Pharmacological but not physiological modulation of cortical acetylcholine release by cholinergic mechanisms in the nucleus basalis magnocellularis

1994 ◽  
Vol 72 (8) ◽  
pp. 893-898 ◽  
Author(s):  
J. C. Szerb ◽  
K. Clow ◽  
D. D. Rasmusson
Keyword(s):  
Acetylcholine Release ◽  
Cholinergic Neurons ◽  
Nucleus Basalis ◽  
Nucleus Basalis Magnocellularis ◽  
Ach Release ◽  
Microdialysis Probe ◽  
Release Of Acetylcholine ◽  
Presynaptic Muscarinic Receptors ◽  
Excitatory Transmitter

The role of muscarinic transmission in the activation of cholinergic neurons ascending to the neocortex from the nucleus basalis magnocellularis (NBM) was investigated. The release of acetylcholine (ACh) from the neocortex of urethane-anesthetized rats was measured using microdialysis, and a second microdialysis probe was inserted into the NBM to apply drugs to the NBM and to measure ACh release from this area. Cholinergic neurons in the NBM were activated synaptically by stimulating the pedunculopontine tegmentum (PPT). Systemically administered scopolamine greatly increased the PPT stimulation evoked cortical release of ACh when the cortical probe was perfused with the cholinesterase inhibitor neostigmine. PPT stimulation evoked release was also high when the cortical probe was perfused with atropine plus neostigmine, but it was not increased any further by systemic scopolamine or by scopolamine perfused through the NBM probe. When neostigmine was perfused through the NBM probe, PPT stimulation evoked cortical ACh release was halved, but the release was restored when the NBM solution also contained scopolamine. The resting release of ACh within the NBM was increased by local neostigmine, but evoked release in the NBM was large only in the presence of local scopolamine. Both of these increases were blocked by perfusion of the NBM with tetrodotoxin. These results suggest that muscarinic transmission within the NBM does not control the activation of cholinergic neurons under physiological conditions, when the diffusion of ACh is limited by its hydrolysis. However, when ACh is allowed to diffuse to a wider area, it may inhibit the release of an excitatory transmitter, probably glutamate, via presynaptic muscarinic receptors.Key words: acetylcholine release, nucleus basalis magnocellularis, pedunculopontine tegmentum, presynaptic muscarinic receptors, microdialysis.

Vasoactive intestinal polypeptide provokes acetylcholine release from the myenteric plexus

1986 ◽  
Vol 251 (1) ◽  
pp. G51-G55 ◽  
Author(s):  
M. Kusunoki ◽  
L. H. Tsai ◽  
K. Taniyama ◽  
C. Tanaka
Keyword(s):  
Vasoactive Intestinal Polypeptide ◽  
Myenteric Plexus ◽  
Acetylcholine Release ◽  
Longitudinal Muscle ◽  
Cholinergic Neurons ◽  
Ach Release ◽  
Perfusion Medium ◽  
Release Of Acetylcholine ◽  
Stimulation Of ◽  
Intestinal Polypeptide

Effects of vasoactive intestinal polypeptide (VIP) on the release of acetylcholine (ACh) from longitudinal muscle strips with myenteric plexus (LM) preparations were examined in the guinea pig small intestine. VIP (10(-10) to 10(-6) M) induced a concentration-dependent contraction of LM preparation. The VIP-induced contractions seem to be related to three components, the scopolamine-sensitive, the scopolamine-insensitive, the tetrodotoxin-sensitive, and the tetrodotoxin-insensitive contractions. VIP (10(-10) to 10(-6) M) induced a concentration-dependent increase in the release of [3H]ACh from LM preparations preloaded with [3H]choline. The VIP-evoked [3H]ACh release was inhibited by removal of Ca2+ from the perfusion medium and by treatment with tetrodotoxin but not by scopolamine and hexamethonium. The spontaneous and VIP-evoked [3H]ACh release was not affected by phentolamine, propranolol, methysergide, diphenhydramine, cimetidine, bicuculline, or [D-Pro2, D-Trp7,9]substance P. The result demonstrates that VIP induces contractions of longitudinal smooth muscle directly and indirectly by the stimulation of both cholinergic neurons and noncholinergic excitatory neurons.

Effects of altered cholinergic function on working and reference memory in the rat

1986 ◽  
Vol 64 (3) ◽  
pp. 376-382 ◽  
Author(s):  
Richard J. Beninger ◽  
B. A. Wirsching ◽  
Khem Jhamandas ◽  
Roland J. Boegman ◽  
Sherif R. El-Defrawy
Keyword(s):  
Working Memory ◽  
Choline Acetyltransferase ◽  
Radial Maze ◽  
Cholinergic Neurons ◽  
Reference Memory ◽  
Nucleus Basalis ◽  
Nucleus Basalis Magnocellularis ◽  
Memory Errors ◽  
Biochemical Assays ◽  
Alternation Task

Many data suggest that the brain's cholinergic neurons participate in the control of memory and it has been suggested that cholinergic systems are involved differentially in working and reference memory. To test this hypothesis the effects on memory of unilateral injections of the neurotoxins, quinolinic acid or kainic acid into the cortically projecting cholinergic cells of the nucleus basalis magnocellularis (nbm) were evaluated. In experiment 1, quinolinate-injected (n = 7) and sham-operated (n = 7) rats were tested in a T-maze alternation task that requires working memory. Lesion rats performed significantly more poorly than shams and subsequent biochemical assays of cortical choline acetyltransferase (CAT) activity revealed significant reductions in the lesion rats. In experiment 2, kainate-injected (n = 9) and sham-operated (n = 8) rats were trained in an eight-arm radial maze with only four arms baited. Lesion rats made significantly more working memory errors (entries into baited arms from which the food had already been collected) than reference memory errors (entries into never baited arms). CAT assays showed that the lesion led to a decrease in cortical CAT with no significant change in hippocampal CAT. The results of these studies support the hypothesis that cholinergic neurons of the basocortical system may be differentially involved in working and reference memory.

Origin and modulation of ACh release from rat airway cholinergic nerves

1997 ◽  
Vol 272 (1) ◽  
pp. L8-L14 ◽  
Author(s):  
F. X. Zhu ◽  
X. Y. Zhang ◽  
N. E. Robinson
Keyword(s):  
Synaptic Vesicles ◽  
High Performance ◽  
Electrical Field Stimulation ◽  
Cyclooxygenase Inhibitors ◽  
Ach Release ◽  
Electrical Field ◽  
Parasympathetic Nerves ◽  
Release Of Acetylcholine ◽  
Rat Trachea

The release of acetylcholine (ACh) from airway parasympathetic nerves was studied in rat trachea. We established stimulus parameters, examined the role of extracellular Ca2+, and investigated the origin of the released ACh by use of vesamicol, an inhibitor of ACh uptake in synaptic vesicles. The role of muscarinic autoreceptors and prostanoids on ACh release was also studied. Tracheal rings were incubated in Krebs-Henseleit solution containing neostigmine and guanethidine with or without atropine. ACh release was measured by high-performance liquid chromatography with electrochemical detection. ACh release was dependent on frequency (0.5-16 Hz), voltage (10-25 V), and pulse duration (0.5-4 ms). At 4 Hz, one-fifth of electrical field stimulation-induced ACh release was extracellular Ca2+ independent and vesamicol resistant, indicating its nonvesicular origin. Three-fifths were Ca2+ dependent and vesamicol sensitive, indicating that it was newly synthesized, and one-fifth was Ca2+ dependent but vesamicol resistant, indicating its origin from prestored vesicles. At 16 Hz, two-fifths were nonvesicular and three-fifths were newly synthesized. Blockade of the muscarinic autoreceptor by atropine potentiated the release of ACh four- to fivefold. Neither of the cyclooxygenase inhibitors indomethacin or meclofenamate nor exogenous prostaglandin E2 affected ACh release, indicating that inhibitory prostanoids do not modulate ACh release.

Effects of Ca2+ channel antagonists on nerve stimulation-induced and ischemia-induced myocardial interstitial acetylcholine release in cats

2006 ◽  
Vol 291 (5) ◽  
pp. H2187-H2191 ◽  
Author(s):  
Toru Kawada ◽  
Toji Yamazaki ◽  
Tsuyoshi Akiyama ◽  
Kazunori Uemura ◽  
Atsunori Kamiya ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Acetylcholine Release ◽  
Local Administration ◽  
Ach Release ◽  
Parasympathetic Nerve ◽  
Nonselective Cation Channels ◽  
Voltage Dependent ◽  
Stretch Activated Channels ◽  
Postganglionic Nerve

Although an axoplasmic Ca2+ increase is associated with an exocytotic acetylcholine (ACh) release from the parasympathetic postganglionic nerve endings, the role of voltage-dependent Ca2+ channels in ACh release in the mammalian cardiac parasympathetic nerve is not clearly understood. Using a cardiac microdialysis technique, we examined the effects of Ca2+ channel antagonists on vagal nerve stimulation- and ischemia-induced myocardial interstitial ACh releases in anesthetized cats. The vagal stimulation-induced ACh release [22.4 nM (SD 10.6), n = 7] was significantly attenuated by local administration of an N-type Ca2+ channel antagonist ω-conotoxin GVIA [11.7 nM (SD 5.8), n = 7, P = 0.0054], or a P/Q-type Ca2+ channel antagonist ω-conotoxin MVIIC [3.8 nM (SD 2.3), n = 6, P = 0.0002] but not by local administration of an L-type Ca2+ channel antagonist verapamil [23.5 nM (SD 6.0), n = 5, P = 0.758]. The ischemia-induced myocardial interstitial ACh release [15.0 nM (SD 8.3), n = 8] was not attenuated by local administration of the L-, N-, or P/Q-type Ca2+ channel antagonists, by inhibition of Na+/Ca2+ exchange, or by blockade of inositol 1,4,5-trisphosphate [Ins( 1 , 4 , 5 )P3] receptor but was significantly suppressed by local administration of gadolinium [2.8 nM (SD 2.6), n = 6, P = 0.0283]. In conclusion, stimulation-induced ACh release from the cardiac postganglionic nerves depends on the N- and P/Q-type Ca2+ channels (with a dominance of P/Q-type) but probably not on the L-type Ca2+ channels in cats. In contrast, ischemia-induced ACh release depends on nonselective cation channels or cation-selective stretch activated channels but not on L-, N-, or P/Q type Ca2+ channels, Na+/Ca2+ exchange, or Ins( 1 , 4 , 5 )P3 receptor-mediated pathway.

scholarly journals Degeneration of the Basalocortical Pathway from the Cortex Induces a Functional Increase in Galaninergic Markers in the Nucleus Basalis Magnocellularis of the Rat

2004 ◽  
Vol 24 (11) ◽  
pp. 1255-1266 ◽  
Author(s):  
Alexandra Barbelivien ◽  
Claire Vaussy ◽  
Yannick Marchalant ◽  
Eric Maubert ◽  
Nathalie Bertrand ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Muscarinic Receptors ◽  
Acetylcholine Release ◽  
Cortical Activity ◽  
Nucleus Basalis ◽  
Nucleus Basalis Magnocellularis ◽  
Ischemic Lesion

The present work aimed 1) to evaluate whether an increase in galanin or galanin receptors could be induced in the nucleus basalis magnocellularis (nbm) by degeneration of the basalocortical neurons from the cortex and 2) to analyze the consequences of such an increase on cortical activity. First, a mild ischemic insult to the frontoparietal cortex was performed to induce the degeneration of the basalocortical system; galanin immunoreactivity, galanin binding sites, and cholinergic muscarinic receptors were quantified through immunocytochemistry and autoradiography. Second, galanin infusions in the nbm were undertaken to mimic a local increase of the galaninergic innervation; cortical acetylcholine release, cerebral glucose use, and cerebral blood flow were then measured as indices of cortical activity. As a result of the cortical ischemic lesion, the postsynaptic M1 and presynaptic M2 muscarinic receptors were found to be reduced in the altered cortex. In contrast, galaninergic binding capacity and fiber density were found to be increased in the ipsilateral nbm in parallel with a local decrease in the cholinergic markers such as the muscarinic M1 receptor density. Galanin infusion into the nbm inhibited the cortical acetylcholine release and cerebral blood flow increases elicited by the activation of the cholinergic basalocortical system but failed to affect acetylcholine release, cerebral blood flow, and cerebral glucose use when injected alone in the nbm. These results demonstrate that degeneration of the basalocortical system from the cortex induces an increase in galaninergic markers in the nbm, a result that might suggest that the galaninergic overexpression described in the basal forebrain of patients with Alzheimer's disease can result from a degeneration of the cholinergic basalocortical system from the cortex. Because galanin was found to reduce the activity of the basalocortical cholinergic system only when this one is activated, galanin might exert its role rather during activation deficits than under resting conditions such as the resting cortical hypometabolism, which is characteristic of Alzheimer's disease.

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