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New! 31 New Pathways were released on 19-NOV-2011
Released 19 pathways on 28-OCT-2011 (details here)
Released 11 pathways on 08-OCT-2011 (details here)
Released 9 pathways on 01 SEPT 2011 (details here)


New Pathways release forcast: 

Next release due on 10-FEB-2012 ( ~#  of pathways for release = 6 to 10). see below for the list.
Main curation theme is Lysosomal storage diseases and Cancer signaling pathways.
We will publish curated pathways on the following diseases:


Lysosomal storage diseases
  • Cystinosis disease pathway
  • Lysosomal storage defect induced autophagy
  • Pompe disease pathway (glycogen storage disease type II or acid maltase deficiency)
  • i cell disease pathway
  • Overview Map of Cellular Biology of Lysosomal Storage disorder
  • Other lysosomal storage diseases
Metabolic disease pathways
Cancer signaling Pathways
  • Regulatory role of stathmin1 in breast cancer signaling pathway
  • Colorectal Cancer Metastasis Signaling Pathway
  • Glioma Signaling Pathway
  • Thyroid Cancer Signaling Pathway

ER Stress and Apoptosis Pathways



Number of pathways/Maps currently being validated for release in near future by iPAVS :  40

Preview: see the slide show of pathway diagrams under validation and scheduled to be released

To be published




Please write to support _ at _ cidms.org if you have a request for a pathway. We may have one in our curation pipeline and we could reassign the priority so that you can see the pathway you need available on iPAVS immediately in our next release.


Showing 57 items
Pathway NameSummaryStatusExpected Release
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Aromatic_L-Aminoacid_Decarboxylase_Deficiency_Metabolite_pathway Aromatic L-Aminoacid Decarboxylase Deficiency(Dopa decarboxylase; DDC) is an autosomal recessive disease caused by a mutation in the DDC gene which codes for aromatic-L-aminoacid decarboxylase.  Finished Newly Released 
17-Beta Hydroxysteroid Dehydrogenase III Deficiency metabolite pathway Defects in 17-beta hydroxysteroid dehydrogenase III (HSD17B3) are the cause of male pseudohermaphrodism with gynecomastia.  Finished Newly Released 
Alkaptonuria_metabolite_pathway Alkaptonuria (Homogentisic acid oxidase deficiency) is an autosomal recessive disease caused by a mutation in the HGD gene which codes for homogentisate 1,2-dioxygenase.  Finished Newly Released 
beta3_integrin_mediated_Ub_for_NFkB_activation beta3 integrin mediated ubiquitination activates surivival signaling during myocardial hypertrophy Finished Newly Released 
beta_AR_stimulation_of_CICR_in_the_heart_involves_cAMP_activation A endogenous PKA-independent betaAR-signaling pathway through cAMP-dependent Epac activation, Rap, and PLC(epsilon) that enhances intracellular Ca(2+) release in cardiac myocytes. cAMP aciviate Epac. Finished Newly Released 
Regulation_of_BetaAR_turnover_via_desensitization_and_sequestration_mechanisms Regulation of beta-adrenoceptor turnover via desensitization and sequestration mechanisms. The desensitization and the associated uncoupling or down-regulation of beta-AR relate to their adaptational responses to various forms of stress. Finished Newly Released 
positive_and_negative_inotropic_effects_induced_by_beta2AR_agonists_in_mamalian_right_papillary_muscles Signaling pathways is involved in positive and negative inotropic effects induced by beta2-adrenoceptor (AR) agonists in guinea pig right papillary muscles. Beta2-adrenoceptor partial agonists induce an unexpected NO-mediated biphasic negative inotropic effect in guinea pig right papillary muscles. Finished Newly Released 
Biotinidase_Deficiency_metabolite_pathway Biotinidase deficiency (Multiple carboxylase deficiency) is an autosomal recessive disease caused by a mutation in the BTD gene which does for biotinidase.  Finished Newly Released 
Canavan_diseaes_metabolite_pathway Canavan Disease (Canavan-Van Bogaert-Bertrand Disease; Aminoacylase 2 Deficiency; Spongy Degeneration of the Central Nervous System; Aspartoacylase Deficiency; ASP Deficiency; ACY2 Deficiency; ASPA) is a rare autosomal recessive disease caused by a defect in the ASPA gene which codes for aspartoacylase.  Finished Newly Released 
Congenital_Erythropoietic_Porphyria_metabolite_pathway Congenital Erythropoietic Porphyria (CEP) or Gunther Disease is a rare inborn error of porphyrin-heme synthesis inherited that is as an autosomal recessive trait. This disorder of bone marrow heme synthesis is caused by a defect in the UROS gene which codes for uroporphyrinogen-III synthase.  Finished Newly Released 
GABA_Transaminase_Deficiency_Metabolite_pathway GABA-Transaminase Deficiency (Gamma-amino butyric acid transaminase deficiency; GABA-T) is caused by a defect in the gene coding for gamma-aminobutyrate transaminase, which is responsible for catabolism of gamma-aminobutyric acid (GABA), an important, mostly inhibitory neurotransmitter in the central nervous system, into succinic semialdehyde.  Finished Newly Released 
Glutaric_aciduria_type3_metabolite_pathway Glutaric Aciduria Type III is an extremly rare metabolic abnormality of peroxisomal metabolism presumed to be cause by a deficiency in peroxisomal glutaryl-CoA oxidase.  Finished Newly Released 
Obesity_Metabolic_Syndrome_metabolite_pathway In Obesity/Metabolic Syndrome, high plasma fatty acids regulate genes responsible for increase insulin resistance, visceral fat deposits, fatty acid oxidation, and thermogenesis.  Finished Newly Released 
Primary_Hyperoxaluria_Type1_Metabolite_pathway Primary hyperoxaluria type 1 (PH1) is an atypical peroxisomal disorder, as befits a deficiency of alanine:glyoxylate aminotransferase (AGT), which is itself an atypical peroxisomal enzyme. PH1 is characterized by excessive synthesis and excretion of the metabolic end-product oxalate and the progressive accumulation of insoluble calcium oxalate in the kidney and urinary tract.  Finished Newly Released 
Pyrimidine salvage reactions In pyrimidine salvage reactions, nucleosides and free bases generated by DNA and RNA breakdown are converted back to nucleotide monophosphates, allowing them to re-enter the pathways of pyrimidine biosynthesis (interconversion). Validation One Month 
activation of focal adhesion by Tie2 Tek signaling pathway The TEK signaling pathway appears to be critical for endothelial cell-smooth muscle cell communication in venous morphogenesis Validation One Month 
Refsum_disease_metabolite_pathway Refsum's disease (hereditary motor sensory neuropathy type IV, heredopathia atactica polyneuritiformis) is an autosomal recessive disorder the clinical features of which include retinitis pigmentosa, blindness, anosmia, deafness, sensory neuropathy, ataxia and accumulation of phytanic acid in plasma- and lipid-containing tissues Finished Newly Released 
AKT PI3K pathway in cardiovasclar tissue The PI3K/AKT/mTOR pathway is an intracellular signalling pathway important in apoptosis and hence cancer e.g. breast cancer and non-small-cell lung cancer. In heart it has Cardioprotective Effects. Validation One Month 
Obesity_Metabolic_Syndrome_pathway In Obesity/Metabolic Syndrome, high plasma fatty acids regulate genes responsible for increase insulin resistance, visceral fat deposits, fatty acid oxidation, and thermogenesis. Many of these responses have a role in metabolic syndrome, obesity and diabetes. Finished Newly Released 
Leigh_Syndrome_metabolic_pathway Leigh’s disease (Encephalopathy), a form of Leigh syndrome, also known as Subacute Necrotizing Encephalomyelopathy (SNEM), is a rare neurometabolic disorder that affects the central nervous system. It is an inherited disorder that usually affects infants between the age of three months and two years, but, in rare cases, teenagers and adults as well.  Finished Newly Released 
Galactosemia_Metabolic_pathway Galactosemia (GALT Deficiency; GALT; Galactose-1-Phosphate Uridylyltransferase Deficiency) is a rare genetic disorder caused by a mutation in the GALT gene which codes for galactose-1-phosphate uridylyltransferase.  Finished Newly Released 
Histidinemia_metabolic_pathway Leigh’s disease (Encephalopathy), a form of Leigh syndrome, also known as Subacute Necrotizing Encephalomyelopathy (SNEM), is a rare neurometabolic disorder that affects the central nervous system. It is an inherited disorder that usually affects infants between the age of three months and two years, but, in rare cases, teenagers and adults as well.  Finished Newly Released 
Glycerol_Kinase_Deficiency_metabolic_pathway _metabolic_pathway Glycerol Kinase Deficiency (Hyperglycerolemia; Glyceroluria; GK Deficiency; GKD) is a rare metabolic disease caused by a deficiency in the GK gene which codes for glycerol kinase. Finished Newly Released 
Richner-Hanhart_syndrome_metabolite_pathway A defect in this enzyme results in accumulation of tyrosine in both blood and urine; increased excretion of 4-hydroxyphenylpyruvic acid, hydroxyphenyllactic acid, and p-hydroxyphenylacetic acid in urine. Symptoms often begin in early childhood, they include excessive tearing, abnormal sensitivity to light (photophobia), eye pain and redness, and painful skin lesions on the palms and soles. Finished Newly Released 
Refsum_disease_metabolic_pathway Adult Refsum Disease (Classic Refsum Disease; Phytanic Acid Oxidase Deficiency; Heredopathia Atactica Polyneurtiformis; Hereditary Motor and Sensory Neuropathy IV; HSMN4; Adult Refsum Disease I; Adult Refsum Disease II), can be caused by mutations in the PHYH (or PAHX) gene, which encodes Phytanoyl-CoA hydroxylase (, the first enzyme in the Phytanic Acid Peroxisomal Oxidation pathway) on chromosome 10 (adult Refsum disease I), and by mutation of the PEX7 gene. Finished Newly Released 
Sialuria_or_French_Type_Sialuria_Metabolic_pathway Sialuria is caused by mutation in the gene encoding uridinediphosphate-N-acetylglucosamine 2-epimerase (UDP-GlcNAc 2-epimerase, which causes an excessive synthesis of sialic acid (N-acetylneuraminic acid, NeuAc).This causes accumulation of sialic acid in the urine. Symptoms of sialuria include hepatosplenomegaly, hypotonia, frequent upper respiratory infections, gastroenteritis and seizures.  Finished Newly Released 
Electron Transport Chain An electron transport chain (ETC) couples electron transfer between an electron donor (such as NADH) and an electron acceptor (such as O2) with the transfer of H+ ions (protons) across a membrane. The resulting electrochemical proton gradient is used to generate chemical energy in the form of adenosine triphosphate (ATP). Electron transport chains are the cellular mechanisms used for extracting energy from sunlight in photosynthesis and also from redox reactions, such as the oxidation of sugars (respiration). Validation One Month 
Maple_Syrup_Urine_Disease_Metabolite_pathway Maple syrup urine disease is an inherited disorder in which the body is unable to process certain protein building blocks (amino acids) properly. The condition gets its name from the distinctive sweet odor of affected infants' urine. Beginning in early infancy, this condition is characterized by poor feeding, vomiting, lack of energy (lethargy), and developmental delay. If untreated, maple syrup urine disease can lead to seizures, coma, and death. Finished Newly Released 
Methionine_Adenosyltransferase_Deficiency_metabolite_pathway Methionine adenosyltransferase deficiency is an inborn error of metabolism resulting in isolated hypermethioninemia. Most patients have no clinical abnormalities, although some neurologic abnormalities have been reported in rare cases with severe loss of enzyme activity (Mudd et al., 2003|PubMed: 7573050). Finished Newly Released 
Malonic aciduria metabolic pathway Malonic Aciduria, is an autosomal recessive metabolic disorder caused by a genetic mutation which disrupts the activity of Malonyl-Coa decarboxylase.  Finished Newly Released 
Saccharopinuria(Hyperlysinemia) II metabolic pathway Saccharopinuria (an excess of saccharopine in the urine), also called saccharopinemia or saccharopine dehydrogenase deficiency, or alpha-aminoadipic semialdehyde synthase deficiency, is a variant form of hyperlysinemia caused by a partial deficiency of the enzyme aminoadipic semialdehyde synthase (AASS), which has lysine ketoglutarate reductase (LKR) and saccharopine dehydrogenase (SDH) activity Finished Newly Released 
Tyrosinemia Type3 metabolic pathway Tyrosinemia type 3, one of the 3 types of tyrosinemia, is caused by a defect in the HPD gene which codes for 4-hydroxyphenylpyruvate dioxygenase.  Finished Newly Released 
Prostaglandin Metabolic Pathway prostaglandins were first detected in human seminal fluid. prostaglandins are found throughout the animal kingdom, even in species as lowly as insects, shellfish and corals.Prostaglandins are a subset of a larger family of substances called eicosanoids. Other subgroups include thromboxanes, leukotrienes and lipoxins. Eicosanoids are localized tissue hormones that seem to be the fundamental regulating molecules in most forms of life. They do not travel in the blood like hormones, but are created in the cells to serve as catalysts for a large number of processes including the movement of calcium and other substances into and out of cells, dilation and contraction, inhibition and promotion of clotting, regulation of secretions including digestive juices and hormones, and control of fertility, cell division and growth Finished Newly Released 
Lidocaine Local Anaesthetic Pathway Lidocaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons.  Finished Newly Released 
ABCIXIMAB Drug Pathway Abciximab (previously known as c7E3 Fab), is a glycoprotein IIb/IIIa receptor antagonist manufactured by Centocor and distributed by Eli Lilly under the trade name ReoPro, is a platelet aggregation inhibitor mainly used during and after coronary artery procedures like angioplasty to prevent platelets from sticking together and causing thrombus (blood clot) formation within the coronary artery. It is a glycoprotein IIb/IIIa inhibitor. Finished Newly Released 
Oxaprozin Drug Pathway Oxaprozin is a nonsteroidal anti-inflammatory drug (NSAID) with analgesic and antipyretic properties. Finished Newly Released 
Mefenamic Acid Drug Pathway Mefanamic Acid Pathway Most NSAIDs, including mefanamic acid, are non-selective prostaglandin G/H synthase (better known as cyclooxygenase or COX) inhibitors that act on both prostaglandin G/H synthase 1 and 2 (COX-1 and -2).  Finished Newly Released 
Von Gierke disease-metabolite pathway Glycogen storage disease type 1A (GSD1A), or von Gierke disease, is caused by a defect in the G6PC gene which codes for Glucose-6-phosphatase. Glucose-6-phosphatase hydrolyzes glucose-6-phosphate to glucose and is responsible for the regulation of blood glucose level. A defect in this enzyme results in accumulation of glycogen in affected tissues, like liver and kidney; decreased glucose level; and accumulation of lactate.  Finished Newly Released 
Androgen and Estrogen Metabolic Pathway This pathway describes the inactivation and catabolism of male (androgen) and female (estrogen) hormones. Many steroid hormones are transformed by sulfatases, dehydrogenases and glucuronide transferases to enhance their solubility and to facilitate their elimination. Inactivation refers to the metabolic conversion of a biologically active compound into an inactive one. Peripheral inactivation (e.g. by liver enzymes) is required to ensure steady-state levels of plasma androgens and estrogens.  Finished Newly Released 
Benzocaine Local Anaesthetic Pathway Benzocaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Benzocaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Therefore benzocaine preferentially inhibits neurons that are actively firing. Finished Newly Released 
Bupivacaine Local Anaesthetic Pathway Bupivacaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Bupivacaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Therefore bupivacaine preferentially inhibits neurons that are actively firing Finished Newly Released 
Chloroprocaine Local Anaesthetic Pathway Chloroprocaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Chloroprocaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Therefore chloroprocaine preferentially inhibits neurons that are actively firing. Finished Newly Released 
Cocaine Local Anaesthetic Pathway Cocaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Cocaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Therefore cocaine preferentially inhibits neurons that are actively firing. Finished Newly Released 
Dibucaine Local Anaesthetic Pathway Dibucaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Dibucaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Therefore dibucaine preferentially inhibits neurons that are actively firing. Finished Newly Released 
Diclofenac Drug Pathway Diclofenac is an acetic acid nonsteroidal anti-inflammatory drug (NSAID) with analgesic and antipyretic properties. Diclofenac is used to treat pain, dysmenorrhea, ocular inflammation, osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, and actinic keratosis. The antiinflammatory effects of diclofenac are believed to be due to inhibition of both leukocyte migration and the enzyme cylooxygenase (COX-1 and COX-2 or prostaglandin G/H synthase 1 and 2), leading to the peripheral inhibition of prostaglandin synthesis.  Finished Newly Released 
Diflunisal Drug Pathway Diflunisal is a non-selective prostaglandin G/H synthase (better known as cyclooxygenase or COX) inhibitor that acts on both prostaglandin G/H synthase 1 and 2 (COX-1 and -2). COX catalyzes the conversion of arachidonic acid to a number of prostaglandins involved in fever, pain, swelling, inflammation, and platelet aggregation. Diflunisal antagonizes COX by binding to the upper portion of the active site and preventing its substrate, arachidonic acid, from entering the active site. The analgesic, antipyretic and anti-inflammatory effects of diflunisal occur as a result of decreased prostaglandin synthesis. Diflunisal also inhibits the migration of leukocytes into sites of inflammation and prevents the production of thromboxane A2, an aggregating agent, by platelets. Finished Newly Released 
Ibuprofen Drug Pathway Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) used for its analgesic, antipyretic and anti-inflammatory properties. Like most NSAIDs, ibuprofen is a non-selective inhibitor of prostaglandin G/H synthase 1 and 2, better known as cyclooxygenase 1 and 2 or simply COX-1 and -2. COX catalyzes the conversion of arachidonic acid to a number of prostaglandins involved in fever, pain, swelling, inflammation, and platelet aggregation. Ibuprofen antagonizes COX by binding to the upper portion of the active site, preventing its substrate, arachidonic acid, from entering the active site. The analgesic, antipyretic and anti-inflammatory effects of ibuprofen occurs as a result of decreased prostaglandin synthesis. Ibuprofen is slightly more potent than aspirin and produces analgesic effects at lower doses than aspirin. Unlike aspirin, ibuprofen is a reversible COX inhibitor and thus it is not used as an antiplatelet agent. Finished Newly Released 
Indomethacin Drug Pathway Indomethacin, an NSAID, is a prostaglandin G/H synthase (a.k.a. cyclooxygenase or COX) inhibitor that acts on both prostaglandin G/H synthase 1 and 2 (COX-1 and -2). Prostaglandin G/H synthase catalyzes the conversion of arachidonic acid to a number of prostaglandins involved in fever, pain, swelling, inflammation, and platelet aggregation. Indomethacin antagonizes COX by binding to the upper portion of the active site, preventing its substrate, arachidonic acid, from entering the active site. Indomethacin, unlike other NSAIDs, also inhibits phospholipase A2, the enzyme responsible for releasing arachidonic acid from phospholipids. Indomethacin is more selective for COX-1 than COX-2, which accounts for its increased adverse gastric effects relative to other NSAIDs. COX-1 is required for maintaining the protective gastric mucosal layer. The analgesic, antipyretic and anti-inflammatory effects of indomethacin occur as a result of decreased prostaglandin synthesis. Finished Newly Released 
Ketoprofen Drug Pathway Ketoprofen is a nonsteroidal antiinflammatory drug (NSAID) with analgesic and antipyretic properties. Ketoprofen has pharmacologic actions similar to those of other prototypical NSAIDs, that is thought to be associated with the inhibition of prostaglandin synthesis. Ketoprofen is used to treat rheumatoid arthritis, osteoarthritis, dysmenorrhea, and to alleviate moderate pain. Its anti-inflammatory effects are believed to be due to inhibition of both prostglandin G/H synthase 1 and 2 (better known as cylooxygenase-1 (COX-1) and cylooxygenase-2 (COX-2)), which leads to the inhibition of prostaglandin synthesis. Antipyretic effects may be due to action on the hypothalamus, resulting in an increased peripheral blood flow, vasodilation, and subsequent heat dissipation. Finished Newly Released 
Levobupivacaine Local Anaesthetic Pathway Levobupivacaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Levobupivacaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Therefore levobupivacaine preferentially inhibits neurons that are actively firing.  Finished Newly Released 
Mepivacaine Local Anaesthetic Pathway Mepivacaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Mepivacaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Therefore mepivacaine preferentially inhibits neurons that are actively firing. Finished Newly Released 
Nabumetone Drug Pathway Most NSAIDs, including Nabumetone, are non-selective prostaglandin G/H synthase (better known as cyclooxygenase or COX) inhibitors that act on both prostaglandin G/H synthase 1 and 2 (COX-1 and -2). Prostaglandin G/H synthase catalyzes the conversion of arachidonic acid to prostaglandin G2 and prostaglandin G2 to prostaglandin H2. Prostglandin H2 is the precursor to a number of prostaglandins involved in fever, pain, swelling and inflammation (e.g. PGE2). Mefanamic acid antagonizes COX by binding to the upper portion of the active site, preventing its substrate, arachidonic acid, from entering the active site. The analgesic, antipyretic and anti-inflammatory effects of mefanamic acid occur as a result of decreased prostaglandin synthesis. Finished Newly Released 
Oxybuprocaine Local Anaesthetic Pathway Oxybuprocaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Oxybuprocaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Finished Newly Released 
Prilocaine Local Anaesthetic Pathway Prilocaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Prilocaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Therefore prilocaine preferentially inhibits neurons that are actively firing. Finished Newly Released 
Procaine Local Anaesthetic Pathway Procaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Procaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Therefore procaine preferentially inhibits neurons that are actively firing. Finished Newly Released 
Proparacaine Local Anaesthetic Pathway Proparacaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Proparacaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Therefore proparacaine preferentially inhibits neurons that are actively firing. Finished Newly Released 
Ropivacaine Local Anaesthetic Pathway Ropivacaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Ropivacaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Therefore ropivacaine preferentially inhibits neurons that are actively firing. Finished Newly Released 
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Pradeep Kumar Sreenivasaiah,
Dec 15, 2011, 11:14 PM
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Pradeep Kumar Sreenivasaiah,
Dec 15, 2011, 11:13 PM
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