Selective Immunolesion of the Basal Forebrain Cholinergic Neurons: Effects on Hippocampal Activity During Sleep and Wakefulness in the Rat

Bassant, M.H.; Apartis, Emmanuelle; Jazat-Poindessous, F.; Wiley, Ronald G.; Lamour, Y.

doi:10.1006/neur.1995.0007

Cited by 72 publications

(47 citation statements)

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“…Figure 6 summarizes the overall levels of sleep in rats with 192-IgG-Sap lesions. Consistent with previous experiments (Bassant et al, 1995;Kapas et al, 1996), there was no change in overall levels of wake, non-REM sleep, or REM sleep ( Fig. 6; Tables 4, 5).…”

Section: Experiments 2: Evaluation Of Sleep Homeostasissupporting

confidence: 91%

Adenosine and Sleep Homeostasis in the Basal Forebrain

et al. 2006

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It is currently hypothesized that the drive to sleep is determined by the activity of the basal forebrain (BF) cholinergic neurons, which release adenosine (AD), perhaps because of increased metabolic activity associated with the neuronal discharge during waking, and the accumulating AD begins to inhibit these neurons so that sleep-active neurons can become active. This hypothesis grew from the observation that AD induces sleep and AD levels increase with wake in the basal forebrain, but surprisingly it still remains untested. Here we directly test whether the basal forebrain cholinergic neurons are central to the AD regulation of sleep drive by administering 192-IgGsaporin to lesion the BF cholinergic neurons and then measuring AD levels in the BF. In rats with 95% lesion of the BF cholinergic neurons, AD levels in the BF did not increase with 6 h of prolonged waking. However, the lesioned rats had intact sleep drive after 6 and 12 h of prolonged waking, indicating that the AD accumulation in the BF is not necessary for sleep drive. Next we determined that, in the absence of the BF cholinergic neurons, the selective adenosine A 1 receptor agonist N6-cyclohexyladenosine, administered to the BF, continued to be effective in inducing sleep, indicating that the BF cholinergic neurons are not essential to sleep induction. Thus, neither the activity of the BF cholinergic neurons nor the accumulation of AD in the BF during wake is necessary for sleep drive.

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Section: Experiments 2: Evaluation Of Sleep Homeostasissupporting

confidence: 91%

Adenosine and Sleep Homeostasis in the Basal Forebrain

et al. 2006

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“…The effects on total sleep/wake amounts appear to be short lasting or absent (Bassant et al, 1995;Kapas et al, 1996;Gerashchenko et al, 2001;Blanco-Centurion et al, 2006). Starkly discrepant from the present NBM/SI injection results are the normal homeostatic responses to 6 h of SD after complete depletion of both rostral and presumably caudal BF cholinergic neurons (Blanco-Centurion et al, 2006).…”

contrasting

confidence: 83%

“…Nonselective BF lesions increased delta power in the EEG (Buzsaki et al, 1988;Riekkinen et al, 1990Riekkinen et al, , 1991Vanderwolf et al, 1993), whereas lesions highly selective to cholinergic neurons had relatively minor or no effect on spontaneous EEG or sleep-wake states (Bassant et al, 1995;Kapas et al, 1996;Berntson et al, 2002;Blanco-Centurion et al, 2006).…”

Section: Introductionmentioning

confidence: 91%

Effects of Ibotenate and 192IgG-Saporin Lesions of the Nucleus Basalis Magnocellularis/Substantia Innominata on Spontaneous Sleep and Wake States and on Recovery Sleep after Sleep Deprivation in Rats

Kaur¹,

Junek²,

Black³

et al. 2008

J. Neurosci.

115

110

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The basal forebrain (BF) is known for its role in cortical and behavioral activation, and has been postulated to have a role in compensatory mechanisms after sleep loss. However, specific neuronal phenotypes responsible for these roles are unclear. We investigated the effects of ibotenate (IBO) and 192IgG-saporin (SAP) lesions of the caudal BF on spontaneous sleep-waking and electroencephalogram (EEG), and recovery sleep and EEG after 6 h of sleep deprivation (SD). Relative to artificial CSF (ACSF) controls, IBO injections decreased parvalbumin and cholinergic neurons in the caudal BF by 43 and 21%, respectively, and cortical acetylcholinesterase staining by 41%. SAP injections nonsignificantly decreased parvalbumin neurons by 11%, but significantly decreased cholinergic neurons by 69% and cortical acetylcholinesterase by 84%. IBO lesions had no effect on sleep-wake states but increased baseline delta power in all states [up to 62% increase during non-rapid eye movement (NREM) sleep]. SAP lesions transiently increased NREM sleep by 13%, predominantly during the dark phase, with no effect on EEG. During the first 12 h after SD, animals with IBO and SAP lesions showed lesser rebound NREM sleep (32 and 77% less, respectively) and delta power (78 and 53% less) relative to ACSF controls. These results suggest that noncholinergic BF neurons promote cortical activation by inhibiting delta waves, whereas cholinergic BF neurons play a nonexclusive role in promoting wake. Intriguingly, these results also suggest that both types of BF neurons play important roles, probably through different mechanisms, in increased NREM sleep and EEG delta power after sleep loss.

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“…The correspondence between effects of immunolesions of the MS/ VDB and neurotoxic hippocampal lesions on CS processing suggests that cholinergic projections from the MS/ VDB to the hippocampus are involved in regulating certain attentional functions of the hippocampus. One possible mechanism might be via an effect on the amplitude of hippocampal theta rhythm; selective removal of hippocampal cholinergic input does not disrupt the rate of hippocampal theta but does decrease its amplitude dramatically (Jenkins et al, 1993;Lee et al, 1994;Bassant et al, 1995). By this view, cholinergic projections from the MS/ VDB to the hippocampus modulate the processing of information that occurs in the hippocampus itself.…”

Section: Discussionmentioning

confidence: 99%

Disruption of Decrements in Conditioned Stimulus Processing by Selective Removal of Hippocampal Cholinergic Input

1997

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The attention directed to environmental stimuli can be modified by experience. For example, preexposure of a conditioned stimulus (CS) in the absence of reinforcement can retard subsequent conditioning of that stimulus when it is paired directly with an unconditioned stimulus, a phenomenon referred to as latent inhibition. Similarly, consistent pairings of a CS with another event can slow the acquisition of new information about that CS. Such phenomena suggest that reductions in the processing of CSs occur when they are made behaviorally irrelevant or consistent predictors of other events. On the basis of the observation that hippocampal lesions prevented such reductions in CS processing, we hypothesized that damage to basal forebrain cholinergic neurons that project to the hippocampus, using microinjections of the selective immunotoxin 192 IgG-saporin into the medial septum/vertical limb of the diagonal band (MS/VDB), also would disrupt normal reductions in CS processing. Lesions of hippocampal cholinergic input disrupted decreases in CS processing, manifested in both an absence of latent inhibition and a lack of reduced processing of a CS that had been a consistent predictor of another CS. These results indicate that cholinergic neurons in the MS/VDB play a role in the regulation of CS processing. Furthermore, these findings (in conjunction with previous findings) implicate both rostral (hippocampal-projecting) and caudal (corticalprojecting) regions of the basal forebrain cholinergic system in the modulation of attention.

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Selective Immunolesion of the Basal Forebrain Cholinergic Neurons: Effects on Hippocampal Activity During Sleep and Wakefulness in the Rat

Cited by 72 publications

References 0 publications

Adenosine and Sleep Homeostasis in the Basal Forebrain

Adenosine and Sleep Homeostasis in the Basal Forebrain

Effects of Ibotenate and 192IgG-Saporin Lesions of the Nucleus Basalis Magnocellularis/Substantia Innominata on Spontaneous Sleep and Wake States and on Recovery Sleep after Sleep Deprivation in Rats

Disruption of Decrements in Conditioned Stimulus Processing by Selective Removal of Hippocampal Cholinergic Input

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