BIOMAT Database Logo BIOMAT Database Logo

Synaptic transmission in ammonia intoxication. 1987

W Raabe

Ammonia intoxication allegedly plays a significant role in the pathophysiology of hepatic encephalopathy. In order to understand the pathogenesis of this encephalopathy it is necessary to know the effects of ammonia on the mechanisms by which neurons communicate, i.e., excitatory and inhibitory synaptic transmissions. NH4+ decreases excitatory synaptic transmission mediated by glutamate. Possibly, this effect is related to a depletion of glutamate in presynaptic terminals. NH4+ decreases inhibitory synaptic transmission mediated by hyperpolarizing Cl(-)-dependent inhibitory postsynaptic potentials. This effect is related to the inactivation of the extrusion of Cl- from neurons by NH4+. By the very same action, NH4+ also decreases the hyperpolarizing action of Ca2+- and voltage-dependent Cl- currents. These currents may modify the efficacy of the synaptic input to neurons and increase neuronal excitability. Estimates derived from experimental observations suggest that an increase of CNS tissue NH4+ to 0.5 mumol/g is sufficient to disturb excitatory and inhibitory synaptic transmission and to initiate the encephalopathy related to acute ammonia intoxication. Chronic portasystemic shunting of blood, as in hepatic encephalopathy, significantly changes the relation between CNS NH4+ and function of synaptic transmission. A portacaval shunt increases the tissue NH4+ necessary to disturb synaptic transmission. However, after a portasystemic shunt, synaptic transmission becomes extremely sensitive to any acute increase of NH4+ in the CNS.

UI MeSH Term Description Entries
D008564 Membrane Potentials The voltage differences across a membrane. For cellular membranes they are computed by subtracting the voltage measured outside the membrane from the voltage measured inside the membrane. They result from differences of inside versus outside concentration of potassium, sodium, chloride, and other ions across cells' or ORGANELLES membranes. For excitable cells, the resting membrane potentials range between -30 and -100 millivolts. Physical, chemical, or electrical stimuli can make a membrane potential more negative (hyperpolarization), or less negative (depolarization). Resting Potentials,Transmembrane Potentials,Delta Psi,Resting Membrane Potential,Transmembrane Electrical Potential Difference,Transmembrane Potential Difference,Difference, Transmembrane Potential,Differences, Transmembrane Potential,Membrane Potential,Membrane Potential, Resting,Membrane Potentials, Resting,Potential Difference, Transmembrane,Potential Differences, Transmembrane,Potential, Membrane,Potential, Resting,Potential, Transmembrane,Potentials, Membrane,Potentials, Resting,Potentials, Transmembrane,Resting Membrane Potentials,Resting Potential,Transmembrane Potential,Transmembrane Potential Differences
D009433 Neural Inhibition The function of opposing or restraining the excitation of neurons or their target excitable cells. Inhibition, Neural
D009435 Synaptic Transmission The communication from a NEURON to a target (neuron, muscle, or secretory cell) across a SYNAPSE. In chemical synaptic transmission, the presynaptic neuron releases a NEUROTRANSMITTER that diffuses across the synaptic cleft and binds to specific synaptic receptors, activating them. The activated receptors modulate specific ion channels and/or second-messenger systems in the postsynaptic cell. In electrical synaptic transmission, electrical signals are communicated as an ionic current flow across ELECTRICAL SYNAPSES. Neural Transmission,Neurotransmission,Transmission, Neural,Transmission, Synaptic
D011167 Portacaval Shunt, Surgical Surgical portasystemic shunt between the portal vein and inferior vena cava. Eck Fistula,Portacaval Anastomosis,Portacaval Shunt,Shunt, Surgical Portacaval,Surgical Portacaval Shunt,Anastomoses, Portacaval,Anastomosis, Portacaval,Fistula, Eck,Portacaval Anastomoses,Portacaval Shunts,Portacaval Shunts, Surgical,Shunt, Portacaval,Shunts, Portacaval,Shunts, Surgical Portacaval,Surgical Portacaval Shunts
D001921 Brain The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM. Encephalon
D006501 Hepatic Encephalopathy A syndrome characterized by central nervous system dysfunction in association with LIVER FAILURE, including portal-systemic shunts. Clinical features include lethargy and CONFUSION (frequently progressing to COMA); ASTERIXIS; NYSTAGMUS, PATHOLOGIC; brisk oculovestibular reflexes; decorticate and decerebrate posturing; MUSCLE SPASTICITY; and bilateral extensor plantar reflexes (see REFLEX, BABINSKI). ELECTROENCEPHALOGRAPHY may demonstrate triphasic waves. (From Adams et al., Principles of Neurology, 6th ed, pp1117-20; Plum & Posner, Diagnosis of Stupor and Coma, 3rd ed, p222-5) Encephalopathy, Hepatic,Portosystemic Encephalopathy,Encephalopathy, Hepatocerebral,Encephalopathy, Portal-Systemic,Encephalopathy, Portosystemic,Fulminant Hepatic Failure with Cerebral Edema,Hepatic Coma,Hepatic Stupor,Hepatocerebral Encephalopathy,Portal-Systemic Encephalopathy,Coma, Hepatic,Comas, Hepatic,Encephalopathies, Hepatic,Encephalopathies, Hepatocerebral,Encephalopathies, Portal-Systemic,Encephalopathies, Portosystemic,Encephalopathy, Portal Systemic,Hepatic Comas,Hepatic Encephalopathies,Hepatic Stupors,Hepatocerebral Encephalopathies,Portal Systemic Encephalopathy,Portal-Systemic Encephalopathies,Portosystemic Encephalopathies,Stupor, Hepatic,Stupors, Hepatic
D000641 Ammonia A colorless alkaline gas. It is formed in the body during decomposition of organic materials during a large number of metabolically important reactions. Note that the aqueous form of ammonia is referred to as AMMONIUM HYDROXIDE.

Related Publications

W Raabe
[Ammonia intoxication in cirrhotics].
March 1968, Cahiers d'anesthesiologie,
W Raabe
Ammonia intoxication in hepatic coma.
January 1984, JPMA. The Journal of the Pakistan Medical Association,
W Raabe
Ammonia intoxication in surgical patients.
November 1955, Annals of the Royal College of Surgeons of England,
W Raabe
AMMONIA INTOXICATION IN PORTAL HYPERTENSION.
January 1964, Biochemical clinics,
W Raabe
CHEMISTRY OF AMMONIA INTOXICATION.
January 1964, Biochemical clinics,
W Raabe
[On ammonia intoxication in acute peritonitis].
July 1968, Vestnik khirurgii imeni I. I. Grekova,
W Raabe
Acute anhydrous ammonia intoxication in cattle.
September 2006, Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc,
W Raabe
Cerebral alpha-ketoglutarate in ammonia intoxication.
November 1967, Gastroenterology,
W Raabe
Ammonia intoxication in portal systemic encephalopathy.
October 1982, JPMA. The Journal of the Pakistan Medical Association,
W Raabe
Liver disease and ammonia intoxication.
March 1963, Gut,
Copied contents to your clipboard!