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PubMed1981

Metabolism of allylglycine and cis-crotylglycine by Pseudomonas putida (arvilla) mt-2 harboring a TOL plasmid.

Spontaneous mutants which acquired the ability to utilize d-allylglycine (d-2-amino-4-pentenoic acid) and dl-cis-crotylglycine (dl-2-amino-cis-4-hexenoic acid) but not l-allylglycine or dl-trans-crotylglycine could be readily isolated from Pseudomonas putida mt-2 (PaM1). Derivative strains of PaM1 putatively cured of the TOL (pWWO) plasmid were incapable of forming mutants able to utilize the amino acids for growth; however, this ability could be regained by conjugative transfer of the TOL (pWWO) plasmid from a wild-type strain of mt-2 or of the TOL (pDK1) plasmid from a related strain of P. putida (HS1), into cured recipients. dl-Allylglycine-grown cells of one spontaneous mutant (PaM1000) extensively oxidized dl-allylglycine and dl-cis-crotylglycine, whereas only a limited oxidation was observed toward l-allylglycine and dl-trans-crotylglycine. Cell extracts prepared from PaM1000 cells contained high levels of 2-keto-4-hydroxyvalerate aldolase and 2-keto-4-pentenoic acid hydratase, the latter enzyme showing higher activity toward 2-keto-cis-4-hexenoic acid than toward the trans isomer. Levels of other enzymes of the TOL degradative pathway, including toluate oxidase, catechol-2,3-oxygenase, 2-hydroxymuconic semialdehyde hydrolase, and 2-hydroxymuconic semialdehyde dehydrogenase, were also found to be elevated after growth on allylglycine. Whole cells of a putative cured strain, PaM3, accumulated 2-keto-4-pentenoic acid from d-allylglycine, which was shown to be rapidly degraded by cell extracts of PaM1000 grown on dl-allylglycine. These same cell extracts were also capable of catalyzing the dehydrogenation of d- but not l-allylglycine and were further found to metabolize the amino acid completely to pyruvate and acetaldehyde. Differential centrifugation of crude cell extracts localized d-allylglycine dehydrogenase activity to membrane fractions. The results are consistent with a catabolic pathway for d-allylglycine and dl-cis-crotylglycine involving the corresponding keto-enoic acids as intermediates, the further metabolism of which is effected by the action of TOL plasmid-encoded enzymes.

Acetaldehyde↗
PubMed1988

Injection of L-allylglycine into the posterior hypothalamus in rats causes decreases in local GABA which correlate with increases in heart rate.

Injection of the GABA antagonist, bicuculline methiodide into the posterior hypothalamus of rats has been shown to cause marked increases in heart rate and lesser elevations in blood pressure. Allylglycine is a potent inhibitor of the synthetic enzyme for GABA, glutamic acid decarboxylase, only after in vivo biotransformation into its active form, 2-keto-4-pentenoic acid, through a stereospecific amino acid oxidase. The posterior hypothalamus is thought to contain substantial activity only of L-amino acid oxidase. In this study, the stereoisomers of allylglycine were injected into the posterior hypothalamus at a site also shown to be reactive to bicuculline. Injection of L-allylglycine but not D-allylglycine caused substantial increases in heart rate but only slight increases in blood pressure. Injection of the GABA agonist muscimol prior to treatment with L-allylglycine prevented these cardiovascular changes. In another series of experiments, levels of GABA in the posterior hypothalamus and adjacent areas were measured 90 min after unilateral injection of L-allylglycine (12.5 or 25 micrograms), D-allylglycine (25 micrograms) or saline into the posterior hypothalamus. Only L-allylglycine caused increases in heart rate and blood pressure and decreases in levels of GABA. Quantitatively, the increases in heart rate at sacrifice were strongly correlated with the decreases in levels of GABA in the injected posterior hypothalamus (r = -0.94; P less than 0.002) but not in other regions.(ABSTRACT TRUNCATED AT 250 WORDS)

Allylglycine↗
PubMed1973

Seizures induced by allylglycine, 3-mercaptopropionic acid and 4-deoxypyridoxine in mice and photosensitive baboons, and different modes of inhibition of cerebral glutamic acid decarboxylase.

1. DL-C-Allyglycine, 4-deoxypyridoxine hydrochloride and 3-mercaptopropionic acid have been studied with reference to their convulsant effects in mice and in baboons (Papio papio) with photosensitive epilepsy, and their action on the cerebral enzyme synthesizing gamma-aminobutyric acid (L-glutamate-1-carboxy-lyase).2. In mice, the ED(50) values for seizures following intraperitoneal injection were allylglycine 1.0 mmol/kg body weight, 4-deoxypyridoxine 1.1 mmol/kg and 3-mercaptopropionic acid 0.27 mmol/kg. Latency to seizure onset was longest after allylglycine (44-240 min), intermediate after 4-deoxypyridoxine (9-114 min) and shortest after 3-mercaptopropionic acid (2.5-8 min).3. In Papio papio intravenous administration of subconvulsant doses of allylglycine (0.87-3.1 mmol/kg), or of 4-deoxypyridoxine (0.21-0.53 mmol/kg) enhanced the occurrence and persistence of myoclonic responses to intermittent photic stimulation, and augmented the associated electroencephalographic abnormalities, without modifying their character or distribution. Higher doses produced brief seizures recurring at regular intervals, between 2-14 h after allylglycine (4.0-4.3 mmol/kg) or 1-4 h after 4-deoxypyridoxine (0.53-0.87 mmol/kg). Electroencephalographically these seizures originated unilaterally in the occipital or posterior parietal cortex.4. In Papio papio photically-induced epileptic responses were enhanced 5-10 min after the intravenous injection of 3-mercaptopropionic acid (0.09-0.28 mmol/kg). A sequence of brief generalized seizures followed by complete recovery occurred 4-17 min after the injection of 3-mercaptopropionic acid (0.28-0.38 mmol/kg). Fatal status epilepticus followed the injection of 3-mercaptopropionic acid (0.57-0.75 mmol/kg). E.E.G. records showed generalized cortical involvement at the onset of the seizures.5. L-Glutamate 1-carboxy-lyase (GAD) activity was determined in whole brain homogenates from mice killed at various intervals after receiving i.p. a convulsant dose of one of the compounds. Inhibition of GAD activity was evident 30-60 min before seizure onset following allylglycine or 4-deoxypyridoxine administration, and was maximal (40-60%) just before or during seizure activity. Addition of pyridoxal phosphate to the brain homogenate relieved inhibition produced by 4-deoxypyridoxine but not that produced by allylglycine. Inhibition of GAD activity in brain homogenates from animals killed 2 or 4 min after injection of a convulsant dose of 3-mercaptopropionic acid varied from 0-49% depending on the dose of 3-mercaptopropionic acid and the concentration of substrate in the assay system.6. Kinetic analysis of the inhibition of GAD activity following direct addition of the compounds to mouse brain homogenates indicated that 3-mercaptopropionic acid (0.01-0.5 mM) was competitive with respect to the substrate. A comparable percentage inhibition of GAD activity was obtained only with much higher concentrations of 4-deoxypyridoxne, i.e. 10-50 mM. Allylglycine in vitro was a very weak inhibitor of GAD activity.7. Three biochemically different mechanisms underlie the inhibition of cerebral GAD activity that precedes seizures induced by ailylglycine, 4-deoxypyridoxine and 3-mercaptopropionic acid. The data are consistent with a critical reduction in the rate of synthesis of gamma-aminobutyric acid being responsible for the onset of seizures.

Allyl Compounds↗
PubMed1987

Redistribution of transmitter amino acids in rat hippocampus and cerebellum during seizures induced by L-allylglycine and bicuculline: an immunocytochemical study with antisera against conjugated GABA, glutamate and aspartate.

The effects of the convulsants L-allylglycine and bicuculline on the distribution of gamma-amino-butyric acid (GABA), glutamate and aspartate in rat brains were assessed immunocytochemically, using antisera raised against glutaraldehyde-protein conjugates of the respective amino acids. In accord with previous biochemical studies of GABA content, L-allylglycine treatment was followed by a decreased immunoreactivity for GABA in the hippocampus and cerebellum, whereas treatment with bicuculline led to an increased immunoreactivity in the hippocampus, but not in the cerebellum. Different cells and zones were affected differentially. With both convulsants the hippocampus showed the most pronounced changes in the neuropil of the pyramidal and granular cell layers. L-Allylglycine treatment led to a substantial decrease in the concentration of detectable GABA-immunoreactive bouton-like dots in the stratum oriens, radiatum and lacunosum-moleculare and in the deep hilar region, but did not produce statistically significant changes in this parameter in the outer and intermediate zones of the dentate molecular layer. In the cerebellum, the decrease in GABA immunoreactivity after L-allylglycine treatment was less in the basket cell terminals than in other GABA-containing elements. Neither convulsant altered the average staining intensity for aspartate or glutamate in the two regions studied, but L-allylglycine reduced the level of aspartate-like immunoreactivity in hippocampal hilar cells. All the changes described were evident after 20 min of seizure activity and were qualitatively similar after 60 min of seizure (animals paralysed and ventilated). Our results indicate that L-allylglycine or bicuculline given intravenously exerts specific effects on cerebral amino acid metabolism. The nature and magnitude of these effects show inter-regional variations and also differ among cellular compartments within each region. Amino acid immunocytochemistry may prove to be a valuable tool for the investigation of metabolic changes associated with epileptic seizures and should be particularly useful in regions showing heterogeneous changes that would tend to cancel each other in biochemical analyses.

Allylglycine↗
PubMed2005

Ring-closing metathesis of C-terminal allylglycine residues with an N-terminal beta-vinyl-substituted phosphotyrosyl mimetic as an approach to novel Grb2 SH2 domain-binding macrocycles.

Ring-closing metathesis (RCM) of peptides often requires insertion of allylglycines at the intended sites of ring juncture, which can result in the displacement of residues that are needed for biological activity. This type of side-chain deletion can be avoided by appending beta-vinyl substituents onto the parent residues at the intended sites of ring juncture, thereby effectively converting them into functionalized allylglycine equivalents. Such an approach has been previously applied in modified form to growth-factor receptor bound 2 (Grb2) SH2 domain-binding peptides by using an N-terminal beta-vinyl-functionalized phosphotyrosyl mimetic and C-terminal 2-allyl-3-aryl-1-propanamides that lacked the alpha-carboxyl portion of allylglycine residues. These C-terminal moieties involved lengthy synthesis and once prepared, required an individual total synthesis of each final macrocycle. Work reported herein significantly enhances the versatility of the original approach through the use of C-terminal allylglycine amides that can be prepared from commercially available L- and D-allylglycines and suitable amines. This methodology could be generally useful where macrocylization is desired with maintenance of functionality at a site of ring juncture.

Adaptor Proteins, Signal Transducing↗
PubMed1979

Proconvulsant, convulsant and other actions of the D- and L-stereoisomers of allylglycine in the photosensitive baboon, Papio papio.

The effects of the intravenous or intracerebroventricular injection of the stereoisomers, and the racemic mixture, of allylglycine (2-amino-pent-4-enoic acid) have been studied in baboons, Papio papio, with photosensitive epilepsy. Enhancement of the natural syndrome of photosensitivy epilepsy is seen 1-12 h (maximally at 3-8 h) after L-allyglycine, 100 mg/kg, intravenously, or D,L-allyglycine, 200 mg/kg, intravenously. Such enhancement is seen with a slower onset, and to a lesser, and more variable, extent after D-allyglycine, 500-750 mg/kg, intravenously. Brief focal or generalised seizures occurred (in the absence of intermittent photic stimulation) after L-allyglycine, 150-200 mg/kg, intravenously. This effect is similar to that previously observed after D,L-allyglycine, 300-400 mg/kg. D-Allyglycine, 780 mg/kg, intravenously produced episodes of vertical nystagmus with increased extensor motor tone, but no 'spontaneous' seizures. Intracerebroventricular injection of L-allylglycine, D-allyglycine or D,L-allyglycine, 100 mg in 1 ml saline, did not modify the natural syndrome of photosensitive epilepsy. D-Allylglycine, or D,L-allyglycine, 100 mg intracerebroventricularly, after 1-2 h gave rise to a syndrome with vomiting, sustained vertical nystagmus, and intermittent extensor spasms. The results are interpreted in terms of regional differences in the metabolism of the two isomers to active compounds that can inhibit glutamic acid decarboxylase. D-Allylglycine is active only at the brain stem and cerebellum because D-amino acid oxidase is largely confined to these brain areas.

Allylglycine↗
PubMed1991

Allylglycine-induced seizures in male and female rats.

The possibility that a sex difference in gamma-aminobutyric acid (GABA) activity might be an underlying cause of the previously reported sex differences in picrotoxin-induced seizures was investigated. Male and female rats were injected (IP) with the GABA antagonist, L-allylglycine (100, 150, 200, or 250 mg/kg), and observed for behavioral signs of five categories of seizures induced by picrotoxin: myoclonic, focal, generalized tonic extension, generalized clonic, and generalized seizures with tonic and clonic components. The latency to the first occurrence of each seizure category was scored. Of the five categories of seizures investigated, only focal and generalized tonic extension seizures were observed after allylglycine in the doses tested. Female rats were significantly more susceptible than male rats to allylglycine-induced focal (p less than 0.007) and generalized tonic extension (p less than 0.05) seizures. The results suggest that male-female differences in presynaptic GABA activity may have relevance for sex differences in the occurrence of focal and tonic extension seizures. Differences in the seizure profiles associated with allylglycine and picrotoxin suggests that pre- and postsynaptic antagonism of GABA activity may have different consequences for specific seizure categories and the sex differences associated with those categories.

Allylglycine↗
PubMed1986

Effects of allylglycine on photosensitivity in the lateral geniculate-kindled cat.

The effects of DL-allylglycine, an inhibitor of GABA synthesis, on the responses to photic stimulation were studied in the cat kindled in the lateral geniculate body (GL). For 3 to 8 h after the injection of DL-allylglycine at a subconvulsant dose (30 or 40 mg/kg, i.v.), the kindled cat showed a stable level of photosensitivity without any toxic effects and responded with various degrees of myoclonus or a generalized tonic-clonic convulsion when photic stimulation was repeated at hourly intervals. The incidence of photically induced myoclonus reached its plateau during this period. Our results suggest that photosensitivity of the lateral geniculate-kindled cat is related to the modification of GABAergic mechanisms, and that when the GL-kindled cat is pretreated with DL-allylglycine it is a reliable model of photosensitive epilepsy.

Allylglycine↗
PubMed1989

Allylglycine and brain excitability. Electrophysiological investigation in cats.

The effect of DL-allylglycine (DL-AG) in two doses (40 and 60 mg/kg i.v.) was studied on cats under acute conditions. DL-AG provoked the appearance of epileptiform EEG patterns either spontaneous or in response to intermittent light stimulation with a frequency of 5-25 Hz. The effect was dose-dependent. The paroxysmal EEG was restricted to or began in the cortex and later it appeared in the thalamus and mesencephalic reticular formation. This finding together with the observation that after DL-AG the visual evoked potentials increased in the primary visual cortex and decreased in the centre median nucleus and in the reticular formation support the view about the role of the cortex in the increased brain excitability and in the increased photosensitivity after allylglycine. The photosensitive of spontaneous epileptiform EEG activity in cats pretreated with DL-allylglycine could be an useful experimental model of epilepsy for assessing the efficacy of anticonvulsant drugs.

Allylglycine↗
PubMed1985

Strychnine and L-allylglycine but not bicuculline and picrotoxin induce transsynaptic degeneration following transection of the inferior alveolar nerve in adult rats.

The effects of the convulsants strychnine, bicuculline, picrotoxin and L-allylglycine on the transsynaptic destruction of medullary dorsal horn neurons were examined following transection of the inferior alveolar nerve in adult rats. Strychnine and L-allylglycine enhanced the transsynaptic effect of nerve transection and caused degeneration of many dorsal horn neurons, while bicuculline and picrotoxin did not. The removal of glycinergic and GABAergic postsynaptic inhibition appears to enhance the transsynaptic destructive activity which follows the peripheral nerve transection.

Allylglycine↗
PubMed1985

Bicuculline- and allylglycine-induced epilepsy in developing rats.

The development of bicuculline- and allylglycine-induced epilepsy has been studied in developing rats (6 to 30 days old). The results showed that during the first period of life, in both experimental models, the behavioral modifications were atypical and poorly correlated to corresponding epileptic EEG changes. Successively, a gradual evolution of the electroclinical patterns was observed, with similar characteristics in both bicuculline- and allylglycine-treated animals. Only from the 3rd week did electroclinical patterns similar to those of adult animals and more specific for the type of the convulsant agent appear. These data suggest that during the 1st 2 weeks after birth, the level of global cerebral immaturity, rather than the type of the epileptogenic substance, is the prominent element in the characterization of epileptic manifestations. From the 3rd week, the more advanced level of anatomical, biochemical, and neurophysiologic maturation of the CNS allows a more selective involvement of various cerebral structures with subsequent well defined epileptic features.

Allylglycine↗
PubMed1979

Effects of some anti-epileptic, neuroleptic and gabaminergic drugs on convulsions induced by D,L-allylglycine.

The antagonism of various seizure and time-related components of the convulsions resulting after IV injection of D,L-allylglycine into male Wistar rats were assessed in a standard test procedure. Trimethadione and ethosuximide did not antagonize the seizure components, whereas clonazepam, phenobarbital, diphenylhydantoin, primidone, valproate sodium, aminoxyacetic acid, etomidate, acetazolamide, flunarizine, pipamperone and baclofen did. The allylglycine test may thus represent a relatively specific method of differentiating between drugs effective against partial or generalized convulsive seizures from those effective against absence seizures. The neuroleptics haloperidol and pimozide were completely inactive in contrast to their reported antagonism of bicuculine seizures. The spectra of the active substances are discussed with respect to Principal Component and Cluster Analysis. Noteworthy are the similarities between baclofen and etomidate; between aminoxyacetic acid, phenobarbital and valproate sodium; and between diphenylhydantoin and flunarizine.

Allylglycine↗
PubMedDate not supplied

Early changes in the rat hippocampus following seizures induced by bicuculline or L-allylglycine: a light and electron microscope study.

Status epilepticus was induced in thirteen paralysed and ventilated rats by the injection of either bicuculline or L-allylglycine. After 1-2 h of seizure activity the animals were intracardially perfused with a 2% glutaraldehyde/3% paraformaldehyde solution. Hippocampal blocks from each rat were processed for light and electron microscopy. The effects of L-allylglycine were more severe than those of bicuculline. Changes include perivascular and perineuronal swelling of astrocytic processes, and neuronal alterations which were graded as follows: Grade I (least severe), neuronal cytoplasm appears slightly darker than usual; Grade II, condensed or dark neurons, usually with microvacuoles; and Grade III classical 'ischaemic cell change'--the cytoplasm and karyoplasm is dark and shrunken, with or without microvacuoles. Many of the microvacuoles originate from mitochondria. In a few cases swollen and disrupted mitochondria are also seen is distended basal dendrites of the CA3 and CA1 pyramidal neurons. Dentate granule cells appear unaffected. The hippocampal neuronal alterations induced by seizure activity include those of 'ischaemic cell change'. The pathogenetic factors common to hypoxia/ischaemia and status epilepticus remain to be identified.

Allylglycine↗
PubMed1984

Changes in regional neurotransmitter amino acid levels in rat brain during seizures induced by L-allylglycine, bicuculline, and kainic acid.

Changes in amino acid concentrations were studied in the cortex, cerebellum, and hippocampus of the rat brain, after 20 min of seizure activity induced by kainic acid, 47 mumol/kg i.v.; L-allylglycine, 2.4 mmol/kg i.v.; or bicuculline, 3.27 mumol/kg i.v. in paralysed, mechanically ventilated animals. Metabolic changes associated with kainic acid seizures predominate in the hippocampus, where there are decreases in aspartate (-26%), glutamate (-45%), taurine (-20%), and glutamine (-32%) concentrations and an increase in gamma-aminobutyric acid (GABA) concentration (+ 26%). L-Allylglycine seizures are associated with generalized decreases in GABA concentrations (-32 to -54%), increases in glutamine concentrations (+10 to +53%), and a decrease in cortical aspartate concentration (-14%). Bicuculline seizures, in fasted rats, are associated with marked increases in the levels of hippocampal GABA (+106%) and taurine (+40%). In the cerebellum, there are increases in glutamine (+50%) and taurine concentrations (+36%). These changes can be explained partially in terms of known biochemical and neurophysiological mechanisms, but uncertainties remain, particularly concerning the cerebellar changes and the effects of kainic acid on dicarboxylic amino acid metabolism.

Allylglycine↗
PubMed1990

Anticonvulsive activity of a barbiturate derivative HB-7 in a model of allylglycine-induced epilepsy in cats.

With the aim of characterizing further the anticonvulsive activity of the newly-synthesized barbituric derivative 2-hydroxylamino-5-ethyl-5-sec. penthylbarbituric acid (HB-7), we studied its effects on allylglycine-induced epileptiform electrocorticogram (ECoG) in cats under acute conditions. Pentobarbital (PB) was used for comparison. Allylglycine (AG) was administered in a dose of 100 mg/kg i.v. to all cats. The control animals were treated with AG only. HB-7 and PB were applied in doses of 20 mg/kg i.p., about 60 min after AG. Intermittent light stimulation (ILS) at flash rate of 8/s and 25/s was applied to some animals. The ILS-stimulated animals were also divided in three groups: controls and animals treated with HB-7 or PB in the same dose. AG led to the appearance of paroxysmal ECoG activity: single and multiple spikes and spike-waves appeared first, to be followed later by generalized seizure activity. No AG-induced convulsions appeared in the cats treated with HB-7, but the AG-induced spikes and spike-waves remained unchanged. The effect of PB on the AG-induced paroxysmal ECoG activity was similar to that of HB-7, but the addition of PB provoked the appearance of slow waves and spindles, mixed with spikes and spike-waves. Although the paroxysmal character of the activity was more pronounced in the ILS-stimulated animals than in the group without ILS, HB-7 and PB (albeit to a lesser extent) inhibited the AG-induced discharges.(ABSTRACT TRUNCATED AT 250 WORDS)

Allylglycine↗
PubMed1987

[Effects of systemic administration of strychnine, L-allylglycine, bicuculline and picrotoxin on the transsynaptic neural destruction in the medullary dorsal horn following transection of the rat inferior alveolar nerve].

Adult rats underwent unilateral transection of the inferior alveolar nerve and subsequent intraperitoneal injection of strychnine (1 mg/kg, 3-23 days) at various posttransectional intervals. When they were sacrificed at 18-30 days posttransectionally, many pyknotic neuronal cell bodies were observed in plastic embedded toluidine blue-stained 1 micron-thick sections of the medullary dorsal horn. They were mostly found in the dorsal part of the dorsal horn ipsilateral to the neurotomy and were more abundant in laminae I/II than in laminae III/IV. Similar pyknotic neurons were found after 1 or 2 days of L-allylglycine administration (55.7 mg/kg/day) at a posttransectional interval of 20 days. Unlike those observed after strychnine treatment, the pyknotic neurons after L-allylglycine treatment were evenly distributed throughout laminae I-IV of the dorsal half of the medullary dorsal horn. Twenty-three days of bicuculline (2 mg/kg/day) or picrotoxin (0.5 mg/kg/day) treatment at an interval of 7 days did not yield pyknotic neurons. The results are discussed in the light of intrinsic synaptic circuitry of the dorsal horn.

Allylglycine↗
PubMed1984

Effects of DL-allylglycine, alone or in combination with morphine, on passive avoidance behaviour in C57BL/6 mice.

In a first set of experiments the posttrial intraperitoneal acute administration of the GAD-inhibitor DL-allylglycine impaired the memory processes of C57BL/6 (C57) mice tested in a passive avoidance apparatus. Memory improvements were, on the contrary, observed following morphine treatment. These effects were dose- and time-dependent. They were, in particular, evident if mice were injected immediately, or 30 min, but not 60 min, after training in the apparatus, and were absent in the no-footshock groups, suggesting lack of proactive effects of the drugs on performance. In a second set of experiments, the posttraining administration of allylglycine, at a per se ineffective dose (5 mg/kg), antagonized the memory improvement exerted by the administration of morphine (0.5 or 1.0 mg/kg). The results support the hypothesis of an involvement of GABAergic mechanisms in the memory consolidation processes, and suggest the possibility that GABAergic systems play a role in the effects of morphine on memory in C57BL/6 mice.

Allylglycine↗
PubMed1975

Hypothermic response following administration of 2-amino-4-pentenoic acid (allylglycine).

Intraperitoneal administration of allylglycine resulted in a hypothermic response in rats. At a dosage of 90 mg/kg, a significant decrease in temperature was noted at 4 and 8 hr after administration, but no significant difference was noted at 12 hr. The same dose administered intraperitoneally to decapitated rats did not result in a hypothermic response, and intraventricular administration resulted in a rapid onset of hypothermia after 1 hr. These findings are indicative of a central site of action for the allylglycine-induced hypothermia. Quantitative assay of hypothalamic monoamines (norepinephrine, serotonin, and dopamine) did not show any significant changes at 4, 8, and 12 hr postadministration when compared to controls. A significant decrease in hypothalamic gamma-aminobutyric acid was noted at each of these time points when compared to controls. These data suggest an important role for gamma-aminobutyric acid in mammalian thermoregulatory control.

Allyl Compounds↗