Effects of some cholinergic agonists on neocortical slow wave activity in rats with basal forebrain lesions

Vanderwolf, C.H.; Raithby, Angela; Snider, Melissa; Cristi, Carolina; Tanner, Carolyn

doi:10.1016/0361-9230(93)90118-u

Cited by 24 publications

(11 citation statements)

References 28 publications

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“…Although they had no effects on behavioral states, IBO lesions (bilateral Ͼ unilateral) robustly increased baseline EEG delta, consistent with previous reports (Buzsaki et al, 1988;Riekkinen et al, 1990Riekkinen et al, , 1991Vanderwolf et al, 1993). We further showed that delta power increased in all states, most prominently during NREM sleep, for at least 27 d postlesion.…”

Section: Discussionsupporting

confidence: 91%

“…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: 93%

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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.

116

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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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 93%

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.

116

110

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“…, 2003). Accordingly, lesions of this region impair performance on tasks designed to test attention, learning and memory (Vanderwolf et al. , 1993; Voytko et al.…”

Section: Introductionmentioning

confidence: 99%

“…As the major source of cholinergic innervation of the neocortex, the BF is well positioned to play an important role in cortical plasticity (Kilgard & Merzenich, 1998;Weinberger, 2003;Conner et al, 2005) and in the processing of sensory information (Linster et al, 2003;Sarter et al, 2003). Accordingly, lesions of this region impair performance on tasks designed to test attention, learning and memory (Vanderwolf et al, 1993;Voytko et al, 1994;Chiba et al, 1995Chiba et al, , 1999Sarter et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Learning‐dependent dynamics of beta‐frequency oscillations in the basal forebrain of rats

Quinn

Nitz

Chiba

2010

Eur J of Neuroscience

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Cholinergic, GABAergic and glutamatergic projection neurons of the basal forebrain (BF) innervate widespread regions of the neocortex and are thought to modulate learning and attentional processes. Although it is known that neuronal cell types in the BF exhibit oscillatory firing patterns, whether the BF as a whole shows oscillatory field potential activity, and whether such neuronal patterns relate to components of cognitive tasks, has yet to be determined. To this end, local field potentials (LFPs) were recorded from the BF of rats performing an associative learning task wherein neutral objects were paired with differently valued reinforcers (pellets). Over time, rats developed preferences for the different objects based on pellet-value, indicating that the pairings had been well learned. LFPs from all rats revealed robust, short-lived bursts of beta-frequency oscillations (∼25 Hz) around the time of object encounter. Beta-frequency LFP events were found to be learning-dependent, with beta-frequency peak amplitudes significantly greater on the first day of the task when object-reinforcement pairings were novel than on the last day when pairings were well learned. The findings indicate that oscillatory bursting field potential activity occurs in the BF in freely behaving animals. Furthermore, the temporal distribution of these bursts suggests that they are probably relevant to associative learning.

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“…Increasing cortical ACh release by electrical stimulation of the basal forebrain of cats or rats (Belardetti et al 1977;Casamenti et al 1986;Metherate and Ashe 1991), or the administration of direct-acting cholinergic agonists in cats or rabbits (Bremer and Chatonnet 1949;Cuculic et al 1968) produces neocortical LVFA. In rats, cholinergic agonists also can reverse the effect of basal forebrain damage on the ECoG (Vanderwolf et al 1993), as can tissue grafts of embryonic basal forebrain tissue placed in the neocortex (Vanderwolf et al 1990b).…”

Section: Introductionmentioning

confidence: 99%

Neocortical activation: modulation by multiple pathways acting on central cholinergic and serotonergic systems

1997

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The present experiments examined the central systems which mediate the electrocorticographic activation induced by electrical stimulation of forebrain and midbrain areas known to play a role in cerebral activation. In urethane-anesthetized rats, 100-Hz electrical stimulation of the amygdaloid cmplex or dorsal raphe changed neocortical electrocorticographic activity from large irregular slow activity (LISA; 1-6 Hz, up to 2 mV) to low voltage fast activity (LVFA; less than 0.5 mV, including frequencies above 10 Hz). The LVFA during amygdala stimulation, but not that during dorsal raphe stimulation, was completely abolished and replaced by LISA after administration of the anti-muscarinic agent scopolamine (5 mg/kg, i.p.), confirming previous work suggesting that neocortical LVFA is maintained by two distinct neurochemical inputs to the cortex that can be dissociated using anti-muscarinic drugs. Electrical stimulation of the locus coeruleus area or of the superior colliculus also suppressed LISA and induced LVFA. The LVFA during stimulation of the locus coeruleus area was abolished by the anti-muscarinic drug atropine (50 mg/kg, i.p.), whereas the LVFA during superior colliculus stimulation was atropine-resistant but could be abolished by the serotonergic antagonists methiothepin (5 mg/kg, i.p.) or ketanserin (5 mg/kg, i.p.). Stimulation of 44% of electrode sites in the orbitofrontal cortex produced neocortical LVFA which was reduced by atropine and completely abolished by additional administration of methiothepin. Stimulation of the entorhinal or cingulate cortex was ineffective in producing LVFA and often resulted in the appearance of epileptiform activity. Single-pulse electrical stimulation of those sites that effectively induced atropine-sensitive LVFA (amygdala, locus coeruleus area) produced excitation of over 65% of those extracellularly recorded basal forebrain neurons that fired at higher rates during the presence of neocortical LVFA relative to LISA. About 80% of basal forebrain cells that were more active during LISA relative to LVFA were inhibited by single-pulse stimulation of the amygdala or locus coeruleus area. The present results suggest that widely distributed neuronal systems can produce electrocorticographic activation by acting through mechanisms sensitive to anti-muscarinic or anti-serotonergic drugs, suggeting that these activating influences involve the release of acetylcholine and/or serotonin. Those neural systems that produce atropine-sensitive (i.e., putative cholinergic) LVFA, believed to be dependent on the cholinergic innervation of the cortex arising in the basal forebrain, may produce electrocorticographic activation by exciting basal forebrain cells that appear to contribute to neocortical LVFA, while concurrently inhibiting cells that may contribute to LISA.

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Effects of some cholinergic agonists on neocortical slow wave activity in rats with basal forebrain lesions

Cited by 24 publications

References 28 publications

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

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

Learning‐dependent dynamics of beta‐frequency oscillations in the basal forebrain of rats

Neocortical activation: modulation by multiple pathways acting on central cholinergic and serotonergic systems

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