Neurotransmitters
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Neurotransmitters

NEUROTRANSMITTERS

M.Prasad Naidu

MSc Medical Biochemistry,

Ph.D.Research Scholar


Epilepsy

  • Definition : - The chemical substance helpful for signal transmission in central nervous system &peripheral nervous system (via) the chemical synapses is neurotransmitters.

  • Synaptic transmission is the predominant means by which neurons communicate with each other.


Epilepsy

  • The criteria for Chemical neurotransmitter

  • 1) found in presynaptic axon terminal.

  • 2) enzymes necessary for synthesis are present in presynaptic neuron .

  • 3) stimulation under physiological conditions results in release.

  • 4) mechanism exist for rapid termination of action.

  • 5) direct application to postsynaptic terminal mimics the activation of nerve stimulus.


Epilepsy

  • 6) drugs that modify metabolism of the neurotransmitter should have predictable physiological effects invivo assuming that the drug is transported to the site where neurotransmitter acts.

  • Not all neuron to neuron transmission is by neurotransmitters , gap junctions provides direct neuron to neuron electrical conduction.


Epilepsy

  • Neurotransmitter is stored in synaptic vesicle released in response to nerve impulse & controled by calcium influx.

  • Release of neurotransmitter is quantal event , that is a nerve impulse reaching presynaptic terminal result in release of transmitter from a fixed number of synaptic vesicle.

  • Neurotransmitter action is terminated by metabolic degradation , reuptake , or diffusion into other cell types.


Epilepsy

  • Class :- 1 acetylcholine

  • Class : -2 The biogenic amines

    norepinephrine , epinephrine

    dopamine , serotonin .

  • Class : - 3 amino acids

    gamma amino butyric acid (GABA) ,

    glycine , glutamate , aspartate.

  • Class : - 4 nitric acid (NO)

    carbonmonoxide ( co )


Epilepsy

  • In addition to classical neurotransmitters many neuropetides are identified as definite or probable neurotransmitters,

    eg : - substance p , neurotensin , enkephalin , β – endorphin , histamine,

    vasoactive intestinal polypeptide,

    cholecystokinin , neuropeptide Y

    & somatostatin.


Epilepsy

  • Neurotransmitters modulate the function of post synaptic cells by binding to specific receptors of 2 types

  • 1) ionotropic receptors ( direct ion channels that open after binding of neurotransmitters. )

    2) metabotropic receptors ( interact with G proteins stimulating production of second messengers & activating protein kinases , which modulate the cellular events. )


Epilepsy

  • G proteins couple several receptors to intra cellular signaling system , linking neuronal excitability to energy metabolism & second messenger systems.

  • G protein binding receptors include adenosine , Ach ( muscarnic ), norepinephrine , dopamine , serotonin


Epilepsy

  • Kinetics of ionotropic receptors are fast , (< 1 ms ) , because neurotransmitters directly alter the electrical property of the postsynaptic cell.

  • Kinetics of metabotropic receptors functions over longer time periods.

    This contributes to the potential for selective & finely modulated signaling by neurotransmitters


Epilepsy

  • The membrane of neuronal cell maintains an asymmetry of inside outside voltage , & is electrically excitable.

  • Neuronal membranes are polarized to a potential of -90 mV by the activity of Na+_k+ ATPase transport system.


Epilepsy

  • Factors that control the neuroexcitability

    1)voltage gated ion channels

    2) neurotransmitter activated ion channels.

    3)neuromodulators

    4)second messenger system.

  • The control of neuronal activity within normal limits is by the modulation of excitatory & inhibotory events simultaneously.


Epilepsy

  • Ligand gated channels are responsible for communication between cells.

  • Voltage gated sodium channels are involved in propagation of action potential , rapid activation is at -60mV due to opening of fast transient channels.

    Voltage gated potassium channels contribute to repolarization ,this regulate repeated firing of action potential by prolonging after spike repolarization.


Epilepsy

  • Voltage dependent calcium channels trigger neurotransmitter release , at rapid activation is around -70mV.

  • Autoantibodies to ca++ channels in motor nerve terminal leads to decreased release of Ach from nerve terminal , this is seen in eaton lambert myasthenic syndrome.

  • Voltage gated channels determine how inhibitory & excitatory influences are integrated .


Acetyl choline

Acetyl choline

  • Acetyl choline is the neurotransmitter used by all motor axons that arise from spinal cord, that is at neuromuscular junction.

  • Junction consist of a single nerve terminal separated from post synaptic region by synaptic cleft.

  • Motor end plate is the specialized portion of the muscle membrane involved in the junction.


Epilepsy

  • Junctional folds are prominent they contain high density of Ach receptors.

  • Synthesis of Ach takes place in cytosol of nerve terminal .

    choline acetyl transferase

    acetyl coA+ choline Ach + coA

  • Ach is incorporated into membrane bound particle called synaptic vesicles.

  • Assembly of synaptic vesicle with cell membrane resembles assembly of transport vesicle involving SNAREs.


Epilepsy

  • Release of Ach into synaptic cleft occurs by exocytosis , which involves fusion of vesicle with presynaptic membrane.

  • Nerve ending is depolarized by transmission of nerve impulse this opens the voltage gated Ca++ channels , permitting influx of Ca++ from synaptic cleft to nerve terminal , this Ca++ plays a role in exocytosis of Ach vesicle.


Epilepsy

  • Approximately 200 vesicles are released into synaptic space.

  • Each vesicle contains 10000 molecules of Ach.

  • Ach binds Ach receptor , receptor undergoes conformational change opening the channel in the receptor that allows entry of Na+, k+ resulting in depolarization of muscle membrane.


Epilepsy

  • Properties of Ach receptor of NMJ :

    nicotinic receptor (nicotine is an agonist for the receptor)

    a membrane glycoprotein containing 5 subunits. ( 2αβγδ subunits).

    only α subunit binds Ach with high affinity.

    2 molecules of Ach binds receptor to open the ion channel which permits Na+ , K+ the receptor is thus transmitter gated ion channel.

    autoantibodies to receptors are implicated in causation of myasthenia gravis


Epilepsy

  • Snake venom α bungarotoxin binds tightly to the α subunit & can used to label the receptor .

    Formation of autoantibodies to Ach receptors in NMJ

    damage to receptors by autoantibodies

    reduction in number of receptors

    Episodic weekness of muscles supplied by cranial nerves


Epilepsy

  • When the channel closes Ach dissociates & it is hydrolyzed by acetyl choline esterase.

    acetyl choline esterase

    Ach + H2O Acetate +choline

  • Choline is recycled into nerve terminal by active transport , it can be used for synthesis of Ach.


Epilepsy

  • The classical neurotransmitter of autonomic ganglia whether sympathetic or parasympathic is acetyl choline.

  • 2 classes of receptors are present in autonomic nervous system.

  • 1) nicotinic eceptors ,

  • 2) muscarnic recptors.

  • Nicotinic receptors in autonomic ganglia are different from those on skeletal muscle.


Epilepsy

  • Nicotinc & muscarnic receptors mediate excitatory postsynaptic potentials (EPSP) , but these potential have different time course.

  • Stimulation of presynaptic neuron elicits a fast EPSP followed by a slow EPSP.

  • Fast EPSP results from activation of nicotinic receptors which cause of ion channels to open.


Epilepsy

  • Slow EPSP is mediated by activation of muscarnic receptors that inhibit the M current , a current that is produced by K+ conductance.

  • Besides acetyl choline sympathetic preganglion neurons may release enkephalin , substance p , LHRH , neurotensin or somatostatin.


Epilepsy

  • Neurotransmitter in parasympathetic postganglionic neurons is acetyl choline.

  • Actions are mediated by 3 types of muscarnic receptors.

  • 1) M1 receptor (neural ) produces slow excitation of ganglia.

  • 2) M2 receptor (cardiac) activation slows the heart.

  • 3) M3 receptor (glandular) , causing secretion, contraction of visceral smooth muscle , vascular relaxation.


Epilepsy

  • Muscarnic Ach receptors act by way of inosine triphosphate system & they may also inhibit adenyl cyclase & thus decreasing cAMP synthesis.

  • Muscarnic recptors also open or close ion channels particularly K+ or Ca++ this action occurs through G proteins.

  • Muscarnic receptors relax smooth muscle by an effect on endothelial cells which produces nitric oxide (NO) .


Epilepsy

  • Nitric oxide ( NO ) relaxes smooth muscles by stimulating guanylate cyclase & there by increasing levels of cGMP which in turn activates cGMP dependent protein kinases.

  • The number of muscarnic receptors are regulated & exposure to muscarnic agonist decreases the number of receptors by internalization of rceptor.


Epilepsy

  • The betz cells of motor cortex uses acetyl choline as their neurotransmitter.

  • Acetyl choline probably acts as an imporatant neurotransmitter in basal ganglia which is involved in control of movements.

  • Deficits in cholinergic path way in the brain implicated in some form of Alzheimer's disease.


Epilepsy

  • GABA major fast inhibitory neurotransmitter in the fore brain. 30% synapses of C.N.S contain GABA.

  • Glutamic acid dehydrogenase synthesizes

    GABA from glutamate in nerve terminal .

  • 3 types of receptors GABA a

    GABA b

    GABA c


Epilepsy

  • GABA a & GABA c are ionotropic receptors & are post synaptic linked to chloride channel.

  • GABA b receptors are metabotropic may be pre or post synaptic & are coupled to ca+ or k+ ion channels via GTP proteins.

  • Presynaptic GABA b receptors serve autoreceptors to inhibit release from nerve terminal.


Epilepsy

  • Binding of GABA leads to an opening of chloride channels & resultant hyperpolarization.

  • Glycine is inhibitory neurotransmitter in brain stem & spinal cord.

  • Post synaptic receptor for glycine is ligand gated chloride channel that allows influx of Cl- to hyperpolarize the postsynaptic neuron


Epilepsy

  • Glutamate & aspartate are excitatory neurotransmitters.

  • Glutamate is responsible for 75% of excitatory neurotransmission in brain.

  • Synthesis of glutamate & aspartate within central neuron & glial cells is from carbohydrates involved in TCA cycle.


Epilepsy

  • Mitochondrial enzyme aspartate transaminase interconverts glutamate & aspartate.

  • Glia contains glutamine synthase which converts glutamate to glutamine.

  • Glutamine is subsequently transferred to neuron where it is deaminated to glutamate by glutaminase.


Epilepsy

  • Glial inactivation & specific uptake systems for glutamate reduces interstitial glutamate levels to terminate neurotransmitter action & prevent excitotoxic damage.

  • Monosodium glutamate produces migrainous head ache.

  • Excessive glutamate can result in neurotoxicity , celldeath & neurodegeration seen alzheimer’s disease.


Epilepsy

  • The receptors are subdivided into 5 classes.

  • 1 )NMDA (N – methyl –D –aspartate )

  • 2 )AMPA (α amino 3 hydroxy 5 methyl 4 isoxazole propionic acid )

  • 3 )The kainate recptor ( isolated from sea weed)

  • 4 )L –AP 4 ( synthetic agonist )

  • 5 )Metabotropic receptors.

  • First four receptors are cation channels .


Epilepsy

  • Metebotropic receptors are linked to intracellular production of diacylglycerol,& inositol triphosphate by phosphoinositide path way.

  • NMDA is receptor is complex contains 5 distinct sites for binding

    1 ) site for transmitter binding glutamate

    2 ) a regulatory site that binds glycine.

    3 ) a voltage dependent Mg++ binding site

    4 ) a site that binds phencyclidine

    5 ) a site that binds Zn++.


Epilepsy

  • NMDA receptor opens when glutamate binds & allows influx of Ca++ & Na++ into the cell.

  • Mg++ , zn++ , poly amines , & steroids can also modulate NMDA.

  • one of the most important controls on the ionic conductance through the NMDA receptor is voltage sensitive blocking by Mg++


Epilepsy

  • Activation of AMPA receptor channels may depolarize the neuron sufficiently to remove the voltage dependent Mg++ block & activate NMDA channels.

  • AMPA & NMDA are co activated & are present on the same part of the neuron.


Epilepsy

  • A separate site that modulates the gating of NMDA channel binds polyamines such as spermine & spermidine which are synthesized by neurons.different concentration dependent effects have observed.

  • Endogenous Zn reduces NMDA activated current.

  • Zinc is present in high concentrations in the hippocampus & released with some neurotransmitter in nervous system.


Epilepsy

  • Hydrogen ions also modulate the ion conductance which is maximal at slightly alkaline pH , & reduces with increasing acidity.

  • During hypoxic ischemic injury , progressive acidification resulting from glycolytic metabolism , may turn off the NMDA receptor channel.


Epilepsy

  • AMPA receptor is coupled to both Na++ , & K ++ channels. it’s activation opens the above channels, depolarizes the neuronal cell rapidly, it is responsible for the majority of rapid excitatory neurotransmission.

  • Kainate receptor is also coupled to Na++ , k++ channels.

  • Kainate receptor has slower rate of depolarizing capacity than AMPA receptor.


Epilepsy

  • Excitatory aminoacids are also able to interact with metabotropic recptors that activate the second messenger system, these receptors are found both pre & post synaptically.

  • Activation result in presynaptic inhibition & post synaptic excitation.


Epilepsy

  • The spectrum of neurological disorders mediated by excitotoxicity include epilepsy, stroke , neurodegerative disorders ( parkinson’s disease , amyotropic lateral sclerosis , AIDS dementia )

  • Most strokes are caused by thromboembolic events causing diminished perfusion resulting in reduction of supply of oxygen & glucose.


Epilepsy

  • 3 subsequent stages are there in the development of brain damage caused by ischemia.

  • 1)induction ,

  • 2)amplification ,

  • 3)expression.

  • Induction : ischemia causes depolarization of the neuronal membrane leading to release of glutamate.


Epilepsy

  • Glutamate overexcites the NMDA receptors in adjacent neuron , leading to abnormally large influxes of Ca++ & Na+ and resultant cell injury or death .

  • In addition glutamate stimulate AMPA – kainate receptor ( leading to additional influx of Na+ ) & also metabotropic receptors , causing the release of ITP & diacylgycerol.


Epilepsy

  • Amplification : further build up of intra cellular calcium occurs by following mechanism ,

    1) increased intracellular Na+ activates Na+ - Ca++ transporters.]

    2)voltage gated Ca++ channels are activated by depolarozation.

    3) ITP release Ca++ into cytosol from within endoplasmic reticulum.


Epilepsy

  • Expression : high levels of intra cellular Ca++ activates Ca++ dependent nucleases , proteases , & phospholipases.

    Degradation of phospholipids

    formation of platelet activating factor (PAF) & release of arachidonic acid

    eicosanoids (vasoconstriction)

    damage by oxygen free radicals

    This is called glutamate cascade.


Epilepsy

  • Huntington disease characterized by selective neuronal death in corpus striatum & glial proliferation .

  • Apoptosis , protein aggregation , & excitotoxins may all contribute cell death in huntington disease.

  • Excitotoxicity is by glutamate cascade.


Epilepsy

  • The dopaminergic neurons are found in nigrostrital , mesolimbic , mesocortical tuberohypophysial systems.

  • Dopamine synthesis occurs from tyrosine , tyrosine hydroxylase is rate limiting enzyme in formation.


Epilepsy

  • Entry of dopamine into synaptic vesicle is is driven by pH gradient established by a protein in vesicular membrane that pumps protons into vesicle at the expense of ATP

  • Release of dopamine involves exocytosis.

  • Dopamine has 5 post synaptic recptors

    D 1 receptor family(D1 & D5)

    D 2 receptor family(D2, D3, D4)

  • D4 receptor exhibits 5 polymorphic variants.


Epilepsy

  • The effect of dopamine is to increase direct path way by D 1 recptor, & supress indirect path way by D 2 receptor.

  • D 1 receptor activation augments adenylate cyclase ( linked to stimulatory G protein).

  • D 2 receptor activation decreases the activity of adenylate cyclase ( linked to inhibitory G protein ).


Epilepsy

  • ATP dependent reuptake of dopamine achieved by a high affinity transporter in presynatic membrane , this is incorporated into vesicles & reused again.

  • Degradation of dopamine occurs within synaptic cleft or following reuptake ,within presynatic terminal.

  • Mono amino oxidase B present in the outer membrane of mitochondria & also in synaptic cleft.


Epilepsy

  • MAO –B & MAO – A are distinguished from each other by preference for different substrates & by their different susceptibility to various inhibitors.

  • Both the above enzymes acts on dopamine to produce 3 – hydroxyphenyl acetaldehyde (DOPAC).

  • DOPAC converted to homovanillic acid by the action of catechol o methyl transferase.


Epilepsy

  • parkinson disease is due to loss of dopaminergic activity & excessive cholinergic activity in basal ganglia.

  • Signs of parkinson disease reflects a deficiency of dopamine in the substantia nigra , corpus striatum ( caudate nucleus & putamen )


Epilepsy

  • Basal ganglia are important for motor control they include putamen

    caudate nucleus

    globus pallidum

    substantia nigra

    subthalamic nucleus .

  • All circuits in basal ganglia are inhibitory utilizing GABA except glutamatergic subthalamic input to globus pallidum internum(GPi) which is excitatory.


Epilepsy

  • Cell damage in parkinson disease reflect a process of ageing , 13 % of cells of substantia nigra are lost per decade from 25 age onwards . ( parkinson disease rarely occurs befor 40 years )

  • Mutattions in gene encoding α synuclein , a presynaptic protein involved in neuronal plasticity is associated with parkinson disease.

  • Lewy bodies are found strongly stained with antibodies of α synuclein .


Epilepsy

  • Signs of parkinson disease appear when the level of dopamine is droped in nigrosriatal system by 80%.

  • Exposure to high levels of Manganese

    ( miners) leads to parkinson disease.

  • Reserpine inhibit dopamine storage & many neuroleptics block dopamine receptors.


Epilepsy

  • Schizophrenia is a manifestation of hyperdopaminergia .

  • Measurement of dopamine metabolite homovanillic acid in CSF is high in schizophrenics.

  • Level of D2 receptors appears to be increased in the brains of schizophrenics.

  • Dopamine mimetic drugs ( L dopa) induces schizophrenia


Epilepsy

  • Low dopamine activity in prefrontal cortex of the brain of schizophrenics correlate well with the negative symptoms .

  • Low dopamine activity in prefrontal cortex releases the inhibitory action on subcortical dopamine neurons resulting in elevated dopaminergic activity.


Epilepsy

  • Adrenergic neurotransmission is by norepinephrine & epinephrine.

  • The adrenergic neurons of locus ceruleus , pons , & medulla project to every area of brain & spinal cord.

  • Sympathetic postganglionic neurons typically release norepinephrine.

  • NE & E serve important role in the regulation of blood volume & blood pressure.


Epilepsy

  • Norepinephrine is synthesized from tyrosine .

    dopamine β hydroxylase

    dopamine norepinephrine

    cu

    dopamine β hydroxylase is bound to inner membrane of synaptic vesicle & release norepinephrine in a tetrameric glycoprotein form.


Epilepsy

  • The overall system of epinephrine synthesis , storage & secretion from adrenal medulla are regulated by neuronal controls & also by glucocorticoid hormones synthesized in & secreted from adrenal cortex in response stress.

  • Secretion of epinephrine is signaled by neural response to stress , which is transmitted to adrenal medulla by way of a preganglionic acetyl cholinergic neuron.


Epilepsy

  • A small number of neurons in the medulla contain phenyl ethenolamine –N- methyl tranferase enzyme that converts norepinephrine to epinephrine with SAM as methyl donor.

  • These neurons project to the thalamus, brainstem , spinal cord.

  • Concentration of epinephrine secreting terminals in the paraventricular nucleus suggests a role in secreton of oxytocin & vasopressin.


Epilepsy

  • Dense innervation of dorsal motor nucleus of vagus , & nucleus solitarius suggets role in regulating cardiovascular & respiratory reflexes.

  • Receptors on target cells may be either α or β adrenergic receptors.

  • Receptors are further sub divided into α1, α2, β1 , β2 , β3.


Epilepsy

  • α1 receptor are located postsynaptically but α2 receptors may be either pre or postsynaptic .

  • Receptors located presynaptically are autoreceptors inhibit release of neurotransmitter.

  • The effects of α1 receptors are mediated by activation of ITP/ diacyl glycerol second messenger system.

  • β receptors can be antagonized by action of α1 receptor.


Epilepsy

  • α2 receptors decease the rate of synthesis of cAMP through an action on inhibitory G protein.

  • β1&β2 receptors activates stimulatory G protein to increase cellular cAMP levels.

  • Activation of β receptor result in coactivation of β adrenergic receptor kinase (BARK), this phosphorylates the receptor.

  • Phophorylation is prominent mechanism of receptor desensitization.


Epilepsy

  • Number of β receptors is regulated .

  • β receptor is phosphorylated & desensitized their number also decreased if they become internalized.

  • β receptors can also be increased by denervation.

  • The number of α receptor is also regulated.


Epilepsy

  • β1 adrenergic receptors principally found in heart & cerebral cortex.

  • β2 receptors principally found in lung & cerebellum.

  • β1 receptors equally prefer NE & E as agonist.

  • β2 receptors prefer epinephrine to norepinephrine.


Epilepsy

  • In synaptic neurons norepinephrine decreases the amplitude of calcium spikes.

  • Excitatory effects of norepinephrine in various parts of CNS & sympathetic ganglion neuron results from α1 receptor activation. This activity primarily depends on blockade of a resting K+ conductance as a result neuron depolarizes & firing rate increases.


Epilepsy

  • Inhibitory effects of norepinephrine results from α2 receptor activation , which results in increase of K+ conductance this hyperpolarizes the neuron & decreases it’s firing rates.

  • NE acting at α2 receptor also block Ca++ current.

  • Both the above inhibitory mechanisms account for the autoreceptor function of α2 receptors which decreases neurotransmitter release.


Epilepsy

  • α1 adreno receptor activation results in , 1)vasoconstriction ,

    2) relaxation of gastrointestinal smooth muscle,

    3) salivary secretion ,

    4)hepatic glcogenolysis.


Epilepsy

  • α2 adreno receptor activation results in

    1) inhibition of transmitter release, (including NE & Ach from autonomic nerves)

    2) platelet aggregation

    3) contraction of vascular smooth muscle.

    4) inhibition of insulin release.


Epilepsy

  • β1 adreno receptors activation results in

    1) increased cardiac rate & force

  • β2 adreno receptors activation results in 1) bronchodilatation ,

    2) vasodilation,

    3) relaxation of visceral smooth muscle,

    4) hepatic glycogenolysis,

    5) muscle tremor.

  • β3 adreno receptor activation results in lipolysis.


Epilepsy

  • The action of catecholamine neurotransmitters is terminated by reuptake into presynaptic neuron by specific transporters.

  • Enzymes involved in metabolism are catechol 0 methyl transferase & monoamino oxidase .

  • End product of norepinephrine & epinephrine metabolism is 3 methoxy 4 hydroxy mandelic acid.


Serotonin

serotonin

  • More than 95% of body’s serotonin is stored in platelets & GI tract , only 5% is seen in brain.

  • Serotonin is distributed in brain regions that affect behaviour especially the hypothalamus & limbic system.


Epilepsy

  • Availability of tryptophan is the main factor regulating synthesis of tryptophan.

  • Process of synthesis , storage , release , reuptake & degradation are similar to catecholmines.

  • Urinary 5 HIAA provides a measure of 5 –HT turn over.


Epilepsy

  • Functions associated with 5-HT path ways

    1)hallucination & behavioural changes,

    2)sleep, wakefulness & mood ,

    3) feeding behaviour,

    4)control of sensory pathway including nociception,

    5) vomiting.

  • Serotonin receptors are metabotropic.

  • Melatonin a derived product of 5-HT has role in establishing circadian rhythm.


Epilepsy

  • Histamine has neurotransmitter role in brain.

  • Acts on metabotropic receptors.

  • H1 receptors are excitatory & H2 , H3 receptors are inhibitory.

  • H1 receptors in cortex & RAS contributes to arousal & wakefulness.

  • Has role in food & water intake, thermoregulation


Epilepsy

  • Nitric oxide synthase is present in many CNS neurons.

  • NO production is increased by mechanisms that raise intracellular Ca++ concentration( eg: transmitter action).

  • NO affects neuronal functions by increasing cGMP formation ,producing both inhibitory & excitatory effects on neurons.


Epilepsy

  • ATP functions as neurotransmitter , it acts via ionotropic receptors as fast excitatory transmitter , via metabotropic receptors acts as neuro modulator.

  • Adenosine exerts inhibitory effects through metabotropic receptors.

  • Neurons contain CO generating enzyme, heme oxygenase , have role in cerebellum & olfactory neurons which have cGMP sensitive ion channels.


Epilepsy

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