Integrated physiology of the lower urinary tract
Jacques Corcos, David Ginsberg, Gilles Karsenty in Textbook of the Neurogenic Bladder, 2015
The micturition reflex can be modulated at the level of the spinal cord by interneuronal mechanisms activated by afferent input from cutaneous and striated muscle targets. The micturition reflex can also be modulated by inputs from other visceral organs.1,4,7,73,84,107–110 Stimulation of afferent fibers from various regions (anus, colon/rectum, vagina, uterine cervix, penis, perineum, and pudendal nerve) can inhibit the firing of sacral interneurons evoked by bladder distension.83 This inhibition may occur as a result of presynaptic inhibition at primary afferent terminals or because of direct postsynaptic inhibition of the second-order neurons. Direct postsynaptic inhibition of bladder PGN can also be elicited by stimulation of somatic afferent axons in the pudendal nerve or by visceral afferents from the distal bowel.108,111
Pathophysiology of Spasticity
Anand D. Pandyan, Hermie J. Hermens, Bernard A. Conway in Neurological Rehabilitation, 2018
In both human and animal experiments, presynaptic inhibition has been found to be strongly regulated by supraspinal control centres (Burke 2012, Meunier 1999, Rudomin et al. 2004). During voluntary movement including locomotion presynaptic inhibition is turned into a highly focused modulatory mechanism that shapes the sensory inflow to spinal motoneurons and interneurons according to the needs of the given task and the central command (Dietz et al. 1990, Faist et al. 1996). Activation of some muscles may thereby be facilitated by removing presynaptic inhibition of the sensory afferents, while ensuring that unwanted activation of other muscles (such as antagonists) does not take place (Crone and Nielsen 1989b, Hultborn et al. 1987, Nielsen and Kagamihara 1993). This regulation of presynaptic inhibition in relation to voluntary movement is of significance for the functional relevance of spasticity and will be further described in Chapter 3.
The Physiology of Pain
Bernard J. Dalens, Jean-Pierre Monnet, Yves Harmand in Pediatric Regional Anesthesia, 2019
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.
Short-term effects of spinal thrust joint manipulation on postural sway in patients with chronic mechanical neck pain: a randomized controlled trial
Published in Disability and Rehabilitation, 2022
Raúl Romero del Rey, Manuel Saavedra Hernández, Cleofás Rodríguez Blanco, Luis Palomeque del Cerro, Raquel Alarcón Rodríguez
In this respect, the cervical spine is of great importance [12]. Firstly, this is because the cervical musculature is a major source of proprioceptive information, especially the suboccipital muscles, which contain a large number of mechanoreceptors [13]. In addition, these muscles also have relationships with the central nervous system, vestibular system and visual system [10], which explains why a proprioceptive information disorder in the cervical spine may affect sensory integration [13]. On the other hand, pain may be the cause of an increase in presynaptic inhibition of muscular input and may affect the central sensory modulation of proprioceptive information that comes from neuromuscular spindles [14]. As a result, this may cause a decrease in motor control, and subsequently, a decrease in postural stability.
Related Knowledge Centers
- Action Potential
- Axon Terminal
- Membrane Potential
- Synaptic Vesicle
- Cannabinoid
- Neuron
- Axo-Axonic Synapse
- Γ-Aminobutyric Acid
- Retrograde Signaling
- Cannabinoid Receptor 1