative Features Accompanying Alzheimer's Disease: Effects on Locomotor Activity and Memory Functions in Rats

Traissard

Herbeaux

Cosquer

et al. 2006

Neuropsychopharmacol

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In Alzheimer's disease (AD), cognitive decline is linked to cholinergic dysfunctions in the basal forebrain (BF), although the earliest neuronal damage is described in the entorhinal cortex (EC). In rats, selective cholinergic BF lesions or fiber-sparing EC lesions may induce memory deficits, but most often of weak magnitude. This study investigated, in adult rats, the effects on activity and memory of both lesions, alone or in combination, using 192 IgG-saporin (OX7-saporin as a control) and L-N-methyl-D-aspartate to destroy BF and EC neurons, respectively. Rats were tested for locomotor activity in their home cage and for working-and/or reference-memory in various tasks (water maze, Hebb-Williams maze, radial maze). Only rats with combined lesions showed diurnal and nocturnal hyperactivity. EC lesions impaired working memory and induced anterograde memory deficits in almost all tasks. Lesions of BF cholinergic neurons induced more limited deficits: reference memory was impaired in the probe trial of the water-maze task and in the radial maze. When both lesions were combined, performance never improved in the water maze and the number of errors in the Hebb-Williams and the radial mazes was always larger than in any other group. These results (i) indicate synergistic implications of BF and EC in memory function, (ii) suggest that combined BF cholinergic and fiber-sparing EC lesions may model aspects of anterograde memory deficits and restlessness as seen in AD, (iii) challenge the cholinergic hypothesis of cognitive dysfunctions in AD, and (iv) contribute to open theoretical views on AD-related memory dysfunctions going beyond the latter hypothesis.

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“…These impairments may be due to effects on motor performance or other variables rather than effects on memory (Waite et al 1999;Lehmann et al 2000). Intraventricular 192 IgG-saporin lesions not only damage basal forebrain cholinergic neurons, but also cerebellar Purkinje cells Waite et al 1995), and the motor impairments following cerebellar damage are severe (Berger-Sweeney et al 1994;Waite et al 1995Waite et al , 1999. They are also dependent on the dose of 192 IgG-saporin (Waite et al 1995), as would be expected if the neurotoxic action of the immunotoxin is mediated via an influence on cell populations outside the basal forebrain.…”

Section: Lesions Of the Medial Septum Or Its Projectionsmentioning

confidence: 99%

“…192 IgG-saporin with those of i.c.v. OX7-saporin, a toxin that damages cerebellar Purkinje cells but not basal forebrain cholinergic neurons (Waite et al 1999;Wrenn and Wiley 2001). OX7-saporin lesions themselves can produce severe impairments in memory as well as in motor and sensory abilities (Waite et al 1999;Gandhi et al 2000).…”

Section: Lesions Of the Medial Septum Or Its Projectionsmentioning

confidence: 99%

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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Deficit in Selective and Divided Attention Associated with Cholinergic Basal Forebrain Immunotoxic Lesion Produced by 192-Saporin; Motoric/Sensory Deficit Associated with Purkinje Cell Immunotoxic Lesion Produced by OX7-Saporin

Cited by 76 publications

References 61 publications

Disconnection of the amygdala central nucleus and the substantia innominata/nucleus basalis magnocellularis disrupts performance in a sustained attention task.

Disconnection of the amygdala central nucleus and the substantia innominata/nucleus basalis magnocellularis disrupts performance in a sustained attention task.

Combined Damage to Entorhinal Cortex and Cholinergic Basal Forebrain Neurons, Two Early Neurodegenerative Features Accompanying Alzheimer's Disease: Effects on Locomotor Activity and Memory Functions in Rats

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

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