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Central Modulation of Pain
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
γ-Aminobutyric acid and glycine are involved in tonic inhibition of nociceptive input, and loss of their inhibitory action can result in features of neuropathic pain such as allodynia. Both GABAA and GABAB receptors have been implicated at both pre- and postsynaptic sites. However, GABAA-receptor-mediated inhibition occurs through largely postsynaptic mechanisms. In contrast, GABAB mechanisms may be preferentially involved in presynaptic inhibition via suppression of excitatory amino acid release from primary afferent terminals.
Electrophysiological Studies of 5-Hydroxytryptamine Receptors on Enteric Neurons
Published in T.S. Gaginella, J.J. Galligan, SEROTONIN and GASTROINTESTINAL FUNCTION, 2020
As membrane hyperpolarizations induced by 5-HT1A agonists are never observed in submucosal neurons, it has been suggested that the nerve fibers releasing the mediators of the sEPSP recorded from submucosal AH neurons arise from cell bodies in the myenteric plexus. The assumption is that receptors expressed on the nerve cell body would be expressed on the terminals of these neurons. Hyperpolarization of the nerve terminal would be a mechanism of presynaptic inhibition.47
The Physiology of Pain
Published in Bernard J. Dalens, Jean-Pierre Monnet, Yves Harmand, Pediatric Regional Anesthesia, 2019
Bernard Jacques Dalens, Brigitte Storme
The mechanisms for the inhibition of pain are complex. They can be presynaptic or postsynaptic.28 Both types of inhibitory mechanisms reduce the effectiveness of adjacent excitatory synapses. Presynaptic inhibition is assumed to act by releasing transmitters which depolarize the second terminal ending of the synapse, thus reducing the propagation of nociceptive impulses in a manner similar to the neuromuscular blockade produced by depolarizing muscle relaxants. Inhibition can also be postsynaptic: in most instances, the released transmitters hyperpolarize the postsynaptic terminal;31 this type of inhibition usually applies to inhibitory synapses.
A dopamine D1 receptor agonist improved learning and memory in morphine-treated rats
Published in Neurological Research, 2018
Qiaofeng Liu, Yanxia Li, Yang Liu, Yanshuang Zhao, Xuemei Li, Yiping Zhang, Chenyi Wang, Wenli Huang, Xin Wang
Two mechanisms may explain the effect of GAD67 on learning and memory. First, increasing GAD67 may reduce the neurotoxic effects of excitatory amino acids by increasing the decarboxylation of accumulated extracellular glutamate to generate GABA, thus decreasing glutamate damage to neurons. Excessive glutamate release can cause neurons to become hyperactive in a variety of pathophysiological conditions, leading to degeneration, necrosis, and apoptosis, i.e. neurotoxicity [24]. Second, higher GAD67 levels may have a protective effect on neurons. GAD67 increases GABA production, and GABA can promote a postsynaptic Cl− influx, hyperpolarizing the postsynaptic membrane. This can reduce cell metabolism and oxygen consumption, thereby protecting postsynaptic neurons. Presynaptic inhibition can also reduce the release of glutamate and reduce the neuronal death [25]. Given these findings, increased levels of GAD67 in the PAG may play a role in D1 agonist-induced improvements in learning and memory in addiction.
Intervention effect of gamma aminobutyric acid on anxiety behavior induced by phthalate (2-ethylhexyl ester) in rats
Published in International Journal of Neuroscience, 2018
Huan Liu, Youting Guo, Tongwang Yang, Zhicheng Fan, Minhao Huang, Shuqin Liang, Chunhong Liu
GABA is the most important inhibitory neurotransmitter in mammalian CNS [35]. Receptors of GABA include ionotropic receptors (GABARA and GABARC) and metabotropic receptors (GABARB) [36]. GABA might interfere with neurotoxicity of DEHP in two ways. First, GABA binds to GABARA, alters chloride ion permeability of nerve cell membrane to inhibit postsynaptic potentials, and inhibits nerve cell activity in anxiety state [37]. In addition, Krajnc et al. [38] indicated that GABA might reduce GLU release by presynaptic inhibition, and finally ameliorate anxiety. Second, researches showed that GABA could bind to GABARB with high affinity, and inhibit Ca2+ influx by activating G protein bound in the membrane, leading to presynaptic inhibition of the release of other excitatory neurotransmitters [39–41]. Therefore, anxiety might be alleviated by reduced NOS and NO contents, which might be resulted in by inhibition of Ca2+ influx induced by extrinsic GABA intake.
Presynaptic inhibition in restless legs syndrome
Published in International Journal of Neuroscience, 2021
Şule Aydin Türkoglu, Elif Sultan Bolac, Serpil Yildiz, Oya Kalaycioglu, Nebil Yildiz
Presynaptic inhibition (PreI) is a very strong inhibition mechanism that has frequently been studied; however, its function has not yet been completely clarified. PreI prevents the excessive loading of sensory systems by decreasing an afferent entry to the spinal cord and brain stem [15]. Although PreI is absent at birth, its maturation starts in the first weeks after birth [16]. Researchers have started to discuss spinal cord hyper excitability and pathologies in the etiopathogenesis of patients with RLS in recent years [17–20]. PreI has numerous sources, constitutes inhibitory modulation of monosynaptic reflexes under numerous conditions such as standing, walking and running. PreI is critical to neural control of movement by gating sensory feedback to spinal cord [21].