Basal Forebrain ; Cholinergic Agents ; Cholinergic Neurons ; Humans ; Receptors, Histamine H1 ; Schizophrenia

To investigate whether BF-7, extracted from Bombyx mori, improved learning and memory of ordinary people, Rey-Kim Memory Test was performed with placebo group (32 persons), 200 mg BF-7 treated group (33 persons) and 400 mg BF-7 treated group (34 persons). BF-7 enhanced significantly learning and memory function in a dose-dependent manner. To know how BF-7 plays such a positive role, we measured the concentration of acetylcholine in the brain from memory impairment animal model. Treatment of BF-7 significantly increased the concentration of acetylcholine. So, it is supposed that the protection of cholinergic neuron and/or keeping proper concentration of acetylcholine might be one of the mechanisms by which BF-7 improve brain function. So, our results suggest that the BF-7 is effective material for improving learning and memory ability.
Acetylcholine ; Bombyx ; Brain ; Cholinergic Neurons ; Humans ; Learning* ; Memory* ; Models, Animal

Acetylcholine (ACh) is an important neuromodulator in various cognitive functions. However, it is unclear how ACh influences neural circuit dynamics by altering cellular properties. Here, we investigated how ACh influences reverberatory activity in cultured neuronal networks. We found that ACh suppressed the occurrence of evoked reverberation at low to moderate doses, but to a much lesser extent at high doses. Moreover, high doses of ACh caused a longer duration of evoked reverberation, and a higher occurrence of spontaneous activity. With whole-cell recording from single neurons, we found that ACh inhibited excitatory postsynaptic currents (EPSCs) while elevating neuronal firing in a dose-dependent manner. Furthermore, all ACh-induced cellular and network changes were blocked by muscarinic, but not nicotinic receptor antagonists. With computational modeling, we found that simulated changes in EPSCs and the excitability of single cells mimicking the effects of ACh indeed modulated the evoked network reverberation similar to experimental observations. Thus, ACh modulates network dynamics in a biphasic fashion, probably by inhibiting excitatory synaptic transmission and facilitating neuronal excitability through muscarinic signaling pathways.
Cholinergic Agents/pharmacology* ; Acetylcholine/metabolism* ; Neurons/metabolism* ; Synaptic Transmission/physiology*

beta-amyloid[Abeta] peptide consisting of 40 of 42 amino acids peptide is the principal constituent of senile plaques in Alzheimer`s disease. Recently, it has been demonstrated that this peptide and its constituent fragments are toxic to neuron. Basal forebrain cholinergic neurons are preferentially damaged early in the course of Alzheimer`s disease, and the degree of cholinergic decrement correlates well with the severity of dementia. Taking into consideration of toxic properties of Abeta and the selective vulnerability of the cholinergic system, possible effects of beta-amyloid on the cultured basal forebrain cholinergic neurons were tested. Our result showed tha Abeta1-40 induced marked neurodegenerative changes including loss of cell body and dystrophic neurites in the basal forebrain neuronal cultures at 20micrometer. Immunocytochemical study showed that Abeta1-40 causes apparent loss of choline acetyltransferase[ChAT] immunoreactivity and acetycholine esterase[AchE] positive neuritic intergrity in large basal forebrain cholinegic neurons. However, the number of ChAT immunoreactive neurons was not significantly decreased as compared to other neurons in mixed culture system. These results suggest that the basal forebrain neurons are not particularly vulnearable to Abeta and that preferential injury to basal forebrain cholinergic neurons in Alzheimer`s disease may be caused by some other medchanism.
Amino Acids ; Choline ; Cholinergic Neurons* ; Dementia ; Neurites ; Neurons ; Plaque, Amyloid ; Prosencephalon*

The diagnostic concept of age-associated memory impairment (AAMI) suggests that clinically recognized memory dysfunction could be a feature of normal aging. Although the memory impairment associated with aging is well recognized, underlying neurobiological mechanisms of cognitive decline remain unclear. There are a number of age-related structural and physiological changes in the brain that could have implications for cognitive decline in the elderly. The impact of these age-related changes in the brain on cognition has been studied using postmortem neurochemical, neuropathological findings or neuroimaging techniques. The available evidence from studies in aged and demented humans suggested that cognitive deficits related to aging might involve concomitant alterations of various neurochemical systems in several brain regions such as the striatum, the hippocampus or the cortex. It also seems that these alterations occur in a complex way which affects dopaminergic, glutamaterigc and serotonergic neurotnasmission in addition to the loss of cholinergic neurons in the basal forebrain, However, data collected to explain the mechanism of AAMI are still limited, the definite interpretation of these findings must await futher studies.
Aged ; Aging ; Brain ; Cholinergic Neurons ; Cognition ; Dopamine ; Glutamic Acid ; Hippocampus ; Humans ; Memory* ; Neurobiology* ; Neuroimaging ; Prosencephalon

Acetyl-L-carnitine (ALC), an acetylated form of L-carnitine, is able to influence the activity of cholinergic neurons, cell membrane stabilization and enhancing mitochondrial function. A 52-year-old woman was referred to neurology clinic for memory impairment within 1 year. She was administered ALC as dose of 1,500 mg per day for improving memory decline. After 14 days from administrating ALC, she complained vivid dreams at every night. Vivid dream was disappeared after ceasing ALC. Another patient, a 72-year-old man, visited neurology clinic for cognitive decline for 2 years. After 20 days from administering ALC with dose of 1,500 mg per day, he also suffered from vivid dreams at every night. His previous stable sleep was also restored after ceasing ALC. ALC supplementation may present vivid dreams as a side effect. Possibility of vivid dream as a side effect should be considered during the management with oral ALC.
Acetylcarnitine* ; Aged ; Carnitine ; Cell Membrane ; Cholinergic Neurons ; Dreams* ; Female ; Humans ; Memory ; Middle Aged ; Neurology

OBJECTIVE: To observe the effect of electroacupuncture (EA) at sensitized acupoints on choline acetyltransferase positive (ChAT METHODS: A total of 79 male SD rats were randomized into five groups, i.e. a normal group (20 rats), a normal plus sensitized acupoint group (5 rats), a model group (34 rats), an EA RESULTS: The EB extravasating areas were distributed in the segments from T CONCLUSION The segmental dominance (acupoints) from T
Acupuncture Points ; Animals ; Cholinergic Neurons ; Colon ; Electroacupuncture ; Male ; Rats ; Rats, Sprague-Dawley

BACKGROUND/AIMS: Gastric peristalsis begins in the orad corpus and propagates to the pylorus. Directionality of peristalsis depends upon orderly generation and propagation of electrical slow waves and a frequency gradient between proximal and distal pacemakers. We sought to understand how chronotropic agonists affect coupling between corpus and antrum. METHODS: Electrophysiological and imaging techniques were used to investigate regulation of gastric slow wave frequency by muscarinic agonists in mice. We also investigated the expression and role of cholinesterases in regulating slow wave frequency and motor patterns in the stomach. RESULTS: Both acetycholinesterase (Ache) and butyrylcholine esterase (Bche) are expressed in gastric muscles and AChE is localized to varicose processes of motor neurons. Inhibition of AChE in the absence of stimulation increased slow wave frequency in corpus and throughout muscle strips containing corpus and antrum. CCh caused depolarization and increased slow wave frequency. Stimulation of cholinergic neurons increased slow wave frequency but did not cause depolarization. Neostigmine (1 muM) increased slow wave frequency, but uncoupling between corpus and antrum was not detected. Motility mapping of contractile activity in gastric muscles showed similar effects of enteric nerve stimulation on the frequency and propagation of slow waves, but neostigmine (> 1 muM) caused aberrant contractile frequency and propagation and ectopic pacemaking. CONCLUSIONS: Our data show that slow wave uncoupling is difficult to assess with electrical recording from a single or double sites and suggest that efficient metabolism of ACh released from motor neurons is an extremely important regulator of slow wave frequency and propagation and gastric motility patterns.
Animals ; Cholinergic Neurons ; Cholinesterases* ; Metabolism ; Mice* ; Motor Neurons ; Muscarinic Agonists ; Muscle, Smooth ; Muscles ; Neostigmine ; Peristalsis ; Pylorus ; Stomach

Cholinergic modulation of GABAergic spontaneous miniature inhibitory postsynaptic currents (mIPSCs) by the activation of muscarine receptors was investigated in mechanically dissociated rat nucleus basalis of the Meynert neurons using the conventional whole-cell patch recording configuration. Muscarine (10microM) reversibly and concentration-dependently decreased mIPSC frequency without affecting the current amplitude distribution. Muscarine action on GABAergic mIPSCs was completely blocked by 1microM methoctramine, a selective M2 receptor antagonist, but not by 1microM pirenzepine, a selective M1 receptor antagonist. NEM (10microM), a G-protein uncoupler, attenuated the inhibitory action of muscarine on GABAergic mIPSC frequency. Muscarine still could decrease GABAergic mIPSC frequency even in the Ca2+-free external solution. However, the inhibitory action of muscarine on GABAergic mIPSCs was completely occluded in the presence of forskolin. The results suggest that muscarine acts presynaptically and reduces the probability of spontaneous GABA release, and that such muscarine-induced inhibitory action seems to be mediated by G-protein-coupled M2 receptors, via the reduction of cAMP production. Accordingly, M2 receptor-mediated disinhibition of nBM neurons might play one of important roles in the regulation of cholinergic outputs from nBM neurons as well as the excitability of nBM neurons themselves.
Animals ; Cholinergic Neurons ; Colforsin ; gamma-Aminobutyric Acid ; GTP-Binding Proteins ; Inhibitory Postsynaptic Potentials ; Muscarine* ; Neurons* ; Pirenzepine ; Rats*

gamma-Aminobutyric acid (GABA) has been reported to enhance exocrine secretion evoked not only by secretagogues but also by intrinsic neuronal excitation in the pancreas. The pancreas contains cholinergic neurons abundantly that exert a stimulatory role in exocrine secretion. This study was undertaken to examine effects of GABA on an action of cholinergic neurons in exocrine secretion of the pancreas. Intrinsic neurons were excited by electrical field stimulation (EFS; 15 V, 2 msec, 8 Hz, 45 min) in the isolated, perfused rat pancreas. Tetrodotoxin or atropine was used to block neuronal or cholinergic action. Acetylcholine was infused to mimic cholinergic excitation. GABA (30microM) and muscimol (10microM), given intra-arterially, did not change spontaneous secretion but enhanced cholecystokinin (CCK; 10 pM) -induced secretions of fluid and amylase. GABA (3, 10, 30microM) further elevated EFS-evoked secretions of fluid and amylase dose-dependently. GABA (10, 30, 100microM) also further increased acetylcholine (5microM) -induced secretions of fluid and amylase in a dose-dependent manner. Bicuculline (10microM) effectively blocked the enhancing effects of GABA (30microM) on the pancreatic secretions evoked by either EFS or CCK. Both atropine (2microM) and tetrodotoxin (1microM) markedly reduced the GABA (10microM) -enhanced EFS- or CCK-induced pancreatic secretions. The results indicate that GABA enhances intrinsic cholinergic neuronal action on exocrine secretion via the GABAA receptors in the rat pancreas.
Acetylcholine ; Amylases ; Animals ; Atropine ; Bicuculline ; Cholecystokinin ; Cholinergic Neurons ; gamma-Aminobutyric Acid* ; Muscimol ; Neurons ; Pancreas* ; Rats* ; Receptors, GABA ; Tetrodotoxin