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A neurotransmitter is a signaling molecule secreted by a neuron to affect another cell across a synapse. The cell receiving the signal,or target cell,may be another neuron,but could also be a gland or muscle cell.
Chemical synapses are biological junctions through which neurons' signals can be sent to each other and to non-neuronal cells such as those in muscles or glands. Chemical synapses allow neurons to form circuits within the central nervous system. They are crucial to the biological computations that underlie perception and thought. They allow the nervous system to connect to and control other systems of the body.
In neuroscience,synaptic plasticity is the ability of synapses to strengthen or weaken over time,in response to increases or decreases in their activity. Since memories are postulated to be represented by vastly interconnected neural circuits in the brain,synaptic plasticity is one of the important neurochemical foundations of learning and memory.
An inhibitory postsynaptic potential (IPSP) is a kind of synaptic potential that makes a postsynaptic neuron less likely to generate an action potential. The opposite of an inhibitory postsynaptic potential is an excitatory postsynaptic potential (EPSP),which is a synaptic potential that makes a postsynaptic neuron more likely to generate an action potential. IPSPs can take place at all chemical synapses,which use the secretion of neurotransmitters to create cell-to-cell signalling. EPSPs and IPSPs compete with each other at numerous synapses of a neuron. This determines whether an action potential occurring at the presynaptic terminal produces an action potential at the postsynaptic membrane. Some common neurotransmitters involved in IPSPs are GABA and glycine.
In neuroscience,an excitatory postsynaptic potential (EPSP) is a postsynaptic potential that makes the postsynaptic neuron more likely to fire an action potential. This temporary depolarization of postsynaptic membrane potential,caused by the flow of positively charged ions into the postsynaptic cell,is a result of opening ligand-gated ion channels. These are the opposite of inhibitory postsynaptic potentials (IPSPs),which usually result from the flow of negative ions into the cell or positive ions out of the cell. EPSPs can also result from a decrease in outgoing positive charges,while IPSPs are sometimes caused by an increase in positive charge outflow. The flow of ions that causes an EPSP is an excitatory postsynaptic current (EPSC).
In neurophysiology,long-term depression (LTD) is an activity-dependent reduction in the efficacy of neuronal synapses lasting hours or longer following a long patterned stimulus. LTD occurs in many areas of the CNS with varying mechanisms depending upon brain region and developmental progress.
An excitatory synapse is a synapse in which an action potential in a presynaptic neuron increases the probability of an action potential occurring in a postsynaptic cell. Neurons form networks through which nerve impulses travels,each neuron often making numerous connections with other cells of neurons. These electrical signals may be excitatory or inhibitory,and,if the total of excitatory influences exceeds that of the inhibitory influences,the neuron will generate a new action potential at its axon hillock,thus transmitting the information to yet another cell.
Neuropharmacology is the study of how drugs affect function in the nervous system,and the neural mechanisms through which they influence behavior. There are two main branches of neuropharmacology:behavioral and molecular. Behavioral neuropharmacology focuses on the study of how drugs affect human behavior (neuropsychopharmacology),including the study of how drug dependence and addiction affect the human brain. Molecular neuropharmacology involves the study of neurons and their neurochemical interactions,with the overall goal of developing drugs that have beneficial effects on neurological function. Both of these fields are closely connected,since both are concerned with the interactions of neurotransmitters,neuropeptides,neurohormones,neuromodulators,enzymes,second messengers,co-transporters,ion channels,and receptor proteins in the central and peripheral nervous systems. Studying these interactions,researchers are developing drugs to treat many different neurological disorders,including pain,neurodegenerative diseases such as Parkinson's disease and Alzheimer's disease,psychological disorders,addiction,and many others.
Molecular neuroscience is a branch of neuroscience that observes concepts in molecular biology applied to the nervous systems of animals. The scope of this subject covers topics such as molecular neuroanatomy,mechanisms of molecular signaling in the nervous system,the effects of genetics and epigenetics on neuronal development,and the molecular basis for neuroplasticity and neurodegenerative diseases. As with molecular biology,molecular neuroscience is a relatively new field that is considerably dynamic.
In neuroscience,Golgi cells are the most abundant inhibitory interneurons found within the granular layer of the cerebellum. Golgi cells can be found in the granular layer at various layers. The Golgi cell is essential for controlling the activity of the granular layer. They were first identified as inhibitory in 1964. It was also the first example of an inhibitory feedback network in which the inhibitory interneuron was identified anatomically. Golgi cells produce a wide lateral inhibition that reaches beyond the afferent synaptic field and inhibit granule cells via feedforward and feedback inhibitory loops. These cells synapse onto the dendrite of granule cells and unipolar brush cells. They receive excitatory input from mossy fibres,also synapsing on granule cells,and parallel fibers,which are long granule cell axons. Thereby this circuitry allows for feed-forward and feed-back inhibition of granule cells.
Neurotransmission is the process by which signaling molecules called neurotransmitters are released by the axon terminal of a neuron,and bind to and react with the receptors on the dendrites of another neuron a short distance away. A similar process occurs in retrograde neurotransmission,where the dendrites of the postsynaptic neuron release retrograde neurotransmitters that signal through receptors that are located on the axon terminal of the presynaptic neuron,mainly at GABAergic and glutamatergic synapses.
Depolarization-induced suppression of inhibition is the classical and original electrophysiological example of endocannabinoid function in the central nervous system. Prior to the demonstration that depolarization-induced suppression of inhibition was dependent on the cannabinoid CB1 receptor function,there was no way of producing an in vitro endocannabinoid mediated effect.
Synaptic potential refers to the potential difference across the postsynaptic membrane that results from the action of neurotransmitters at a neuronal synapse. In other words,it is the “incoming”signal that a neuron receives. There are two forms of synaptic potential:excitatory and inhibitory. The type of potential produced depends on both the postsynaptic receptor,more specifically the changes in conductance of ion channels in the post synaptic membrane,and the nature of the released neurotransmitter. Excitatory post-synaptic potentials (EPSPs) depolarize the membrane and move the potential closer to the threshold for an action potential to be generated. Inhibitory postsynaptic potentials (IPSPs) hyperpolarize the membrane and move the potential farther away from the threshold,decreasing the likelihood of an action potential occurring. The Excitatory Post Synaptic potential is most likely going to be carried out by the neurotransmitters glutamate and acetylcholine,while the Inhibitory post synaptic potential will most likely be carried out by the neurotransmitters gamma-aminobutyric acid (GABA) and glycine. In order to depolarize a neuron enough to cause an action potential,there must be enough EPSPs to both depolarize the postsynaptic membrane from its resting membrane potential to its threshold and counterbalance the concurrent IPSPs that hyperpolarize the membrane. As an example,consider a neuron with a resting membrane potential of -70 mV (millivolts) and a threshold of -50 mV. It will need to be raised 20 mV in order to pass the threshold and fire an action potential. The neuron will account for all the many incoming excitatory and inhibitory signals via summative neural integration,and if the result is an increase of 20 mV or more,an action potential will occur.
Neurotransmitter transporters are a class of membrane transport proteins that span the cellular membranes of neurons. Their primary function is to carry neurotransmitters across these membranes and to direct their further transport to specific intracellular locations. There are more than twenty types of neurotransmitter transporters.
The Calyx of Held is a particularly large synapse in the mammalian auditory central nervous system,so named after Hans Held who first described it in his 1893 article Die centrale Gehörleitung because of its resemblance to the calyx of a flower. Globular bushy cells in the anteroventral cochlear nucleus (AVCN) send axons to the contralateral medial nucleus of the trapezoid body (MNTB),where they synapse via these calyces on MNTB principal cells. These principal cells then project to the ipsilateral lateral superior olive (LSO),where they inhibit postsynaptic neurons and provide a basis for interaural level detection (ILD),required for high frequency sound localization. This synapse has been described as the largest in the brain.
Potassium-chloride transporter member 5 is a neuron-specific chloride potassium symporter responsible for establishing the chloride ion gradient in neurons through the maintenance of low intracellular chloride concentrations. It is a critical mediator of synaptic inhibition,cellular protection against excitotoxicity and may also act as a modulator of neuroplasticity. Potassium-chloride transporter member 5 is also known by the names:KCC2 for its ionic substrates,and SLC12A5 for its genetic origin from the SLC12A5 gene in humans.
In biochemistry,the glutamate–glutamine cycle is a cyclic metabolic pathway which maintains an adequate supply of the neurotransmitter glutamate in the central nervous system. Neurons are unable to synthesize either the excitatory neurotransmitter glutamate,or the inhibitory GABA from glucose. Discoveries of glutamate and glutamine pools within intercellular compartments led to suggestions of the glutamate–glutamine cycle working between neurons and astrocytes. The glutamate/GABA–glutamine cycle is a metabolic pathway that describes the release of either glutamate or GABA from neurons which is then taken up into astrocytes. In return,astrocytes release glutamine to be taken up into neurons for use as a precursor to the synthesis of either glutamate or GABA.
Axon terminals are distal terminations of the branches of an axon. An axon,also called a nerve fiber,is a long,slender projection of a nerve cell that conducts electrical impulses called action potentials away from the neuron's cell body to transmit those impulses to other neurons,muscle cells,or glands. Most presynaptic terminals in the central nervous system are formed along the axons,not at their ends.
In neuroscience,synaptic scaling is a form of homeostatic plasticity,in which the brain responds to chronically elevated activity in a neural circuit with negative feedback,allowing individual neurons to reduce their overall action potential firing rate. Where Hebbian plasticity mechanisms modify neural synaptic connections selectively,synaptic scaling normalizes all neural synaptic connections by decreasing the strength of each synapse by the same factor,so that the relative synaptic weighting of each synapse is preserved.
Communication between neurons happens primarily through chemical neurotransmission at the synapse. Neurotransmitters are packaged into synaptic vesicles for release from the presynaptic cell into the synapse,from where they diffuse and can bind to postsynaptic receptors. While most presynaptic cells are historically thought to release one vesicle at a time per active site,more recent research has pointed towards the possibility of multiple vesicles being released from the same active site in response to an action potential.
References
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- ↑ "Tom Otis - Google Scholar".
- ↑ "Thomas Otis, Ph.D."
- ↑ Buhl, Eberhard H.; Otis, Thomas S.; Mody, Istvan (1996). "Zinc-Induced Collapse of Augmented Inhibition by GABA in a Temporal Lobe Epilepsy Model". Science. 271 (5247): 369–373. doi:10.1126/science.271.5247.369. PMID 8553076. S2CID 31854030.
- ↑ "'Better research for better health' - A holistic approach to challenges & opportunities".
- ↑ "Tom Otis".
- ↑ "Prof. Tom Otis".
- ↑ "Tom Otis".
- ↑ Otis, Thomas; Zhang, Su; Trussell, Laurence O. (1996). "Direct Measurement of AMPA Receptor Desensitization Induced by Glutamatergic Synaptic Transmission". The Journal of Neuroscience. 16 (23): 7496–7504. doi:10.1523/JNEUROSCI.16-23-07496.1996. PMC 6579098 . PMID 8922405.
- ↑ Otis, Thomas S.; Kavanaugh, Michael P.; Jahr, Craig E. (1997). "Postsynaptic Glutamate Transport at the Climbing Fiber-Purkinje Cell Synapse". Science. 277 (5331): 1515–1518. doi:10.1126/science.277.5331.1515. PMID 9278516.
- ↑ Otis, Thomas S.; Brasnjo, Gabor; Dzubay, Jeffrey A.; Pratap, Meera (2004). "Interactions between glutamate transporters and metabotropic glutamate receptors at excitatory synapses in the cerebellar cortex". Neurochemistry International. 45 (4): 537–544. doi:10.1016/j.neuint.2003.11.007. PMID 15186920. S2CID 26123313.
- ↑ "UCLA Brain Scientists Crack Mystery Of How Alcohol Causes Intoxication".
- ↑ Lee, K. H.; Mathews, P. J.; Reeves, A. M.; Choe, K. Y.; Jami, S. A.; Serrano, R. E.; Otis, T. S. (2015). "Circuit Mechanisms Underlying Motor Memory Formation in the Cerebellum". Neuron. 86 (2): 529–540. doi:10.1016/j.neuron.2015.03.010. PMC 4417109 . PMID 25843404.
- ↑ Scoles, Daniel (5 April 2016). "Targeting ATXN2 Using Antisense Oligonucleotides as a Treatment for Spinocerebellar Ataxia Type 2 (SCA2) (S30.007)". Neurology. 86 (16 Supplement).