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PubMed2003

Stimulation of gamma-aminobutyric acid synthesis activity in brown rice by a chitosan/glutamic acid germination solution and calcium/calmodulin.

Changes in the concentrations of gamma-aminobutyric acid (GABA), soluble calcium ions, glutamic acid, and the activity of glutamate decarboxylase (GAD) were investigated in non-germinated vs. germinated brown rice. Brown rice was germinated for 72 h by applying each of the following solutions: (1) distilled water, (2) 5 mM lactic acid, (3) 50 ppm chitosan in 5 mM lactic acid, (4) 5 mM glutamic acid, and (5) 50 ppm chitosan in 5 mM glutamic acid. GABA concentrations were enhanced in all of the germinated brown rice when compared to the non-germinated brown rice. The GABA concentration was highest in the chitosan/glutamic acid that germinated brown rice at 2,011 nmol/g fresh weight, which was 13 times higher than the GABA concentration in the non-germinated brown rice at 154 nmol/g fresh weight. The concentrations of glutamic acid were significantly decreased in all of the germinated rice, regardless of the germination solution. Soluble calcium and GAD were higher in the germinated brown rice with the chitosan/glutamic acid solution when compared to the rice that was germinated in the other solutions. GAD that was partially purified from germinated brown rice was stimulated about 3.6-fold by the addition of calmodulin in the presence of calcium. These data show that the germination of brown rice in a chitosan/glutamic acid solution can significantly increase GABA synthesis activity and the concentration of GABA.

Calcium↗
PubMed1985

Involvement of growth hormone-releasing factor in growth hormone secretion induced by gamma-aminobutyric acid in conscious rats.

Intracerebroventricular (icv) injection of gamma-aminobutyric acid (GABA) (10 mumol/rat) resulted in an increase in plasma GH in conscious freely moving rats pretreated with normal rabbit serum (0.5 ml/rat, iv). Rabbit antiserum specific for rat GH-releasing factor (GRF) (0.5 ml/rat, iv) abolished GH release induced by GABA in these animals. Rabbit anti-rat GRF serum also blunted GH release induced by a Met5-enkephalin analog, FK33-824 (10 micrograms/100 g BW, iv) in conscious rats. Considering our previous findings that rat GH release induced by FK33-824 was blunted by GABA antagonists (Endocrinology 103:1033, 1981), these results suggest that GH secretion induced by opioid peptides via GABAergic mechanisms is mediated, at least in part, by hypothalamic GRF in the rat.

Animals↗
PubMed1976

Desensitization to gamma-aminobutyric acid in crustacean muscle fibres.

1. Desensitization to gamma-aminobutyric acid (GABA) was demonstrated in crab muscle fibres by measurements to conductance changes induced by the drug. 2. In standard solutions (containing 34 mM-Ca2+), complete desensitization occurred in the presence of 5 X 10(-4) M-GABA. In Ca2+-free solutions, however, only partial (70-80%) desensitization was observed after the application of the same concentration of GABA. 3. Complete recovery of the membrane sensitivity to GABA was achieved after less than 60 min of continuous washout with standard solution. Only partial (10%) recovery was observed after 1 hr of washout with Ca2+-free solution. 4. The results support the 'receptor hypothesis' of desensitization which assumes transformation of the receptor from an effective to refractory state, as opposed to the 'ionophore hypothesis' which assumes direct inactivation of the synaptic current. 5. The possible mechanism by which Ca ions effect desensitization is discussed in terms of the 'cyclic model' of Katz & Thesleff (1957).

Aminobutyrates↗
PubMed1991

Expression of mammalian gamma-aminobutyric acid receptors with distinct pharmacology in Xenopus oocytes.

Gamma-Aminobutyric acid (GABA), the major inhibitory neurotransmitter in mammalian brain, is known to interact with two classes of GABA receptors denoted GABAA and GABAB. Using Xenopus oocytes, we compared the electrical and pharmacological properties of GABA receptors expressed by poly(A)+ RNA isolated from mammalian brain and retina. RNA from cerebral cortex expressed GABA responses with features characteristic of currents mediated by GABAA receptors. In contrast, RNA from retina expressed responses mediated by GABAA receptors and, in addition, GABA responses that were insensitive to the GABAA antagonist bicuculline and the GABAB agonist baclofen and showed no modulation by barbiturates or benzodiazepines. The bicuculline/baclofen-insensitive GABA response was a Cl- current that was blocked by picrotoxin but showed little desensitization or outward rectification. Our results suggest that mammalian retina contains RNAs encoding GABA receptors with distinct pharmacology.

Animals↗
PubMed1988

Identification of gamma-aminobutyric acid and its binding sites in Caenorhabditis elegans.

Gamma-aminobutyric acid (GABA), glutamate decarboxylase and GABA-transaminase were identified in the nematode Caenorhabditis elegans. The concentration of GABA in C. elegans (0.14 micrograms/mg protein) is approximately 10-fold lower than the concentration of GABA in rat brain. Glutamate decarboxylase and GABA-transaminase, the GABA anabolic and catabolic enzymes, are also present in C. elegans. Crude membrane fractions were prepared from C. elegans and used to study specific [3H] GABA binding sites. GABA binds to C. elegans membranes with high affinity (37 nM) and low capacity (Bmax = 2.25 pmol/mg protein). Muscimol is a competitive inhibitor of specific GABA binding with a KI value of 120 nM. None of the other GABA agonists or antagonists inhibited greater than 40% of the specific GABA binding at concentrations up to 10(-4)M. Thirteen spider venoms were examined as possible GABA agonists or antagonists, the venom from Calilena agelenidae inhibits specific GABA binding with a KI value of 6 nl/ml. These results suggest that GABA has a physiological role as a neurotransmitter in C. elegans.

4-Aminobutyrate Transaminase↗
PubMed1995

gamma-Aminobutyric acid (GABA) metabolism in mammalian neural and nonneural tissues.

4-Aminobutyric acid (GABA), a major inhibitory neurotransmitter of mammalian central nervous system, is found in a wide range of organisms, from prokaryotes to vertebrates. GABA is widely distributed in nonneural tissue including peripheral nervous and endocrine systems. GABA acts on GABAA and GABAB receptors. GABAA receptors are ligand-gated chloride channels modulated by a variety of drugs. GABAB receptors are essentially presynaptic, usually coupled to potassium or calcium channels, and they function via a GTP binding protein. In neural and nonneural tissues, GABA is metabolized by three enzymes--glutamic acid decarboxylase (GAD), which produces GABA from glutamic acid, and the catabolic enzymes GABA-transaminase (GABA-T) and succinic semialdehyde dehydrogenase (SSADH). Production of succinic acid by SSADH allows entry of the GABA carbon skeleton into the tricarboxylic acid cycle. Alternate sources of GABA include putrescine, spermine, spermidine and ornithine, which produce GABA via deamination and decarboxylation reactions, while L-glutamine is an additional source of glutamic acid via deamination. GAD from mammalian brain occurs in two molecular forms, GAD65 and GAD67 (referring to subunit relative molecular weight (Mr) in kilodaltons). These different forms of GAD are the product of different genes, differing in nucleotide sequence, immunoreactivity and subcellular localization. The presence and characteristics of GAD have been investigated in a wide variety of nonneural tissues including liver, kidney, pancreas, testis, ova, oviduct, adrenal, sympathetic ganglia, gastrointestinal tract and circulating erythrocytes. In some tissues, one form (GAD65 or GAD67) predominates. GABA-T has been located in most of the same tissues, primarily through histochemical and/or immunochemical methods; GABA-T is also present in a variety of circulating cells, including platelets and lymphocytes. SSADH, the final enzyme GABA catabolism, has been detected in some of the tissues in which GAD and GABA-T have been identified, although the presence of this enzyme has not been in mammalian pancreas, ova, oviduct, testis or sympathetic ganglia.

Animals↗
PubMed1991

gamma-Aminobutyric acid enhances the tone of human internal anal sphincter.

The effect of gamma-aminobutyric acid (GABA) on the human internal anal sphincter was investigated. Cumulative applications of GABA produced concentration-dependent contractions (10(-8)-10(-5) M) of the isolated human sphincter. Pretreatment with bicuculline (GABAA antagonist) turned them to relaxation. Muscimol, a GABAA agonist, induced concentration-dependent contractions (10(-8)-10(-5) M); however, baclofen (GABAB agonist, 10(-8)-10(-5) M) promoted concentration-dependent relaxation of the strips. These results suggested that both excitatory GABAA receptors and inhibitory GABAB receptors exist in the internal anal sphincter. Oral administration of sodium valproate (1600 mg/day), a GABA transaminase inhibitor, enhanced the anal canal resting pressure in 10 normal volunteers. Anal manometry showed a significant elevation in tonus without affecting amplitudes or frequencies. These results indicated that endogenous GABA, which was increased by sodium valproate, produced elevations in the anal canal resting pressure through its specific receptors in the human internal anal sphincter.

Anal Canal↗
PubMed1994

Intestinal absorption pathway of gamma-aminobutyric acid in rat small intestine.

Intestinal absorption of gamma-aminobutyric acid (GABA), as a model compound for gamma-aminoacids, has not been extensively studied from the kinetic viewpoint. Since data from our laboratory suggested that some competition arises between intestinal absorption of beta-alanine and GABA and since our intent was to maintain the aqueous stagnant diffusion layer in order to approach absorption tests to in vivo physiological conditions, a rat jejunum in situ study was undertaken in order to gain an insight into the mechanism of GABA absorption. In the present paper, results from assays using isotonic perfusion solutions with starting GABA concentrations ranging from 1 to 50 mM are reported. They show that the intestinal absorption of the gamma-aminoacid can be apparently described as a specialized transport mechanism which obeys Michaelis-Menten and first-order kinetics. Parameter values found were Vm = 13.99 +/- 2.37 mM h-1, Km = 3.87 +/- 0.63 mM, and ka(passive) = 0.362 +/- 0.120 h-1. Through the perfusion of 5 mM beta-alanine solutions containing variable concentrations of GABA (from 5 to 50 mM), a partially competitive inhibition of beta-alanine absorption was apparently characterized.

Alanine↗
PubMed1994

Dorsal column inhibition of nociceptive thalamic cells mediated by gamma-aminobutyric acid mechanisms in the cat.

Cells in posterior parts of the cat thalamus were investigated. Responses in single units excited by electrical stimulation in the lateral funiculus (LF), the dorsal column nucleus (DCN) or the canine tooth pulp (TP) were analysed. All cells had a spontaneous resting activity which could be increased by extracellular iontophoretic application of DL-homocysteic acid (DLH) and decreased by gamma-aminobutyric acid (GABA). No effect on the spontaneous firing rate was observed following iontophoresis of the selective GABA-antagonists, picrotoxin (GABA-A receptor antagonist) or saclofen (GABA-B receptor antagonist). However, the decreased firing following GABA application was partially blocked by picrotoxin but not by saclofen. A phasic inhibition induced by DCN stimulation in nociceptive thalamic cells is indicated since simultaneous administration of picrotoxin increased the evoked response. This type of inhibitory mechanism could not be detected following LF or TP stimulation. The extracellular activity evoked by electrical stimulation of LF or TP was significantly depressed by preceding electrical stimulation in the DCN. This inhibition was reversed by simultaneous administration of picrotoxin, indicating an involvement of GABA-A receptors. The reversal of the DCN-induced depression of the late responses following LF stimulation occurred after application of saclofen. It is suggested that this effect is partly mediated via GABA-B receptors. Results from the present study indicate an interaction in the thalamus between presumed low-threshold (DCN) and presumed nociceptive afferents (LF and TP) similar to that previously described in the spinal cord.

Afferent Pathways↗
PubMed1992

Effects of exogenous gamma-aminobutyric acid on experimental arrhythmias.

The effects of exogenous gamma-aminobutyric acid (GABA) 10 mg.kg-1 iv in preventing arrhythmias induced by drugs and ischemia were studied in mice, rats, and guinea pigs. It was found that the threshold dose of aconitine inducing arrhythmia in mice and the recovery rate to normal sinus rhythm increased significantly, ED50 of GABA was 5.4-5.8 mg.kg-1. The duration of ventricular tachycardia (VT) induced by aconitine in rats was shortened (P < 0.01). The incidence and the mortality of ventricular fibrillation (VF) in GABA group were decreased to 0/10 vs 6/10 and 5/10 in control, respectively (P < 0.05). The doses of ouabain to induce ectopic beats (EB), VT, VF, and cardiac arrest (CA) in guinea pigs were increased (P < 0.01). The incidence of VF induced by coronary artery ligation in rats was decreased to 0/5 in GABA group vs 4/5 in control group (P < 0.01). The total amount of EB, total time of VT, and VF were 66%, 41%, and 0% of the control group, respectively. The anti-arrhythmic effects of GABA were dose-dependent and as potent as procainamide (10 or 5 mg.kg-1, iv). The results suggest GABA (10 mg.kg-1, iv) may be useful for the prevention of VT and VF.

Aconitine↗
PubMed1993

Gamma-aminobutyric acid (GABA) immunoreactivity in the mouse adrenal gland.

Gamma-aminobutyric acid (GABA) immunoreactivity was revealed by immunocytochemistry in the mouse adrenal gland at the light and electron microscopic levels. Groups of weakly or faintly GABA immunoreactive chromaffin cells were often seen in the adrenal medulla. By means of immunohistochemistry combined with fluorescent microscopy, these GABA immunoreactive chromaffin cells showed noradrenaline fluorescence. The immunoreaction product was seen mainly in the granular cores of these noradrenaline cells. These results suggest the co-existence of GABA and noradrenaline within the chromaffin granules. Sometimes thick or thin bundles of GABA immunoreactive nerve fibers with or without varicosities were found running through the cortex directly into the medulla. In the medulla, GABA immunoreactive varicose nerve fibers were numerous and were often in close contact with small adrenaline cells and large ganglion cells; a few, however, surrounded clusters of the noradrenaline cells, where membrane specializations were formed. Single GABA immunoreactive nerve fibers, and thin or thick bundles of the immunoreactive varicose nerve fibers ran along the blood vessels in the medulla. The immunoreaction deposits were observed diffusely in the axoplasm and in small agranular vesicles of the GABA immunoreactive nerve fibers. Since no ganglion cells with GABA immunoreactivity were found in the adrenal gland, the GABA immunoreactive nerve fibers are regarded as extrinsic in origin.

Adrenal Medulla↗
PubMed1988

Changes in cerebral receptors for gamma aminobutyric acid in patients with hepatic encephalopathy.

If the gamma-aminobutyric acid (GABA) inhibitory neurotransmitter system plays an important role in the mediation of hepatic encephalopathy (HE) in man, changes in the status of receptors for GABA in the brain may occur in patients with HE. To test this possibility, brains were obtained at autopsy from 11 patients who had died of causes unrelated to liver disease and from 11 patients who had died with chronic liver disease. Eight of the liver disease group had overt HE at the time of death. The specific binding of GABA to synaptic membranes isolated from frontal cortex was determined. Mean specific binding of GABA for patients with cirrhosis without overt HE was similar to that for control patients. In contrast, corresponding means for patients who had mild HE (stages I-III) and for patients who had severe HE (stage IV) were 45% higher (p less than 0.05) and 43% lower, respectively, than that for control patients. The mean specific binding of GABA was significantly greater for patients with mild HE than in patients with severe HE (p less than 0.025). Scatchard plots of the GABA binding data were curvilinear and consistent with a model of GABA receptors with two independent binding sites. Computer-assisted analysis of the binding data indicated that the altered GABA binding observed in patients with HE is attributable to changes in the affinity rather than the density of both GABA receptors (increased affinities in mild HE, and decreased affinities in hepatic coma). These findings are compatible with the hypothesis that alterations in GABAergic neurotransmission are associated with and contribute to the syndrome of HE in man.

Aged↗
PubMed1992

Molecular mechanisms of the partial allosteric modulatory effects of bretazenil at gamma-aminobutyric acid type A receptor.

In central nervous system gamma-aminobutyric acid (GABA) inhibits neuronal activity by acting on GABA type A (GABAA) receptors. These heterooligomeric integral membrane proteins include a GABA-gated Cl- channel and various allosteric modulatory sites where endogenous modulators and anxiolytic drugs act to regulate GABA action. In vivo, various anxiolytic drugs exhibit a wide range of variability in their modulatory efficacy and potency of GABA action. For instance, bretazenil modulatory efficacy is much lower than that of diazepam. Such low efficacy could be due either to a preferential modulation of specific GABAA receptor subtypes or to a low modulatory efficacy at every GABAA receptor subtype. To address these questions we studied drug-induced modifications of GABA-activated Cl- currents in native GABAA receptors of cortical neurons in primary cultures and in recombinant GABAA receptors transiently expressed in transformed human embryonic kidney cells (293) after transfection with cDNAs encoding different molecular forms of alpha, beta, and gamma subunits of GABAA receptors. In cortical neurons the efficacy of bretazenil was lower than that of diazepam, whereas the potency of the two drugs was similar. In cells transfected with gamma 2 subunits and various molecular forms of alpha and beta subunits bretazenil efficacy was always lower than that of diazepam. However, in cells transfected with gamma 1 or gamma 3 subunits and various forms of alpha and beta subunits the efficacy of both diazepam and bretazenil was lower and always of similar magnitude. When bretazenil and diazepam were applied together to GABAA receptors including a gamma 2 subunit, the action of diazepam was curtailed in a manner related to the dose of bretazenil.

Allosteric Regulation↗
PubMed2002

Activation of A-type gamma-aminobutyric acid receptors excites gonadotropin-releasing hormone neurons.

Gamma-aminobutyric acid (GABA), acting through GABA(A) receptors (GABA(A)R), is hypothesized to suppress reproduction by inhibiting GnRH secretion, but GABA actions directly on GnRH neurons are not well established. In green fluorescent protein-identified adult mouse GnRH neurons in brain slices, gramicidin-perforated-patch-clamp experiments revealed the reversal potential (E(GABA)) for current through GABA(A)Rs was depolarized relative to the resting potential. Furthermore, rapid GABA application elicited action potentials in GnRH neurons but not controls. The consequence of GABA(A)R activation depends on intracellular chloride levels, which are maintained by homeostatic mechanisms. Membrane proteins that typically extrude chloride (KCC-2 cotransporter, CLC-2 channel) were absent from the GT1-7 immortalized GnRH cell line and GnRH neurons in situ or were not localized to the proper cell compartment for function. In contrast, GT1-7 cells and some GnRH neurons expressed the chloride-accumulating cotransporter, NKCC-1. Patch-clamp experiments showed that blockade of NKCC hyperpolarized E(GABA) by lowering intracellular chloride. Regardless of reproductive state, rapid GABA application excited GnRH neurons. In contrast, bath application of the GABA(A)R agonist muscimol transiently increased then suppressed firing; suppression persisted 4-15 min. Rapid activation of GABA(A)R thus excites GnRH neurons whereas prolonged activation reduces excitability, suggesting the physiological consequence of synaptic activation of GABA(A)R in GnRH neurons is excitation.

Action Potentials↗
PubMed1994

Expression of GAT-1, a high-affinity gamma-aminobutyric acid plasma membrane transporter in the rat retina.

Gamma-aminobutyric acid (GABA) plasma membrane transporters influence synaptic transmission by high-affinity, Na(+)-dependent transport processes. The cDNA clone, GAT-1, encodes a high-affinity Na(+)- and Cl(-)-dependent GABA plasma membrane transporter, which has kinetic and pharmacological properties similar to those of high-affinity GABA uptake systems associated with neurons. The present study evaluates the distribution and cellular localization of this putative neuronal GABA transporter by RNA blot hybridization and in situ hybridization histochemistry in the rat retina. Northern blot hybridization analysis of total retinal and cerebellar RNA extracts demonstrated a single band of hybridization at 4.2 kilobases. GABA transporter mRNA is expressed by numerous cells that are distributed to the proximal inner nuclear layer and the ganglion cell layer and by a few cells located in the inner plexiform layer. Double label studies combining the retrograde transport of the fluorescent dye Fluorogold from the superior colliculus to identify ganglion cells and in situ hybridization histochemistry demonstrated that most GAT-1 mRNA-containing cells in the ganglion cell layer are displaced amacrine cells, although some ganglion cells containing GAT-1 mRNA were visualized. In freshly dissociated retinal cell preparations, the GAT-1 RNA signal is strong in neurons and weak to moderate in specialized glial cells called Müller cells. Müller cells were identified by both their morphology and the presence of the selective Müller cell marker cellular retinaldehyde-binding protein. Only background labeling is seen with the sense GAT-1 RNA probe in both tissue sections and dissociated retinal cell preparations. These findings demonstrate that GAT-1 mRNA is expressed in both the retina and brain. In the retina, this transporter is predominantly localized to amacrine, displaced amacrine and interplexiform cells, and some ganglion cells. This transporter mRNA is also expressed by Müller cells but at a lower level than by neurons. These observations indicate that GABA transport by GAT-1 plasma membrane transporters in the retina is mediated by both neurons and glia cells.

Animals↗
PubMed1983

Distribution of gamma aminobutyric acid containing neurons and terminals in the septal area. An immunohistochemical study using antibodies to glutamic acid decarboxylase in the rat brain.

The distribution of gamma aminobutyric acid (GABA)-containing neurons and nerve terminals was examined in the rat septal area by using specific antibodies to the enzyme glutamic acid decarboxylase (GAD) in combination with the avidin-biotin immunoperoxidase method. Whereas only a few GAD positive neurons were present in the septum of normal rats, the septal area of rats treated with colchicine, an inhibitor of fast axonal transport, showed numerous GAD-immunoreactive neurons. These neurons were evenly filled with GAD-immunoreactive material throughout the cytoplasm of the soma and proximal parts of the dendrites. Although GAD-positive neurons were present in most parts of the septal area, their density differed greatly in the different septal subnuclei. Both the diagonal band of Broca (vertical and horizontal parts) and the lateral septum were rich in GAD positive cell bodies, whereas the medial septal nucleus and the intermediate parts of the lateral septum contained relatively few. Within the lateral septum itself a larger number of labeled cell bodies was present in its ventral subdivision. The anterior hippocampal rudiment (taenia tecta) contained numerous GAD-positive neurons, while the septal component of the island of Calleja (insula magna) was devoid of them. GAD-immuno-positive neurons found within the septum ranged from small (15 microns) to large (30-35 micron). They were round or multipolar in the diagonal band, medium-sized multipolar in the lateral septum, and pyramidal, round or fusiform in the anterior hippocampal rudiment. GAD-immunoreactive nerve terminals are present in most subdivisions of the septal nuclei, with the exception of myelinated fiber tracts, and throughout all rostrocaudal levels of the septum. However, the density of the innervation is not the same within all individual nuclei. The lateral septum (dorsal and ventral parts) contained high density innervation but the diagonal band of Broca had a lower density of GAD-positive terminals. The lateral border of the islands of Calleja was rich in thick GAD-positive processes that appeared to be continuous with GAD-immunoreactive processes of the substantia inominata. The inner portion of the molecular layer adjacent to the granule cells of the anterior hippocampal rudiment contained a rich GAD-positive terminal field.

Animals↗
PubMed1996

Inhibition of gamma-aminobutyric acid aminotransferase from rat brain mitochondria by chloride and acetate.

10-100 mmol/l of acetate inhibits gamma-aminobutyric acid aminotransferase from rat brain mitochondria by 35-90%. Similarly, 50-100 mmol/l of chloride inhibits this enzyme by 10-30%. In either case, the inhibition is competitive with GABA and noncompetitive with alpha-ketoglutarate. The effect of sodium and potassium is negligible. gamma-Aminobutyric acid aminotransferase from rat liver mitochondria is also inhibited by acetate and chloride. The degree of inhibition of both hepatic and cerebral enzyme is nearly the same.

4-Aminobutyrate Transaminase↗
PubMed1993

Molecular electrostatic potentials from crystal diffraction: the neurotransmitter gamma-aminobutyric acid.

Given the electronic charge parameters obtained from a diffraction study of the charge density distribution in a crystal, a mathematical procedure is presented for deriving the electrostatic potential. The procedure allows the mapping of electrostatic potential for a molecule or group of molecules removed from the crystal structure but with each molecule retaining the effects of polarization owing to the original crystal environment. The method is applied for the neurotransmitter gamma-aminobutyric acid. The potential for a gamma-aminobutyric acid molecule is analyzed in terms of a simple model that is suitable for rapid computations concerned with Coulombic molecular interactions. Outside the molecular envelope at 1.2 A from the atomic nuclei, the total potential is well represented by a sum of spherical atom contributions with V(r) = (q/r) + exp(-beta r2). The most important aspherical component in the potential is the dipole contribution from the hydrogen atoms. This can be represented as V(r, phi) = (0.162 cos phi)/(r2 + 0.615). Here, V is in e/A, r is the distance from each nucleus in A, q is the experimentally determined net atomic charge in electron units, and phi is the angle between r and the bond X-H. We obtain beta = 1.47, 1.66, 1.83 A-2 for C, N, and O respectively. For H, no term in beta is needed.

Biophysical Phenomena↗