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PubMed1993

Protective actions of human recombinant basic fibroblast growth factor on MPTP-lesioned nigrostriatal dopamine neurons after intraventricular infusion.

Basic fibroblast growth factor (bFGF, FGF-2) is a trophic factor for neurons and astrocytes and has recently been demonstrated in the vast majority of dopamine (DA) neurons of the ventral midbrain of the rat. Potential neuroprotective actions of FGF-2 in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model have also been reported. The actions of the FGF-2 have now been further analyzed in a combined morphological and behavioural analysis in the MPTP model of the adult black mouse, using a continuous human recombinant FGF-2 (hrFGF-2) intraventricular (i.v.t.) administration in a heparin-containing (10 IU heparin/ml) mock cerebrospinal fluid (CSF) solution. Tyrosine hydroxylase (TH) immunocytochemistry in combination with computer assisted microdensitometry demonstrated a counteraction of the MPTP-induced disappearance of neostriatal TH-immunoreactive (ir) nerve terminals following the FGF-2 treatment. Unbiased estimates of the total number of nigral TH ir neurons, using stereological methods involving the optical disector (Olympus), showed that the MPTP-induced reduction in the number of nigral TH ir nerve cell bodies counterstained with cresyl violet (CV; by 56%) was partially counteracted by the FGF-2 treatment (by 26%). The behavioral analysis demonstrated an almost full recovery of the MPTP-induced reduction of the locomotor activity after FGF-2 treatment. This action was maintained also 1 week after cessation of treatment. The hrFGF-2 produced an astroglial reaction as determined in the lateral neostriatum and in the substantia nigra (SN) far from the site of the infusion, indicating that the growth factor may have reached these regions by diffusion to activate the astroglia. Immunocytochemistry revealed FGF-2 immunoreactivity (IR) in the nuclei of the astroglia cell population in the dorsomedial striatum and the microdensitometric and morphometric evaluation demonstrated an increase in the number, but not in the intensity, of these profiles on the cannulated side, suggesting the possibility that hrFGF-2 stimulates FGF-2 synthesis in astroglial cells with low endogenous FGF-2 IR. These results indicate that hrFGF-2, directly and/or indirectly via astroglia, upon i.v.t. infusion exerts trophic effects on the nigrostriatal DA system and may increase survival of nigrostriatal DA nerve cells exposed to the MPTP neurotoxin

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMedDate not supplied

Conditioned place preference induced by intraventricular infusions of acetaldehyde.

Multiple intracerebroventricular infusions of acetaldehyde were shown to induce conditioned place preference in laboratory rats. Those animals receiving acetaldehyde infusions displayed an increased preference for environmental cues previously paired with the drug administration. These results indicate that acetaldehyde, when present in the brain, may have reinforcing properties.

Acetaldehyde↗

PubMed2003

Intraventricular infusion of antagonists of IL-1 and TNF alpha attenuates neurodegeneration induced by the infection of Trypanosoma brucei.

Infection of Trypanosoma brucei causes specific patterns of neurodegeneration in association with chronic expression of proinflammatory cytokines in the brain. To investigate whether the induction of proinflammatory cytokines contributed to the observe pathology in this disease, we infected rats with T. brucei and treated them with intracerebral infusion of the cytokine antagonists interleukin-1 receptor antagonist (IL-1ra) and/or soluble type-I receptor of the tumor necrosis factor (sTNFr1). Infusion of IL-1ra, not sTNFr1, restored the reduction of body weight gain induced by the infection. Infusion of IL-1ra+sTNFr1 reduced the expression of IL-1beta and the cytokine response gene IkappaBalpha, but not TNFalpha. Infusion of sTNFr1 reduced trypanosome-induced neurodegeneration. Further reduction of neurodegeneration was seen after IL-1ra+sTNFr1 infusion. Infusion of IL-1ra alone, however, did not significantly affect the patterns of neurodegeneration. These results suggest that TNFalpha is a major mediator for trypanosome-induced neurodegeneration although its neurotoxic effects can be augmented by IL-1.

Animals↗

PubMed1986

Effect of intraventricular infusion of an angiotensin II antagonist on 125I-angiotensin II binding in rats.

The effects of chronic (six day) intracerebroventricular (i.c.v.) infusion of an angiotensin II antagonist, sarcosine1, isoleucine8 angiotensin II ([Sar1, Ile8]Ang II), (500 ng/microliter per hour) was studied. Specific 125I-Ang II binding site density and binding affinity in the hypothalamus-thalamus-septum-midbrain (H-T-S-M) region of the brain and the adrenal medulla did not differ significantly between [Sar1, Ile8]Ang II treated and control (0.9% saline) rats. However, 125I-Ang II binding to the adrenal cortex was significantly reduced by i.c.v. infusion of [Sar1, Ile8]Ang II. The drinking response to microinjection of Ang II was blunted for up to seven days of [Sar1, Ile8]Ang II infusion. Thus, although [Sar1, Ile8]Ang II effectively blocked the central Ang II receptors, chronic infusion of this Ang II antagonist did not appear to cause alterations in brain H-T-S-M Ang II receptors, suggesting that brain Ang II receptors in normal rats do not undergo homologous regulation.

1-Sarcosine-8-Isoleucine Angiotensin II↗

PubMed2004

Intraventricular infusion of the neurotrophic protein S100B improves cognitive recovery after fluid percussion injury in the rat.

Elevated serum S100B levels have been shown to be a predictor of poor outcome after traumatic brain injury (TBI). Experimental data, on the other hand, demonstrate a neuroprotective and neurotrophic effect of this calcium-binding protein. The purpose of this study was to examine the role of increased S100B levels on functional outcome after TBI. Following lateral fluid percussion or sham injury in male Sprague Dawley rats (n = 56), we infused S100B (50 ng/h) or vehicle into the cerebrospinal fluid of the ipsilateral ventricle for 7 days using an osmotic mini-pump. Assessment of cognitive performance by the Morris water maze on days 30-34 after injury revealed an improved performance of injured animals after S100B infusion (p < 0.05), when compared to vehicle infusion. Blood samples for analysis of clinical markers of brain damage, S100B and neuron specific enolase, taken at 30 min, 3 h, 4 h, 2 days, or 5 days showed a typical peak 3 h after injury (p < 0.01), and higher serum levels correlated significantly with an impaired cognitive recovery (p < 0.01). The correlation of higher serum S100B levels with poor water maze performance may result from injury induced opening of the blood-brain barrier, allowing the passage of S100B into serum. Thus while higher serum levels of S100B seem to reflect the degree of blood-brain barrier opening and severity of injury, a beneficial effect of intraventricular S100B administration on long-term functional recovery after TBI has been demonstrated for the first time. The exact mechanism by which S100B exerts its neuroprotective or neurotrophic influence remains unknown and needs to be elucidated by further investigation.

Animals↗

PubMed1994

Behavioral and neuroanatomical consequences of a unilateral intraventricular infusion of AF64A and limitations on the neuroprotective effects of nimodipine.

The monoethylcholine aziridinium ion, AF64A, (3 nmol in 1 microliter) or artificial CSF (1 microliter) was infused unilaterally into the right dorsal lateral ventricle of male adult rats. Treatment with the L-type calcium channel antagonist, nimodipine (70 micrograms/kg b.wt.) or its vehicle was administered beginning before and for seven days following surgery. The infusion of AF64A reduced spontaneous alternation rates in the T-maze when compared to CSF and sham infused animals. AF64A-treated animals also took longer to reach the goal area in a complex maze task on specific trials relative to CSF and sham-infused animals. Locomotion and habituation to the open field did not differ between surgery groups. Unilateral AF64A significantly depleted acetylcholinesterase (AChE) positive terminals in the ipsilateral hippocampus and cell bodies in the ipsilateral medial septal area (MSA). Receptors for nerve growth factor (NGF-R), often colocalized with cholinergic cell bodies and terminals, also were depleted in the ipsilateral MSA of AF64A infused animals. Treatment with nimodipine did not have a neuroprotective effect on AF64A animals in either behavioral or histological results. However, some degree of protection was found in the vehicle-treated rats. This effect was likely a consequence of the stress of the injection procedure rather than the content of the vehicle, largely polyethylene glycol 400. Nimodipine-treated animals, regardless of surgery group, exhibited fewer emotional responses and had lower spontaneous alternation rates than untreated animals. The behavioral alterations found in the nimodipine groups are most easily explained in terms of altered emotionality. Overall our findings indicate that AF64A is a potent cholinotoxin that can selectively eliminate the ipsilateral septohippocampal cholinergic system when unilaterally infused into the lateral ventricle. It is possible that the mechanism of action of AF64A, like other nitrogen mustard analogues, involves disruption of basic processes involved in protein synthesis and DNA activities. Because of this, the toxic effects of the aziridinium mustard are independent of extracellular calcium and thus may not be susceptible to protection by calcium channel antagonists.

Acetylcholinesterase↗

PubMed2000

[Effect of intraventricular infusion of Licvorin on general convulsive activity of rats].

It was studiet anticonvulsive action of the biopreparation licvorin had been made from a cerebrospinal fluid (CSF) of a cattle on the epiliptic activity provoking by korasol. The preparation was infused intraventriculary. Research showed preparation had the antiepileptic effect. It was manifested by decreasing expressiveness of convulsions, averting of general epileptic fit and mortality. Anticonvulsive action of the biopreparation licvorin was registrated in 2 hours and was achieved maximum effect 24 hours after injection. Anticonvulsive properties of the biopreparation licvorin realized by influence his active factors on structures of a brain, specifically on the GABAdependent systems.

Animals↗

PubMed1992

Reduction of hibernation bout duration by intraventricular infusion of met-enkephalin.

The potential of brain met-enkephalin (met-enk) systems to modulate central nervous system (CNS) activity during periods of general depression (modeled by the mammalian hibernation state) was studied in the ground squirrel (Citellus lateralis). Following entrance into hibernation, continuous met-enk infusion into the lateral ventricle (1 microliter/h; 0.2, 1 and 5 micrograms/microliter) produced a dose-dependent reduction in bout duration ranging from 1.2 to 3.9 days (13.8-44.6% of baseline bout duration). We suggest that the activity of met-enk-releasing neurons may serve to increase the excitability of the depressed CNS, thus accelerating the termination of the hibernation bout.

Animals↗

PubMed1993

Expression of c-fos in restricted areas of the basal forebrain and brainstem following single or combined intraventricular infusions of vasopressin and corticotropin-releasing factor.

Vasopressin has been shown to be localized in specific central nervous system (CNS) sites. There is considerable evidence that it can act as a central neurotransmitter and it has been ascribed a variety of putative roles in the CNS. To identify those regions of the brain capable of responding to this peptide, 250 pmol vasopressin were infused into the lateral ventricle intracerebroventricular of conscious, handled male rats, and their brains processed for fos-immunohistochemistry 60 min later. Increases in fos-immunoreactivity, compared with cerebrospinal fluid-infused controls, were found in specific regions of the basal forebrain and brainstem: the central nucleus of the amygdala, ventrolateral septum, parvocellular divisions of the paraventricular nucleus of the hypothalamus, dorsal tuberal nucleus and locus coeruleus. Pre-infusion of 2500 pmol of a V1a antagonist prevented or reduced the expression of c-fos by intracerebroventricular vasopressin in all areas except the dorsal parvocellular paraventricular nucleus, implying that in most (but not all) areas the actions of vasopressin are mediated by the V1a receptor. Central administration of vasopressin had no effect on plasma corticosterone levels. Vasopressin and corticotropin-releasing factor act synergistically on the anterior pituitary to cause release of adrenocorticotropic releasing hormone and have corresponding synergistic interactions on behaviour. Infusion of 250 pmol corticotropin releasing factor produced a similar but not identical pattern of fos-like immunoreactivity to that of vasopressin. Activation of the parabrachial nucleus was observed, but there was no significant effect on the lateral septum and apparent increases in the medial parvocellular division of the paraventricular nucleus and locus coeruleus were not significant. Corticotropin releasing factor also caused a marked rise in plasma corticosterone. When the two peptides were infused together (125 pmol each) no evidence for synergy was found, in terms of the number of neurons activated to express c-fos. The induction of differential patterns of fos-like immunoreactivity by vasopressin and corticotropin-releasing factor in specific regions of the limbic forebrain and brainstem has implications for the individual roles they play in the CNS.

Animals↗

PubMed1977

Reduced food intake following cerebral intraventricular infusion of glucose in Gallus domesticus.

Unanaesthetized hens and cocks were infused into the cerebral lateral ventricle with 0.2 ml of a 6% glucose solution or equal volumes of isotonic saline following a 20-hr total food deprivation period. A more marked suppression of food intake occurred in the next 1-3 hr after glucose rather than after saline. The results provide new evidence that chickens possess central glucoreceptors involved in the regulation of their feeding behavior.

Animals↗

PubMed1980

Central effects of histamine and H1 and H2 receptors agonists and antagonists after intraventricular infusion in fowls.

In adult fowls (Gallus deomesticus) the effects of histamine H2 and H2 histamine receptors angonists and antagonists infused into the III cerebral ventricle were studied on behaviour, electrocortical activity and body temperature. Histamine produced biphasic effects, i.e. an initial period of electrocortical synchronization was followed by a longer-lasting behavioural stimulation, electrocortical desynchronization and shivering. Body temperature was increased in a dose-dependent manner. Dimaprit, an agonist at H2 receptors, produced behavioural and electrocortical sleep and decreased body temperature whereas, 2-(2-thiazolyl-)-ethyl-amine, an agonist at H1 receptors, behavioural stimulation, electrocortical desynchronization, vocalization and hyperthermia. Cimetidine, an antagonist at H2 receptors, produced intense behavioural stimulation and electrocortical desynchronization accompanied by vocalization, tachypnoea, occasional escape responses and stereotypies. Body temperature was increased. Mepyramine, an antagonist at H1 receptors, produced behavioural and electrocortical sleep and prevented behavioural excitation elicited by subsequent infusion of histamine and hyperthermia evoked by 2-(2-thiazolyl -ethylamine. Haloperidol, a neuroleptic drug, sharing with mepyramine membrane stabilizing properties, was unable to antagonize histamine-induced behavioural excitation. In conclusion, present experiments provide pharmacological evidence for the existence of H1 and H2 histamine receptors in avian brain and suggest an involvement of histamine H1 and H2 receptors in the control of arousal-sleep and thermoregulatory mechanisms.

Animals↗

PubMed1992

Regional expression of c-fos antigen in the basal forebrain following intraventricular infusions of angiotensin and its modulation by drinking either water or saline.

The expression of c-fos protein was examined in the basal forebrains of male rats 60 min following intracerebroventricular infusions of 250 pmol angiotensin II. Levels of corticosterone and vasopressin were also measured at the same time point. In animals not allowed access to water after infusion, angiotensin II induced intense c-fos expression in a band of neurons extending throughout the anterior region of the third ventricle region, including the organum vasculosum of the lamina terminalis, the median preoptic nucleus (nucleus medianus) and the subfornical organ. There were also high levels of expression in the hypothalamic supraoptic nucleus and the paraventricular nucleus, particularly its lateral (magnocellular) region, though other, parvicellular areas were also affected. No other area of the hypothalamus was altered. There was increased c-fos expression in the central nucleus of the amygdala and the bed nucleus of the stria terminalis. Allowing rats to drink during the 60-min survival period modified this pattern of response. c-fos was markedly reduced in the supraoptic nucleus and the paraventricular nucleus but not in the other areas examined, including the anterior region of the third ventricle and the amygdala. When water was withheld for 15 min, but then allowed, rats drank the same total volume but c-fos expression was no longer inhibited in either the supraoptic nucleus or paraventricular nucleus. When rats were given 0.9% saline to drink, they ingested about three times as much as water, but angiotensin II-induced c-fos expression was similar to that in rats denied access to water. The pattern was similar following access to 1.8% saline, though levels in the organum vasculosum of the lamina terminalis were reduced. There was a marked correlation between the number of c-fos-positive neurons in the supraoptic nucleus or paraventricular nucleus and plasma levels of corticosterone 60 min after infusion, but not with arginine-vasopressin levels. These experiments show that angiotensin II induces highly localized expression of c-fos in areas known to be concerned with the dipsogenic and endocrine actions of this peptide, and that this pattern is selectively altered by allowing the animal to drink solutions of different tonicity. Immediate-early gene expression is a novel and valuable method of determining the neural response to peptides at the cellular level.

Angiotensin II↗

PubMed1978

Lack of behavioural effects following intraventricular infusion of somatostatin in the conscious goat.

The effect of IV or intracerebroventricular (ICV) administration of somatostatin was studied on the behaviour of conscious goats. The doses of somatostatin infused IV were 100 and 300 microgram for 30 min and 600 microgram for 6 min. The doses infused ICV were 10 and 100 microgram for 30 min and 600 microgram for 6 min. In contrast to earlier reports on experiments with rats ,no behavioral effects whatsoever were seen in goat. IV infusion of 100 to 600 microgram and ICV infusion of 600 microgram of somatostatin caused a difinite reduction in the secretion of insulin and growth hormone, but had no effect on the concentration of blood glucose. The reason why neither IV nor ICV administration of somatostatin had any behavioural effects in the conscious goat, in contrast to the effects in rat, cannot be explained with certainty. This may be due to species specificity, to the amount of somatostatin reaching the central nervous system, or to some metabolic changes in rat but not in goat.

Animals↗

PubMed1994

Regional suppression by water intake of c-fos expression induced by intraventricular infusions of angiotensin II.

Intracerebroventricular (i.c.v.) infusions of angiotensin II (AII) reliably induced c-fos expression in the supraoptic (SON) and paraventricular (PVN) nuclei, as well as other areas of the basal forebrain including the OVLT, subfornical organ (SFO), and bed nucleus (BNST). Double-labelling showed that AII-induced c-fos was observed in both vasopressin (AVP-) and oxytocin (OXY)-containing neurons of the SON and PVN in male rats. Allowing rats to drink water after AII infusions suppressed c-fos expression both AVP- and OXY-stained magnocellular neurons. Intragastric infusions of water were also effective, showing that oro-pharyngeal stimuli were not critical. Maximal suppression occurred in rats in whom water had been infused intragastrically about 5 min before i.c.v. AII infusions, suggesting that changes in osmolarity were responsible. i.c.v. AII also induced c-fos expression in a number of brainstem structures, including the solitary nucleus (NTS), lateral parabrachial nucleus (LPBN), locus coeruleus (LC), and the area postrema (AP). These results indicate that AVP and OXY-containing neurons in the magnocellular parts of the SON and PVN alter their immediate-early gene response to AII after water intake, and that this does not depend upon oro-pharyngeal factors. Furthermore, AII can induce c-fos expression in a number of brainstem nuclei associated with autonomic function, and these do not respond to water intake.

Angiotensin II↗

PubMed1996

Intrastriatal and intraventricular infusion of brain-derived neurotrophic factor in the cynomologous monkey: distribution, retrograde transport and co-localization with substantia nigra dopamine-containing neurons.

The distribution and retrograde transport of brain-derived neurotrophic factor was examined using magnetic resonance imaging guided stereotaxic intracerebroventricular and intrastriatal infusion in the cynomologous monkey. Two intracerebroventricular animals were infused with brain-derived neurotrophic factor at a dose of 3 micrograms/h for 21 and 28 days. A third intracerebroventricular animal received sequential infusions of 15, 30 and 60 micrograms/h brain-derived neurotrophic factor each for seven days using an Alzet 2002 minipump. For the multiple intrastriatal animals (n = 5) a dose of 3 micrograms/h was infused into each site. One intrastriatal monkey was infused with vehicle solution of 10 mM phosphate-buffered saline pH 7.4 for 14 days resulting in no brain-derived neurotrophic factor immunoreactivity. Following the lower dose intracerebroventricular infusion, brain-derived neurotrophic factor immunoreactivity was confined to the ventricular ependymal layer. In the sequential higher dose intracerebroventricular case, the cannula was located mainly within the lateral ventricle, although there was damage to the ependymal wall and adjacent caudate nucleus. Brain-derived neurotrophic factor immunoreactivity revealed spread of injectate within the ipsilateral and to a lesser extent the contralateral caudate nucleus, septum, orbital cortex and ventricular ependymal wall. In this case, retrogradely labelled brain-derived neurotrophic factor neurons were found within the parafascicular thalamus and substantia nigra, pars compacta, as well as within cortex, vertical limb of the diagonal band and nucleus basalis. Brain-derived neurotrophic factor intrastriatal infusion retrogradely labelled perikarya within sensory motor cortex, parafascicular thelamus and substantia nigra, pars compacta. Sections from these cases dual-immunoreacted for brain-derived neurotrophic factor and tyrosine hydroxylase, the synthesizing enzyme for dopamine, revealed a subpopulation of pars compacta dopaminergic neurons which contained retrogradely transported brain-derived neurotrophic factor. These findings indicate that a select subgroup of nigral dopamine neurons retrogradely transport brain-derived neurotrophic factor in the primate. Furthermore it remains to be determined whether select nigral cells are responsive to the trophic influences of brain-derived neurotrophic factor in the normal and neuropathologic condition.

Animals↗

PubMed1992

Intraventricular infusion of N-methyl-D-aspartate. 2. Acute neuronal consequences.

This study documents the ultrastructural features of acute neuronal injury following N-methyl-D-aspartate (NMDA) receptor activation. NMDA (100 nmol/microliters) or vehicle was infused over a 15-min period into the lateral ventricle of adult rats. After perfusion fixation, specimens demonstrating normal and abnormal patterns of vascular permeability to horseradish peroxidase were sampled for ultrastructural analysis. In NMDA-infused rats, brain regions exhibiting protein extravasation contained swollen dendritic profiles and abnormal neuronal perikarya. Although periventricular regions were most severely affected, parenchymal abnormalities were also detected in the cerebral cortex, septum, striatum, thalamus, hypothalamus and cerebellum. Mildly affected dendrites contained dark compact mitochondria, while in severely swollen dendrites mitochondria were enlarged with ruptured cristae. Focal sites of plasma membrane disruption were also detected within swollen dendrites. Swollen neurons commonly displayed peripheral pallor and increased numbers of cytoplasmic vacuoles. Other neurons appeared dark and shrunken, some containing disrupted mitochondria and pyknotic nuclei. Pretreatment with the NMDA antagonist MK-801 (2 mg/kg) attenuated the neuronal and dendritic alterations. In conditions where cerebrospinal fluid levels of glutamate are abnormally elevated, excessive NMDA receptor activation may lead to early vascular and neuronal complications which could work in concert to promote brain injury.

Animals↗

PubMed1996

Learning deficits induced by chronic intraventricular infusion of quinolinic acid--protection by MK-801 and memantine.

The NMDA receptor agonist quinolinic acid (9 mM) was infused i.c.v. via ALZET osmotic minipumps for 2 weeks. This treatment produced a persistent, short-term memory deficit in the T-maze. Autoradiography revealed a decrease in the density of choline uptake sites in the hippocampus. Parallel s.c. infusion by another minipump of the uncompetitive NMDA receptor antagonist memantine (1-amino-3,5-dimethyladamantane, 20 mg/kg per day) or (+)-5-methyl-10,11-dihydro-5H-dibenzocyclohepten-5,10-imine maleate ((+)-MK-801, 0.31 mg/kg day) prevented the learning deterioration induced by quinolinic acid. The treatment with memantine resulted in steady-state serum levels of 1.2 mu M which, based on in vitro data, should assure inhibition of NMDA receptors and are similar to levels seen in the serum of demented patients treated with this agent. In naive animals this treatment had no effect on either learning or on ex vivo induction of long-term potentiation, indicating that under chronic conditions it is possible to obtain neuroprotective effects with NMDA receptor antagonists without negative effects on memory processes. This contrasts to some acute insults (e.g. ischaemia) where high doses of NMDA receptor antagonists that produce side effects are required.

Analysis of Variance↗

PubMed1989

Intraventricular infusion of 2-amino-7-phosphonoheptanoate (APH) mitigates ischaemic brain damage.

Intracerebroventricular infusion of the competitive N-methyl-D-aspartate (NMDA) antagonist 2-amino-7-phosphonoheptanoate (APH) was evaluated as a neuroprotective regimen in a rat transient cerebral ischaemia model allowing long-term recovery. Ventricular delivery of APH via an osmotic minipump was chosen to allow continuous and direct access to brain tissue of this polar molecule, and because of the potential applicability of such a regimen in clinical situations where the brain is at risk from cerebral ischaemia and a ventricular catheter is in place. The highest tolerable concentration of APH, 50 mM, was given at 1 microliter/h. Selective neuronal necrosis was significantly reduced in the cerebral cortex and the incidence of infarction in the substantia nigra pars reticulata (SNPR) was decreased. A borderline protective effect was seen in the hippocampal CA1 pyramidal neurons, and no significant protection was seen in the caudate nucleus. The results suggest a limited usefulness for APH as a cerebral protective agent.

2-Amino-5-phosphonovalerate↗