 |
|||||
|
|||||
|
|||||
|
|||||
|
|||||
The Journal of Neuroscience, January 9, 2008, 28(2):491-504; doi:10.1523/JNEUROSCI.1585-07.2008
Previous Article | Next Article
Behavioral/Systems/Cognitive
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
Satvinder Kaur, Adrienne Junek, Michelle A. Black, andKazue Semba Department of Anatomy and Neurobiology, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia B3H 1X5, Canada
Correspondence should be addressed to Kazue Semba, Department of Anatomy and Neurobiology, Faculty of Medicine, Dalhousie University, 5850 College Street, Halifax, Nova Scotia B3H 1X5, Canada. Email: semba{at}dal.ca
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.
Key words: basal forebrain; ibotenic acid; 192 IgG-saporin; EEG; waking; recovery sleep
Received April 9, 2007; revised Dec. 1, 2007; accepted Dec. 1, 2007.
Correspondence should be addressed to Kazue Semba, Department of Anatomy and Neurobiology, Faculty of Medicine, Dalhousie University, 5850 College Street, Halifax, Nova Scotia B3H 1X5, Canada. Email: semba{at}dal.ca
This article has been cited by other articles:
O. K. Hassani, M. G. Lee, P. Henny, and B. E. Jones
Discharge Profiles of Identified GABAergic in Comparison to Cholinergic and Putative Glutamatergic Basal Forebrain Neurons across the Sleep-Wake Cycle
J. Neurosci., September 23, 2009; 29(38): 11828 - 11840.
[Abstract] [Full Text] [PDF]
H.-K. Wigren, K.-M. Rytkonen, and T. Porkka-Heiskanen
Basal Forebrain Lactate Release and Promotion of Cortical Arousal during Prolonged Waking Is Attenuated in Aging
J. Neurosci., September 16, 2009; 29(37): 11698 - 11707.
[Abstract] [Full Text] [PDF]
M. M. Methippara, T. Bashir, S. Kumar, N. Alam, R. Szymusiak, and D. McGinty
Salubrinal, an inhibitor of protein synthesis, promotes deep slow wave sleep
Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2009; 296(1): R178 - R184.
[Abstract] [Full Text] [PDF]
F. Espinosa, M. A. Torres-Vega, G. A. Marks, and R. H. Joho
Ablation of Kv3.1 and Kv3.3 Potassium Channels Disrupts Thalamocortical Oscillations In Vitro and In Vivo
J. Neurosci., May 21, 2008; 28(21): 5570 - 5581.
[Abstract] [Full Text] [PDF]
|
|
|
|
 |
|