| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
The Journal of Neurophysiology Vol. 87 No. 2 February 2002, pp. 696-704
Copyright ©2002 by the American Physiological Society
Division of Neurology, Department of Medicine, University of Alberta, Edmonton, Alberta T6G 2S2, Canada
Jhamandas, Jack H.,
Kim H. Harris,
David MacTavish, and
Balvinder S. Jassar.
Novel Excitatory Actions of Galanin on Rat Cholinergic Basal
Forebrain Neurons: Implications for Its Role in Alzheimer's
Disease. J. Neurophysiol. 87: 696-704, 2002. Galanin, a 29-amino-acid neuropeptide, is generally viewed as an
inhibitory neuromodulator in a variety of central systems. Galanin
expression is upregulated in the cholinergic basal forebrain nuclei in
Alzheimer's disease (AD) and is postulated to play an important role
in memory and cognitive function. In this study, application of galanin
to acutely dissociated rat neurons from the basal forebrain nucleus
diagonal band of Broca (DBB), caused a decrease in whole cell
voltage-activated currents in a majority of cells. Galanin reduces a
suite of potassium currents, including calcium-activated potassium
(IC), the delayed rectifier
(IK), and transient outward potassium
(IA) conductances, but not calcium or
sodium currents. Under current-clamp conditions, application of galanin
evoked an increase in excitability and a loss of accommodation in
cholinergic DBB neurons. Using single-cell RT-PCR technique, we
determined that galanin actions were specific to cholinergic, but not
GABAergic DBB neurons The notion that galanin plays a deleterious role
in AD is based, in part, on galanin hyperinnervation of cholinergic
cells in the basal forebrain of AD patients, its ability to depress
acetylcholine release and its inhibitory actions at other CNS sites.
However, our results suggest that by virtue of its excitatory actions
on cholinergic neurons, galanin may in fact play a compensatory role by
augmenting the release of acetylcholine from remaining cholinergic
basal forebrain neurons. This action might serve to delay the
progression of AD pathology linked to a reduction in central
cholinergic tone.
This article has been cited by other articles:
|
|
 |
|
  C. Hawkes, J. H. Jhamandas, K. H. Harris, W. Fu, R. G. MacDonald, and S. Kar Single Transmembrane Domain Insulin-Like Growth Factor-II/Mannose-6-Phosphate Receptor Regulates Central Cholinergic Function by Activating a G-Protein-Sensitive, Protein Kinase C-Dependent Pathway J. Neurosci., January 11, 2006; 26(2): 585 - 596. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. K. Robinson Galanin and Cognition Behav Cogn Neurosci Rev, December 1, 2004; 3(4): 222 - 242. [Abstract] [PDF]
|
|
|
|
 |
|
 J. H. Jhamandas, K. H. Harris, C. Cho, W. Fu, and D. MacTavish Human Amylin Actions on Rat Cholinergic Basal Forebrain Neurons: Antagonism of Beta-Amyloid Effects J Neurophysiol, June 1, 2003; 89(6): 2923 - 2930. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. E. Counts, S. E. Perez, S. D. Ginsberg, S. de Lacalle, and E. J. Mufson Galanin in Alzheimer Disease Mol. Interv., May 1, 2003; 3(3): 137 - 156. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. H. Chin, K. Harris, D. MacTavish, and J. H. Jhamandas Nociceptin/Orphanin FQ Modulation of Ionic Conductances in Rat Basal Forebrain Neurons J. Pharmacol. Exp. Ther., October 1, 2002; 303(1): 188 - 195. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Basheer, E. Arrigoni, H. S. Thatte, R. W. Greene, I. S. Ambudkar, and R. W. McCarley Adenosine Induces Inositol 1,4,5-Trisphosphate Receptor-Mediated Mobilization of Intracellular Calcium Stores in Basal Forebrain Cholinergic Neurons J. Neurosci., September 1, 2002; 22(17): 7680 - 7686. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
