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PubMedDate not supplied

Noradrenergic pharmacotherapy, intracerebral infusion and adrenal transplantation promote functional recovery after cortical damage.

The research described in this review briefly summarizes evidence that short term pharmacological enhancement of noradrenergic (NA) synaptic activity, combined with symptom relevant experience (SRE), promotes functional recovery of some symptoms of cortical damage in rat, cat and human beings even when treatment is initiated from days to weeks after injury. A summary is provided of the numerous drugs tested in rodent cortical injury models which have been proven useful for predicting beneficial or harmful effects on behavioral outcome in human stroke. The pattern of drug effects indicates a central role for NA in functional recovery. Additionally, studies of the effects of direct intraventricular infusion of monoamine neurotransmitters are reviewed and further support the hypothesized role of NA in recovery from some symptoms of cortical injury. The site of NA/SRE interaction to promote recovery from hemiplegia apparently involves the cerebellar hemisphere contralateral to the cortical injury. Microinfusions of NA into the contra- but not ipsilateral cerebellar hemisphere dramatically enhance recovery. Furthermore, like its systemic action, microinfusion of the alpha 1-NA receptor antagonist, phenoxybenzamine, reinstates hemiplegia. A "permanent" symptom of motor cortex injury in the cat is the complete loss of tactile placing contralateral to the injury which does not spontaneously recover for as long as seven years after ablation. This postural reflex is temporarily restored for 8-12 hours following amphetamine administration. However, this permanently lost reflex can be enduringly restored by transplanting catecholamine secreting adrenal tissue into the wound cavity. The experiment is reviewed in detail and involves chromaffin cell autografts into the frontal cortex ablation wound cavity producing a restoration of tactile placing for the 7-10 month duration of the study. This enduring restoration of tactile placing is considered a result of the release of catecholamines into the CNS from the grafted chromaffin cells found, by histochemical methods, surviving 7-10 months after transplant. Lastly, we attribute these delayed treatment effects to an attenuation of a diaschisis, or remote functional depression, in morphologically intact areas anatomically connected to the area of injury. The widespread reduction of glycolytic and oxidative metabolism, produced by focal cortical injury, is normalized by the same treatment which alleviates symptoms and is worsened by drugs which exacerbate deficits. These data support the hypothesis that providing SRE during a period of enhanced NA synaptic activity produces an enduring functional recovery after cortical injury by attenuating remote functional depression. This treatment for enhancing recovery is especially attractive since it is effective even when begun weeks after cortical damage.

Adrenal Glands↗
PubMed1998

Effects of intracerebroventricular dizocilpine (MK801) on dehydration-induced dipsogenic responses, plasma vasopressin and c-fos expression in the rat forebrain.

This study determines the interaction between glutamate receptors and dehydration-induced drinking, vasopressin (AVP) release, plasma osmolality and c-fos expression in the brain of conscious rats. The NMDA receptor antagonist dizocilpine (100 nmol infused into the cerebral ventricles) suppressed drinking following either 22 h water deprivation or intragastric injection of hypertonic saline (1.5 M), attenuated the increased plasma vasopressin induced by dehydration, but had no effects on peripheral hyperosmolality caused by either water deprivation or injections of hypertonic saline. Dizocilpine had no inhibitory effects on feeding after 24 h food deprivation. Dizocilpine also suppressed c-fos expression induced by dehydration in the median preoptic nucleus (MPN), the supraoptic and paraventricular nuclei (SON and PVN), but did not influence c-fos expression in the subfornical organ (SFO). The non-NMDA receptor antagonists CNQX (400 nmol) or DNQX (60 nmol) affected neither the animals' drinking nor c-fos expression induced by dehydration. Double staining showed that suppression of c-fos expression following dizocilpine occurred in the NMDA R1 receptor containing neurons in the hypothalamus. These results suggest that the NMDA-type glutamate receptors may be involved in dehydration induced dipsogenic and neuroendocrinological responses. They complement our earlier findings that dizocilpine also attenuates drinking and c-fos expression following intraventricular infusions of angiotensin II.

Animals↗
PubMed2002

Continuous infusion of neurotrophin-3 triggers sprouting, decreases the levels of TrkA and TrkC, and inhibits epileptogenesis and activity-dependent axonal growth in adult rats.

Neurotrophin-3 (NT-3), a member of the neurotrophin family of neurotrophic factors, is important for cell survival, axonal growth and neuronal plasticity. Epileptiform activation can regulate the expression of neurotrophins, and increases or decreases in neurotrophins can affect both epileptogenesis and seizure-related axonal growth. Interestingly, the expression of nerve growth factor and brain-derived neurotrophic factor is rapidly up-regulated following seizures, while NT-3 mRNA remains unchanged or undergoes a delayed down-regulation, suggesting that NT-3 might have a different function in epileptogenesis. In the present study, we demonstrate that continuous intraventricular infusion of NT-3 in the absence of kindling triggers mossy fiber sprouting in the inner molecular layer of the dentate gyrus and the stratum oriens of the CA3 region. Furthermore, despite this NT-3-related sprouting effect, continuous infusion of NT-3 retards the development of behavioral seizures and inhibits kindling-induced mossy fiber sprouting in the inner molecular layer of the dentate gyrus. We also show that prolonged infusion of NT-3 leads to a decrease in kindling-induced Trk phosphorylation and a down-regulation of the high-affinity Trk receptors, TrkA and TrkC, suggesting an involvement of both cholinergic nerve growth factor receptors and hippocampal NT-3 receptors in these effects. Our results demonstrate an important inhibitory role for NT-3 in seizure development and seizure-related synaptic reorganization.

Animals↗
PubMed1987

Acquisition of a brief behavioural experience in the rat is inhibited by the brain-specific monoclonal antibody, F3-87-8.

Intraventricular infusion of the brain-specific monoclonal antibody F3-87-8 is demonstrated to inhibit the acquisition of a passive-avoidance paradigm in a rat model. Antibody was infused prior to, and following, training of a step-down task and recall was assessed after 24 and 48 h. The antibody only inhibited recall when infused prior to training and no effect was seen when administered 6 h after acquisition of the task. No effect was found with absorbed antibody or in sham-operated animals and open field studies showed no alterations in locomotor activity. Results are discussed considering available information on the antigen and current memory/learning theories.

Animals↗
PubMed1998

Nerve growth factor improves evoked potentials and long-term potentiation in the dentate gyrus of presenile rats.

Chronic infusion of nerve growth factor (NGF, 1.2 microg/day) for 14 days to presenile rats (17 months at the beginning of treatment) that showed an initial cognitive impairment led to an improved long-term potentiation in the dentate gyrus. Both the relative increase of the slope of the population excitatory postsynaptic potential and that of the population spike were enhanced by NGF pretreatment after long-term potentiation induction at 400 Hz. The treatment was also able to increase the diminished baseline amplitude of the population spike, an effect not seen when the treatment was applied to older animals [Bergado, J., Fernández, C.I., Gómez-Soria, A., González, O., 1997a. Chronic intraventricular infusion with NGF improves LTP in old cognitively-impaired rats. Brain Res. 770, 1-9] stressing the importance of an early start of trophic therapy to achieve better results.

Animals↗
PubMedDate not supplied

Dopamine receptor elevation by cholecystokinin.

High concentrations of cholecystokinin (CCK) in the striatum and limbic areas of the brain suggest that this peptide may influence dopaminergic transmission. Thus, the effect of CCK on dopamine D2 receptors in the striatum and nucleus accumbens of the rat brain both in vitro and in vivo (central and peripheral administration) was studied by determining the binding of 3H-spiperone. The density (Bmax) of D2 receptors was elevated (a) by 20% in the accumbens upon in vitro co-incubation with 10(-6) M CCK. (A non-significant drop of 10% occurred in the striatum); (b) by about 40% in the accumbens and 25% in the striatum after continuous intraventricular infusion of CCK for 24 hr. The increase in receptor density in the accumbens was maintained for 14 days and in both tissues was specific to CCK (neurotensin infusion did not alter 3H-spiperone binding); (c) by 20% in the accumbens and 15% in the striatum 3 hr after a single IP injection of 50 micrograms/kg CCK or caerulein, and maintained up to 14 days later. These results suggest that CCK elevates dopamine D2 receptors in the accumbens and striatum and may be a physiological modulator of the dopaminergic system.

Animals↗
PubMed1989

Intratumoural and intraventricular human lymphoblastoid alpha interferon (HLBI) for treatment of glioblastoma multiforme.

A series of ten patients with glioblastoma multiforme were treated with human lymphoblastoid alpha interferon (HLBI) as a single therapy after partial surgical resection (5 cases) or stereotactic biopsy (5 cases). Treatment consisted of intratumoural administration of HLBI (15 x 16(6) IU) every month (8 cases) or in the continuous intraventricular infusion of HLBI (1.8 x 10(6) IU daily) in 15-day cycles (2 cases) until rapid growing of the tumour and important neurological deterioration. The treatments were well tolerated. As judged from data from control groups, the patients demonstrated no improvement in mean survival time and follow-up CT-scan showed rapid progression of the tumour in all cases.

Adult↗
PubMed1997

Peroxynitrite reduces myocardial infarct size and preserves coronary endothelium after ischemia and reperfusion in cats.

BACKGROUND: Peroxynitrite (ONOO-) is purported to exert cytotoxic effects at high doses. However, physiologically relevant concentrations of ONOO- inhibit polymorphonuclear neutrophil (PMN) adhesion to the endothelium and attenuate PMN-mediated contractile dysfunction in isolated perfused rat hearts. We are unaware of any reports in vivo showing effects of peroxynitrite in myocardial ischemia and reperfusion (MI/R). Thus, the purpose of this study was to examine the in vivo effects of a physiologically relevant concentration of ONOO- (1 micromol/L) in a feline model of MI/R injury. METHODS AND RESULTS: ONOO- (1 micromol/L) or its vehicle (0.9% NaCl at pH 8.4) was infused intraventricularly, starting 10 minutes before reperfusion in cats subjected to 90 minutes of myocardial ischemia and 4.5 hours of reperfusion. ONOO(-)-treated cats demonstrated marked attenuation of cardiac necrosis after MI/R compared with cats receiving only vehicle (P<.001). Moreover, vasorelaxation of ischemic-reperfused left anterior descending (LAD) coronary artery rings in response to the endothelium-dependent dilators acetylcholine and A23187 was greater in rings isolated from ONOO(-)-treated MI/R cats compared with MI/R cats receiving only vehicle, indicating that postreperfusion coronary vascular endothelial function was preserved by ONOO-. ONOO- also significantly reduced adherence of neutrophils to the ischemic-reperfused LAD coronary endothelium. Immunohistochemical localization of P-selectin was also significantly attenuated in hearts from ONOO(-)-infused MI/R cats. CONCLUSIONS: These data suggest that physiologically relevant concentrations of ONOO- exert significant cardioprotective and vasculoprotective effects in MI/R in cats, at least partially by attenuating PMN-endothelium interactions.

Animals↗
PubMed1985

Ototoxicity of intraventricularly administered gentamicin in adult rabbits.

To determine whether daily intraventricular injection of gentamicin sulfate is ototoxic, adult male rabbits were given 0.2 ml of saline (group 1; n = 8) or 0.25 mg/kg of gentamicin sulfate in 0.2 ml of saline (group 2; n = 7) by intraventricular infusion once a day for 21 d. All rabbits were also given intramuscular gentamicin sulfate, 2 mg/kg, twice daily. Before and after antibiotic treatment, brainstem auditory evoked responses (BAERs) were recorded. During the experimental period, neurologic examinations were performed on all rabbits. After treatment, the animals were euthanized; brain tissue and cochleas were then removed for histopathologic examination. The ratios of neurologic abnormalities observed in group 1 and 2 animals, respectively, were 0/8 and 5/7; of abnormal BAERs, 0/8 and 5/7; of abnormal brain morphology, 2/5 and 6/6; and of abnormal cochlear morphology, 0/6 and 7/7. The electrophysiologic evidence of auditory deficit and the structural evidence of ototoxic insult are significantly associated (p less than or equal to 0.006) with intraventricularly administered gentamicin sulfate. These data suggest that intraventricular gentamicin should be used with caution.

Animals↗
PubMed1996

Diminished noradrenergic stimulation reduces the activity of rolipram-sensitive, high-affinity cyclic AMP phosphodiesterase in rat cerebral cortex.

The present study examined the in vivo regulation of rolipram-sensitive, high-affinity cyclic AMP phosphodiesterase (PDE4) in rat cerebral cortex. The hydrolysis of cyclic AMP, formed by stimulation of beta-adrenergic receptors, was measured in cerebral cortical slices. Hydrolysis of cyclic AMP formed under these conditions was inhibited by the PDE4-selective inhibitor rolipram but not by selective inhibitors of other PDE families. Intraventricular infusion of 6-hydroxydopamine (6-OHDA; 200 micrograms) decreased the rate constant of cyclic AMP hydrolysis and increased the cyclic AMP half-life 17 days, but not 1 or 7 days, following the treatment. A reduction in norepinephrine (NE) content occurred first; the NE level was reduced to 42, 24, and 6% of control at 1, 7, and 17 days after 6-OHDA infusion, respectively. This was followed by the development of supersensitivity of beta-adrenergic receptor-linked adenylyl cyclase, which occurred 7 days after the infusion. The reduction in PDE4 activity occurred last. When a higher dose of 6-OHDA (300 micrograms) was used, the reduction in the rate constant of cyclic AMP hydrolysis occurred by 7 days; at this time NE content was depleted to 6% of control. Similar to 6-OHDA treatment, continuous blockade of beta-adrenergic receptors, produced by chronic propranolol infusion, decreased the rate constant of cyclic AMP hydrolysis. Therefore, the current results indicate that diminished stimulation of beta-adrenergic receptors, either by loss of noradrenergic innervation or by receptor blockade, reduces the activity of PDE4. This suggests that PDE4 regulation may contribute in the homeostasis of the noradrenergic receptor-effector system in the brain.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1990

Physostigmine facilitation of lordosis in naturally cycling female rats.

Both systemic and intracerebral administrations of the cholinergic muscarinic antagonist, scopolamine, have been shown to inhibit naturally occurring sexual behavior in intact, cycling female rats. The present study examined the facilitative effects of the acetylcholinesterase inhibitor, physostigmine (eserine), on sexual behavior in intact, cycling female rats. Cycling was determined by daily monitoring of sexual behavior and vaginal cytology. When administered during either early proestrus or proestrus, physostigmine activated lordosis 15 min and 1 hr after intraventricular infusion (10 micrograms bilaterally). However, infusion of physostigmine failed to facilitate lordosis 15 min after administration during either diestrus I, mid-diestrus, or diestrus II. The administration of this cholinergic agent did not interrupt cyclicity patterns. Because estrogen levels are highest during proestrus and cholinergic facilitation appears to be limited to this time, it is suggested that estrogen priming of central cholinergic systems is necessary for the cholinergic regulation of sexual behavior in intact, cycling female rats.

Animals↗
PubMed1995

Intraventricular administration of antibodies to nerve growth factor retards kindling and blocks mossy fiber sprouting in adult rats.

Repeated subconvulsive electrical stimulation of certain areas of the forebrain leads to kindling, a progressive and permanent amplification of evoked epileptiform activity, which is a model for human temporal lobe epilepsy. Recent studies have shown that kindling induces synthesis of nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) but not neurotrophin-3 (NT-3) in the hippocampus and cortex. Kindling also elicits mossy fiber sprouting and functional synaptogenesis in the supragranular layer, the hilus, and the CA3 region of the hippocampus. Intraventricular administration of antibodies to NGF has been shown to effectively block septohippocampal sprouting in the adult rat, and has been reported to retard amygdaloid kindling. In the present study, we have investigated the possible role of NGF in both kindling and kindling-associated sprouting. We have confirmed a kindling-induced sprouting of the mossy fibers into the stratum oriens of the CA3 region of the hippocampus, utilizing a new semiquantitative method of analysis based on Timm staining. Previous studies found no overt signs of hippocampal damage with this kindling paradigm, indicating that the increased Timm staining likely reflects a purely activity-induced sprouting. Intraventricular infusion of affinity-purified anti-NGF IgGs (which cross-react with NT-3 but not BDNF) resulted in both significant retardation of kindling and inhibition of the kindling-induced mossy fiber sprouting. The findings suggest a role for NGF in both these phenomena.

Animals↗
PubMed1977

Inhibitory effect of sulpiride on cinchophen gastric ulceration in dogs.

An intraventricular administration of sulpiride suppressed the experimental cinchophen ulcer, thereby the effect of repeated administration of the material on cinchophen ulcerogenesis is evident, whereas intermittent administration lacked this effect. Such an effect as reducing experimental cinchophen ulceration, which is due to central neurohumoral mechanism, following intraventricular infusion of sulpiride appears to be ascribable to a chemical blockage of the hypothalamic structure. It can thus be concluded that sulpiride acts principally at the level of hypothalamus. Its inhibitory action on cinchophen gastric ulcer development is probably exerted via the hypothalomo-pituitary-adrenal axis, which is essential to the occurrence of an ulcer, and may be regarded as favoring the central neurohumoral theory of cinchophen ulcerogenesis.

11-Hydroxycorticosteroids↗
PubMed1996

Variations of motor activity following intraventricular (D-Pen2, D-Pen5)-enkephalin administration: interaction with acute uncontrollable foot-shock in mice.

The effects of intraventricular administration of (D-Pen2, D-Pen5)-enkephalin (DPDPE) (0.005, 1.0, and 2.5 micrograms/microlitter in a 1-microlitter vol.) on horizontal activity, rearing, and exploratory head dipping were assessed among CD-1 mice exposed to acute uncontrollable foot-shock 15 min following stressor termination. Foot-shock reduced horizontal activity, rearing, and exploratory head dipping during the immediate 15-min poststressor interval. Mice challenged with 0.005 micrograms DPDPE were behaviorally indistinguishable from vehicle-treated subjects. The 1.0-microgram dose of DPDPE increased horizontal activity in stressed and nonstressed subjects. Intraventricular infusion of 2.5 micrograms DPDPE potentiated horizontal activity in previously stressed mice but had no effect in nonstressed animals. The suppression of rearing and exploratory head dipping following uncontrollable foot-shock was not ameliorated by the delta-receptor agonist, and DPDPE was without effect on rearing and exploratory head dipping in nonstressed animals. Potential neurochemical mechanisms associated with the expression of these stressor associated behaviors are discussed.

Analgesics↗
PubMed1993

Angiotensin and captopril increase alcohol intake.

Reportedly both angiotensin II (ANG II) and angiotensin-converting enzyme (ACE) inhibitors reduce ethanol intake when they are injected SC into certain chronic experimental conditions in the rat. The ACE inhibitors are suggested to reduce ethanol intake by increasing ANG II synthesis in the brain. The present results show that several different methods can produce opposite effects of ANG II and the ACE inhibitor captopril on ethanol intake. Continuous intraventricular infusions of ANG II for 7 days or low doses of oral or SC-infused captopril for up to 12 days increased the intake of ethanol. The only reduction of ethanol intake resulted from a universal blockade of all ACE in both the brain and periphery, a condition in which ANG II could not possibly mediate the decrease. The results contradict the hypothesis that ethanol intake is suppressed by centrally acting or centrally synthesized ANG II. ACE inhibitors may reduce ethanol intake only when they affect the brain as well as the periphery.

Alcohol Drinking↗
PubMed1989

Involvement of protein kinase in the regulation of beta-adrenergic receptors by antidepressants.

The role of serotonin (5-HT) and protein kinases in the regulation of the beta-receptor induced by typical and atypical antidepressants was investigated. Treatment with either mianserin or maprotiline for seven days produced a significant decrease in the beta-receptor density measured 6h after the last dose. The reduction in beta-receptors disappeared within 24h. However, combined treatment of mianserin or maprotiline with either fluoxetine or 5-hydroxytryptophan significantly decreased beta-receptors even 24h after the last dose. Following treatment with p-chlorophenylalanine the reduction in beta-receptors induced by desipramine was reversible within 24h. These results demonstrate that an increase in the synaptic 5-HT availability may contribute to the prolongation of the beta-receptor down-regulation by antidepressants. The intraventricular infusion of 12-0-tetradecanoyl-phorbol-13-acetate (TPA), a potent protein kinase C (PK-C) activator for seven days caused a significant decrease in beta-receptors, while forskolin or dibutyryl cyclic adenosine monophosphate had no influence on the receptor. The TPA-induced and desipramine-induced decreases in beta-receptors were not additive, suggesting that a similar mechanism is involved. The infusion of the PK-C inhibitor 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7) caused an inhibition of the desipramine-induced decrease in beta-receptors. It is suggested that the beta-receptor down-regulation by antidepressants might be also regulated by PK-C through 5-HT-Ca2+-inositol-phospholipid systems.

5,7-Dihydroxytryptamine↗
PubMed1981

Drainage of cerebral interstitial fluid into deep cervical lymph of the rabbit.

Lymph from the jugular lymph trunks of anesthetized rabbits has been continuously collected and radioiodinated albumin (RISA) therein estimated after microinjection of 1 microliter of 131I-albumin into the caudate nucleus, after single intraventricular injections, and during intraventricular infusions. Comparison of lymph at 7 and 25 h after intracerebral microinjection with efflux of radioactivity from whole brain suggests that about 50% of cleared radioactivity goes through lymph. Concentrations, normalized to cerebrospinal fluid (CSF), were much higher in lymph and retropharyngeal nodes after brain injection than after CSF injection or infusion. Also after brain injection, lymph and nodes contained more activity on injected side in contrast to lack of laterality after CSF administration. Calculation suggests that less than 30% of RISA cleared from brain can do so via a pool of well-mixed CSF. Analysis of tissues is compatible with much RISA draining by bulk flow via cerebral perivascular spaces plus passage from subarachnoid space of olfactory lobes into submucous spaces of nose and thus to lymph.

Animals↗