Targeting the Nervous System
Nathan Keighley in Miraculous Medicines and the Chemistry of Drug Design, 2020
Where two neurones meet at a synapse, the nerve impulse is interrupted because there is a gap between the neurones, called the synaptic cleft. In order for the signal travelling down the presynaptic neurone to be continued, it must be propagated in the postsynaptic neurone across the synapse via neurotransmitters, such as acetylcholine. Neurotransmitters are molecules that, upon activation by an action potential, are released from the presynaptic neurone into the synaptic cleft. The neurotransmitter molecules diffuse across the gap and bind to receptors on the postsynaptic neurone, causing a chain of reactions that result in the propagation of the action potential in the postsynaptic nerve and the signal can proceed to its final destination. The actions of the neurotransmitter acetylcholine are instrumental in the operation of the cholinergic nervous system.
The Nervous System and Its Disorders
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss in Understanding Medical Terms, 2020
Transmission from one neuron to another follows a similar course. As an impulse moving down the axon of one neuron reaches the presynaptic terminal (the end before [pre-] the synapse), a neurotransmitter is released into the synapse so it can attach to a receptor on a dendrite of the next nerve. In the neuromuscular junction, the transmitter is always acetylcholine; between nerves, however, the transmitter can excite the next nerve or inhibit it. In the central nervous system, the primary excitatory neurotransmitter is acetylcholine, so these nerves and those that stimulate muscles comprise what is called the cholinergic system (literally, "responding to choline," but actually referring to acetylcholine).
Phytochemistry and pharmacology of component herbs of Shengmai San
Kam-Ming Ko in Shengmai San, 2002
It was suggested that the learning and memory processes are mediated by the central cholinergic systems. Ginsenosides Rb1 and Rg1 have been shown to prevent scopolamine-induced memory deficits in rats by facilitating acetylcholine release from rat brain hippocampal slices and increasing cholinergic activity (Benishin et al. 1992; Yamaguchi et al. 1995). Intraperitoneal administration of ginsenoside Rg1 at a dose of 10 mg/kg to rats enhanced the discrimination between two sounds. It also stimulated the exploratory behavior in rats (Shibata et al. 1985). Recently, Lee et al. (2000) showed that repeated administration of Ginseng total saponins ameliorated the impairing effect of ethanol on acquisition, and the effect of the saponins on ethanol-induced amnesia was dependent on the catecholaminergic, but not serotonergic, neuronal activity. Intraperitoneal administration of Ginseng saponins with low ratios of protopanaxadiol and protopanaxatriol saponin at doses of 50 and 100 mg/kg respectively, also improved scopolamine-induced learning disability and spatial working memory in mice (Jin et al. 1999).
Shaddock (Citrus maxima) peels extract restores cognitive function, cholinergic and purinergic enzyme systems in scopolamine-induced amnesic rats
Published in Drug and Chemical Toxicology, 2022
Ayokunle O. Ademosun, Adeniyi A. Adebayo, Temitope V. Popoola, Ganiyu Oboh
Activities of cholinergic neurotransmitters (acetylcholine and butyrylcholine) are regulated by cholinesterases. Cholinergic system in the central nervous system (CNS) are widely known to play crucial roles in the cognition and memory process (Marisco et al.2013, Hashimoto et al.2014). Studies have related impaired cholinergic system to dementia and other cognitive-related disorder, thus implicating the central cholinergic neurons in the cognitive process (Schliebs and Arendt 2006, Marisco et al.2013, Hashimoto et al.2014, Akinyemi et al.2017). A decrease in (essential) neurotransmitters level causes loss of dissemination of information from the brain and to other parts of the body which results in cognitive impairment. The result revealed that shaddock peels extract administration ameliorated memory dysfunction in scopolamine-treated rats as observed by an improvement of the cholinergic neurotransmitters through inhibition of cholinesterase (AChE and BChE) activities. AChE and BChE inactivate the neurotransmitter acetylcholine (ACh) and are thus viable therapeutic targets in cognitive disorder (Schliebs and Arendt 2006). ACh is a neurotransmitter release from cholinergic neurons, and it has been implicated in cognitive and behavioral functions that are widely disturbed in cognitive-related disorders (Soreq and Seidman 2001, Thanvi and Lo 2004).
Protective effects of cerebrolysin against chemotherapy (carmustine) induced cognitive impairment in Albino mice
Published in Drug and Chemical Toxicology, 2022
Suraj Sharma, Khadga Raj, Shamsher Singh
The cholinergic system plays a crucial role in modulating diverse functions, including cognition, attention, arousal, learning, and memory (Solari and Hangya 2018). Impaired cholinergic transmission is one of the factors implicated in the etiopathogenesis of memory deficit in AD. The destruction of cholinergic neurons and axonal defects lead to reduced release of acetylcholine resulting in cognitive decline. In the present study, the BCNU-treated group showed memory impairment and reduced cognitive ability, which indicates that there were altered levels of Ach, glutamate, and GABA. Treatment with CBN significantly attenuated the BCNU-induced memory impairment and restored neurotransmitters concentration in the brain, which are analyzed by HPLC-ECD. Taken together, our data suggested that CBN restored ACh, GABA levels and decreases glutamate levels indicate its neuroprotective properties.
Nicotine intoxication by e-cigarette liquids: a study of case reports and pathophysiology
Published in Clinical Toxicology, 2020
Gerdinique C. Maessen, Anjali M. Wijnhoven, Rosalie L. Neijzen, Michelle C. Paulus, Dayna A. M. van Heel, Bart H. A. Bomers, Lucie E. Boersma, Burak Konya, Marcel A. G. van der Heyden
The described seizures and myoclonus have two possible explanations, depending on a physician’s definition of these terms. First, nicotinic cholinergic receptors are, besides paravertebrally, situated at the neuromuscular junction. Nicotine acts as a substitute for acetylcholine and as such stimulates more rapid depolarisation of the muscle fibres. In high concentrations, it can induce involuntary contraction of the muscles, even resulting in seizure-like movements [47]. Second, at very high dosage, nicotine can cause epileptic activity in the brain. This mechanism is not yet fully understood, but may be related to desensitisation of the cholinergic receptors after prolonged exposure. The cholinergic receptors in the central nervous system normally stimulate GABAergic interneurons, which in turn have an inhibitory effect on the pyramidal cells. A decrease in cholinergic receptors reduces the GABAergic activity and has an excitatory effect on the pyramidal cells, resulting in seizure [48,49]. The desensitisation of the nicotinic cholinergic receptors eventually induces a similar effect at the neuromuscular junction. Lengthened exposure to nicotine leads to a reduction in available receptors at the muscle cell membrane, followed by decreased cell depolarisation. In this way, partial or complete muscle paralysis may occur [16].
Related Knowledge Centers
- Butyrylcholine
- Choline
- Lecithin
- Sympathetic Nervous System
- Neurotransmitter
- Parasympathetic Nervous System
- Acetylcholine
- Inositol
- Quaternary Ammonium Cation
- Ion