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PubMed1977

Serotonergic afferents to the dorsal raphe nucleus: evdience from HRP and synaptosomal uptake studies.

Afferent connections of the serotonin (5-HT)-containing dorsal raphe nucleus were investigated in the rat utilizing the horseradish peroxidase (HRP) retrograde cell labeling technique. Small quantities (0.1-0.5 mul) of HRP solutions were infused into the dorsal raphe, and the brains were examined 19-72 h later for retrograde transport of the enzyme. Intrinsic connections within the dorsal raphe nucleus were revealed by this mapping technique, as was an input to the dorsal raphe from another serotonergic cell group, the median raphe nucleus. Little evidence was found for projections from other, more remote, brain sites. A serotonergic innervation of the dorsal raphe was also demonstrated by the presence of high affinity uptake of [3H]5-HT (Km=0.17 muM) into synaptosomal suspensions of the dorsal raphe nucleus. Synaptosomal uptake of [3H]5-HT was blocked by selective destruction of serotonergic axon terminals induced by the intraventricular injection of 200 mug of 5,7-dihydroxytryptamine following desipramine HCl pretreatment, but not by destruction of catecholaminergic axon terminals induced by intraventricularly injected 6-hydroxydopamine (2 X 250 mug). The uptake of [3H]-5-HT by synaptosomes of the dorsal raphe was comparable to that of striatal and hypothalamic synaptosomes, and markedly greater than that of synaptosomes from the cerebellum or nearby dorsal central gray or midbrain reticular formation, indicating the presence of a relatively dense serotonergic innervation. These data together indicate that neurons in the dorsal raphe nucleus receive a prominent serotonergic input that is derived, at least in part, from other neurons within the dorsal nucleus and from a neighboring raphe nucleus.

5,6-Dihydroxytryptamine↗
PubMed1987

Gonadal steroid modulation of brain opioid systems.

It is becoming increasingly clear that the effects of the opioids and their synthetic analogs on anterior pituitary function largely depend on the steroid milieu present in the animal at time of drug administration. However, it is still unclear whether gonadal steroids regulate the opioid-modulated mechanisms by affecting the number of opiate receptors in the brain. To further investigate these issues, the effects of opiate agonists and antagonists on LH, FSH and prolactin (Prl) secretion have been studied in: (a) normal and castrated male rats, and (b) normally cycling female rats. The binding characteristics of the brain subclass of mu opiate receptors have been analyzed in the same group of experimental animals; this type of receptors seems to be particularly involved in the control of gonadotropin and Prl release. When injected intraventricularly into normal male rats, morphine (200 micrograms/rat) induced in a significant elevation of serum LH levels at 10 and 20 min. In long-term castrated animals the administration of the drug significantly reduced LH secretion at 40 and 60 min after the injection, the inhibition lasted up to 180 min. Morphine, when given intraventricularly to normal males, induced a conspicuous and significant elevation of serum Prl levels at 10, 20, 40 and 60 min after treatment. However, when the drug was administered to castrated rats, it did not significantly affect Prl release at any time interval considered. Morphine intraventricular injections did not modify serum FSH levels either in normal or in castrated male rats. The concentration of mu opiate receptors was found to be similar when measured in the whole brain of normal and orchidectomized rats. In adult cycling female rats, s.c. injections of naloxone (2.5 mg/kg) stimulated LH release in every phase of the estrous cycle; the magnitude of the responses was highly variable, being particularly elevated at 16.00 h of the day of proestrous and at 10.00, 12.00 and 14.00 h of the day of estrous. Conversely, LH response to naloxone was totally obliterated at 18.00 and 20.00 h of the day of proestrous, when the preovulatory LH surge was found to occur. The concentration of brain opiate receptors of the mu type showed significant variations during the different phases of the estrous cycle, with higher levels at 12.00 h of the day of proestrous and at 18.00 h of the day of estrous.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1968

Role of the chemoreceptor trigger zone in histamine-induced emesis.

1. In unanaesthetized dogs, the emetic action of histamine was studied after its injection into the cerebral venricles through chronically implanted cannulae in order to elucidate the role of the chemoreceptor trigger zone (CT-zone), situated in the area postrema, for this emesis.2. On injection into the lateral cerebral ventricle, about 10 times larger doses of histamine (3 mg) were required regularly to produce emesis, and it occurred after a longer latency than on injection into the fourth ventricle. This is in accord with an action of histamine on the CT-zone.3. After bilateral ablation of the CT-zone, intraventricular injections of histamine no longer produced emesis even when injected in doses which were three to four times greater than those which regularly elicited vomiting in dogs with intact CT-zone. The emesis produced in dogs by intraventricular injections of histamine is thus fully accounted for by an action on the CT-zone.4. Injections of chlorpromazine intramuscularly or of the two antihistamines cyclizine and mepyramine, either intramuscularly or into the lateral ventricle, prevented the emesis caused by histamine injected into the lateral ventricle. This protective action of the antihistamines-which did not extend to the emesis produced by oral copper sulphate-suggests the presence of histaminergic receptors in the CT-zone.

Animals↗
PubMed1980

Neuroendocrine regulation and central dopamine (DA) systems in physical and psychological stress.

Physical and psychological stress cause different patterns of changes in the fluorescence intensity of nigral and tuberoinfundibular DA neurons which point to changes in neuronal activity. In order to investigate possible interactions between alpha-MSH (alpha-melanotropin) and DA systems in stress, systemic and intraventricular injections of antiserum against alpha-MSH were made. The functional state of DA neurons was assessed by histochemical microfluorimetry and hormone levels were measured by radioimmunossay. Antiserum against alpha-MSH was found to affect the functional state of DA neurons, but only thorugh the intravenous route. Under physical stress i.v. injection of antiserum against alpha-MSH was accompanied by elevated levels of activity of the DA neurons of the substantia nigra. An intraventricular injection of the same antiserum was ineffective. In psychological stress, an effect was again seen only after intravenous injection of antiserum against alpha-MSH. In this situation, the activity in DA cell groups of the substantia nigra, ventral tegmental area and tubero-infundibular system was increased after antiserum injection. Possible influences from manipulations were checked; certain effects which depended upon experimental situation were noted. Our data suggest a modulatory influence of circulating alpha-MSH on the functional state of central DA systems.

Animals↗
PubMed1989

[Hemostatic changes after local exposure to low temperatures (frostbite)].

Hemostatic blood potential was studied in experiments on 400 rats, 25 dogs and in 120 patients, during changes of CNS reactivity after intraventricular injection of reserpine, adrenaline, and irritation of the thalamus ventromedial nucleus (VMN) or its destruction. CNS reactivity in dogs changed after intraarterial injections of acetylcholine, reserpine, heparin and fibrinolysin solutions. It was shown that activation of adrenergic structures of the hypothalamus by intraventricular adrenaline injections, or the hypothalamus VMN irritation, stimulated coagulation and depressed anticoagulation mechanisms of the blood, and increased hemostatic blood potential, that led to rejection of frostbitten tissues. Activation of the hypothalamus cholinergic structures by intraventricular injections of reserpine, destruction of the hypothalamus VMN, and intraarterial injections of acetylcholine, reserpine, heparin, fibrilysin and contrycal mixtures stimulated the blood anticoagulation mechanisms, decreased the hemostatic potential, led to retention of cryodestructed tissues.

Animals↗
PubMed1977

beta-Endorphin: pituitary and adrenal glands modulate its action.

Hypophysectomized rats are supersensitive to the hypothermic effects of morphine and beta-endorphin injected intraventricularly as early as 1 week after surgery. At 2 weeks after surgery, there is a significant increase in the antinociceptive potency for these opiates. The route of opiate injection must be considered in interpretations of these results. The enhanced opiate potency following subcutaneous morphine injection in hypophysectomized rats may be partially explained by adrenal dysfunction, as demonstrated by a similar sensitization to subcutaneous morphine following adrenalectomy. By contrast, no enhancement of opiate potency was observed upon direct intraventricular injection of morphine or beta-endorphin in adrenalectomized rats. Furthermore, the potency of intravenous beta-endorphin is profoundly enhanced in adrenalectomized mice; five out of nine animals died when injected with a dose of the peptide that produced only mild analgesia in sham controls. The complete reversal of this intravenous beta-endorphin supersensitivity by dexamethasone implies a possible physiological interplay between the peptide and adrenal function.

Adrenal Glands↗
PubMed1981

The effect of antiserum to S 100 protein on behavior and amount of S 100 in brain cells.

Since antiserum raised against the S 100 protein has an impairing effect on acquisition in behavioral tests, when interacting with S 100 on hippocampal cells, the effect of S 100 antiserum was studied in rats on the S 100 content of the hippocampus and thalamus, as well as on behavior. The operant reversal of handedness test and a light discrimination test were used. S 100 antiserum, 2 X 30 mu l, was injected intraventricularly before and during the sessions of two different learning tests. The S 100 protein was determined by quantitative immunoelectrophoresis. In the antiserum-injected animals, the levels of S 100 protein was increased by up to 30%, the incorporation values of 3H-valine increased in proteins of high molecular weight. Further acquisition was inhibited compared to controls, in which antiserum absorbed with pure S 100 protein was injected intraventricularly. The stimulation of S 100 synthesis, probably by the glia, may have occurred by a negative feedback effect, as has been observed in thymocytes.

Animals↗
PubMed1988

The antinociceptive role of a bulbospinal serotonergic pathway in the rat brain.

The antinociceptive role of spinal serotonin (5-HT) neurons descending from 5-HT cells near the ventrolateral surface of the medulla oblongata was investigated by stimulating these cells in normal rats, in rats with generalized or selective chemical ablation of 5-HT nerves, and in rats with postsynaptic blockade of 5-HT receptors. Electrical stimulation of the lateral medulla elicited analgesia in normal rats; the increase in pain threshold was proportional to the intensity and to the frequency of stimulation. In addition, microinjection of kainic acid or L-glutamate at the same sites also produced analgesia. However, generalized destruction of CNS 5-HT nerves produced by intraventricular injection of 5,7-dihydroxytryptamine (5,7-DHT) or selective destruction of spinal 5-HT nerves produced by intraspinal injection of 5,7-DHT reduced the magnitude of the antinociceptive responses to electrical stimulation. Postsynaptic blockade of CNS 5-HT receptors produced by intraventricular injection of cyproheptadine also reduced the stimulation-produced analgesia. The specificity of the lesions for 5-HT nerves is demonstrated by the lack of effect on the levels of noradrenaline in the same brain regions. The results indicate that the activity of 5-HT nerve cells adjacent to the ventrolateral surface of the medulla oblongata and projecting to the spinal cord serves to elevate pain threshold.

5,7-Dihydroxytryptamine↗
PubMed1985

Neuropeptide Y affects secretion of luteinizing hormone and growth hormone in ovariectomized rats.

Neuropeptide Y (NPY) has recently been localized in the rat hypothalamus. We have evaluated the effects of NPY on hypothalamic and pituitary function by injecting NPY into the third ventricle in vivo and by examining its action on perifused pituitary cells in vitro. Injections of NPY into the third ventricle of conscious ovariectomized rats led to a dramatic and highly significant reduction in plasma luteinizing hormone (LH) relative to pretreatment levels in these animals or to those of controls injected with physiological saline. Significant inhibition was obtained with doses ranging from 0.02 to 5.0 micrograms (4.7-1175 pmol) of NPY. These inhibitory effects on LH release were dose dependent and lasted for at least 120 min after injection of 5.0 micrograms of NPY. Intraventricular injection of NPY also significantly decreased plasma growth hormone; however, the threshold dose was 2.0 micrograms (470 pmol), a dose 100-fold greater than the lowest dose that inhibited LH release. Plasma follicle-stimulating hormone was unaffected by injection of NPY. NPY (10(-6) and 10(-7) M) stimulated secretion of LH, growth hormone, and follicle-stimulating hormone from perifused anterior pituitary cells loaded in a Bio-Gel P-2 column. These results indicate that NPY acts on structures adjacent to the third ventricle to inhibit the secretion of LH and growth hormone but not follicle-stimulating hormone, whereas it can directly stimulate the secretion of all three hormones from the cells of the anterior pituitary in vitro. Since NPY has been found in the hypothalamus and median eminence, it is quite likely that it plays a physiologically significant role at both hypothalamic and pituitary sites: influencing secretion of pituitary hormones.

Animals↗
PubMed1981

Lumiflavin and lumichrome transport in the central nervous system.

The transport of the lipid-soluble sugarless flavins, [14C]lumiflavin and [14C]lumichrome, into an from the isolated choroid plexus and brain slices was studied in vitro. The isolated choroid plexus accumulated both [14C]flavins by a saturable, energy-requiring process that did not depend on binding or intracellular metabolism of the [14C]flavins. Both sugar-containing and sugarless flavins, as well as cyclic organic acids, significantly inhibited [14C]lumiflavin and [14C]lumichrome uptake by the isolated choroid plexus. Within 2.5 min, 75% of the [14C]lumiflavin accumulated by the isolated choroid plexus was released into the medium. Brain slices accumulated [14C]lumiflavin by a saturable process that did not meet all the criteria for active transport. Ninety-five percent of the [14C]lumiflavin accumulated by brain slices was released into the medium within 7.5 min. In vivo, 2 h after the intraventricular injection of 6.5 nmol [14C]lumiflavin, almost all of the [14C]flavin was cleared from the CNS. Addition of 3.5 mumol FMN to the intraventricular injectate significantly decreased the clearance of [14C]lumiflavin from the CNS. These studies document that the sugarless flavins are transported by the flavin transport systems in the CNS.

Animals↗
PubMed1996

Morphological and pharmacological evidence for neuropeptide Y-galanin interaction in the rat hypothalamus.

Galanin (GAL) and neuropeptide Y (NPY) have been shown to play important roles in the regulation of pituitary hormone secretion, as well as ingestive and sexual behaviors, by acting within the hypothalamus. While the mechanism of action of these regulatory peptides is under intensive investigation, less attention has been paid to the possible interaction between them in influencing these central regulatory processes. Because NPY and GAL augment pituitary gonadotropin release, the present study was undertaken to evaluate the nature of morphological and functional relationships between these excitatory hypothalamic peptidergic systems. Double immunolabeling for NPY and GAL was carried out on vibratome sections taken from the hypothalamus of colchicine-pretreated female rats. Avidinbiotin peroxidase technique and a dark blue diaminobenzidine reaction was used to visualize NPY profiles, while the GAL neurons were labeled with a light brown diaminobenzidine reaction using either the avidin-biotin peroxidase or the peroxidase antiperoxidase technique. Light microscopic examination of the immunostained material showed that in the arcuate nucleus, paraventricular nucleus, supraoptic nucleus, anterior hypothalamus, and medial preoptic area, an abundant network of NPY-immunoreactive axons surrounded GAL-immunostained cells. Numerous dark blue NPY-containing putative boutons were observed in close proximity to GAL-immunolabeled cell bodies and dendrites. Correlated light and electron microscopic examination revealed that most of the immunoreactive NPY axon terminals established synaptic connections with GAL-expressing cells. Synaptic connections were most frequently found in the medial preoptic area and in the magnocellular region of the paraventricular nucleus and arcuate nucleus. Fewer connections were observed in the supraoptic nucleus. These morphological observations demonstrate the existence of a strong NPY input to hypothalamic GAL neurons, thereby suggesting a modulatory role for NPY in monitoring GAL release. To evaluate the functional relevance of this anatomical relationship, the effects of intraventricular injection of a GAL receptor antagonist, galantide, were examined on NPY-induced LH release in ovarian steroid-primed ovariectomized rats. As expected, intraventricular injection of NPY readily stimulated LH release. Although, while on its own, galantide was ineffective in altering basal LH release, it markedly attenuated the NPY-induced LH response, thereby suggesting that GAL released in response to NPY administration may, in part, mediate the excitatory effects of NPY. These experimental results, taken together with the morphological observations, document the involvement of an NPY --> GAL signaling modality in the release of gonadotropins and, likewise, raise the possibility of a similar signaling process in the release of other pituitary hormones and elicitation of behavioral effects attributed to NPY and GAL.

Analysis of Variance↗
PubMed1981

Yohimbine diastereoisomers: cardiovascular effects after central and peripheral application in the rat.

The cardiovascular effects of four yohimbine diastereoisomers, yohimbine, rauwolscine, corynanthine, and 3-epi-alpha-yohimbine, were compared in urethane-anaesthetized and conscious, normotensive Sprague-Dawley rats. Intravenous cumulative infusions (10--500 microgram) of the drugs to anaesthetized rats decreased blood pressure and blunted the pressor response to intravenous adrenaline injections. Corynanthine was the most potent isomer in this regard, followed by yohimbine, rauwolscine, and 3-epi-alpha-yohimbine. Depressor responses following intravenous bolus doses (40 microgram) showed a similar ranking. Intraventricular injections of yohimbine to anaesthetized rats decreased blood pressure dose-dependently, as did injections of corynanthine and rauwolscine. Responses indicated the ranking to be yohimbine greater or equal to rauwolscine greater than corynanthine for this effect at the 40 microgram dose. Heart rate was also decreased by these isomers, but not in a dose-dependent fashion. In conscious rats, the intraventricular injection of these isomers (20 microgram) increased blood pressure and heart rate. No differences were noted in terms of blood pressure responses; but, in causing tachycardia, the ranking was rauwolscine greater than yohimbine greater than corynanthine. These data suggest that after intraventricular application in anaesthetized rats, the effects of these alpha-adrenoceptor blockers are related to their individual affinity for the alpha 2 adrenoceptor.

Animals↗
PubMed1985

Evidence for a spinal site at which opioids may act to inhibit the milk-ejection reflex.

Morphine was injected into the lumbar subarachnoid space of anaesthetized lactating rats (7-10 days post partum) to examine its effect on the milk-ejection reflex at a spinal level. Although the delay until the first milk-ejection response to the suckling of hungry pups was variable (3-60 min) the subsequent responses occurred at regular intervals of 7.5 +/- 0.4 min; milk-ejection responses were detected by measurement of intramammary pressure and by the characteristic behaviour of the pups. Injection of morphine (4-50 micrograms) via a cannula inserted into the spinal subarachnoid space inhibited reflex milk ejection in a dose-related manner without affecting the sensitivity of the mammary gland to exogenous oxytocin (1 mu., i.v.); injection extradurally was without effect. The opiate antagonist naloxone (10 micrograms), when injected intrathecally, did not significantly alter the pattern of reflex milk ejection or the amplitude of the intramammary pressure response, but prevented the inhibitory effect of morphine when administered with the opiate. Pethidine (250 and 400 micrograms) also inhibited the milk-ejection reflex. It is unlikely that the effect of spinal administration of morphine occurred as the result of the transportation to a supraspinal site since release of oxytocin evoked by intraventricular injection of hypertonic sodium chloride (3 mol/l) was blocked by intraventricular injection of morphine (4 micrograms) but not by a much larger dose (40 micrograms) injected intrathecally.

Animals↗
PubMed1975

[Ventriculography with methylglucamine iocarmate (Dimer-X). Experimental and Clinical study (author's transl)].

Evaluation of 60% solution of Methylglucamine iocarmate (Dimer-X) for ventriculography in animal experiment and clinical cases was reported. The experimental result was compared with that of Conray 60 and Angiografin, which was reported in our previous papers. In seven intraventricular injections of 2.0 ml, administered to 6 dogs, convulsion was observed on three occasions, facial myoclonus on 1 and no symptoms on the remaining three. However, in 7 intraventricular injections of 1.5 ml for 6 dogs, 6 were symptom-free and only residual one showed convulsion. And no dog died in either experiment. No changes were seen in a subsequent ventriculogram one month after the 1st ventriculography with Dimer-X and also no histological changes of the ventricular wall were revealed one month after the first experiment. These experimental results suggested less toxicity of Dimer-X than Conray 60 or Angiografin. Clinically, in 17 neurosurgical patients, ventriculography was performed with 1-5 ml of Dimer-X. No patients showed convulsive complication, but there was one episode of vomiting in each of 2 cases and slight headache in one case. From our experimental and clinical studies, it is concluded that the Dimer-X is to be considered the best watersoluble contrast medium for ventriculography at present.

Adolescent↗
PubMed1976

Behavioral effects of phenoxybenzamine administered intraventricularly in rats.

Phenoxybenzamine (PNB) injected into the lateral ventricle of the brain weakens spontaneous motility of rats and antagonizes hyperactivity induced with noradrenaline, amphetamine and caffeine. Body temperature rises briefly, sleep induced with chloral hydrate is shortened, and high doses enhance amphetamine-induced stereotypy. PNB injected intraventricularly intensifies turnover of noradrenaline but it has no effect on turnover of dopamine in rat brains. The results confirm a blocking influence of PNB on the cerebral noradrenaline receptors.

Animals↗
PubMed1989

Intraventricular or epidural injection of morphine for severe pain.

Intraventricular or epidural injection of morphine through implantable infusion devices was used for severe pain in 50 patients with advanced cancer, arachnoiditis, or spinal injury. Intraventricular catheter was inserted for injection of morphine in 21 patients, 29 were treated through epidural infusion. For the evaluation of results the multimodal evoked potential (MEP) has been obtained before and after each treatment. 80% of the patients experienced good results. No significant side effects have been noted in patients with either epidural or intraventricular injection of morphine. These may be excellent methods for pain control in well selected patients.

Adult↗
PubMed2006

Intraventricular ascorbic acid administration decreases hypoxic-ischemic brain injury in newborn rats.

Neuronal cell damage following hypoxic-ischemic (HI) brain injury is partly caused by production of free radicals and reactive oxygen species (ROS). Ascorbic acid (AA) is a potent antioxidant, which scavenges various types of ROS. Some studies have shown that it is neuroprotective, however, the issue is still controversial. In this study, we examined the effect of intraventricular AA administration on immature HI brain using the Rice-Vannucci model. After unilateral carotid artery ligation under isoflurane anesthesia, 7-day-old rat pups received varying concentrations of AA (0.04, 0.2, 1 and 5 mg/kg) by intraventricular injection and were exposed to 8% oxygen for 90 min. Vehicle controls received an equal volume of phosphate saline buffer. We assessed the neuroprotective effect of AA at 7 days post-HI. The percent brain damage measured by comparing the wet weight of the ligated side of hemisphere with that of contralateral one was reduced in both 1 and 5 mg/kg groups but not in either 0.04 or 0.2 mg/kg groups compared to vehicle controls (5 mg/kg 16.0 +/- 4.3%, 1 mg/kg 10.9 +/- 5.0%, vs. controls 36.7 +/- 3.6%, P < 0.05). Macroscopic evaluation of brain injury revealed the neuroprotective effect of AA in both 1 and 5 mg/kg groups (5 mg/kg 1.1 +/- 0.4, 1 mg/kg 0.4 +/- 0.3, vs. controls 2.9 +/- 0.3, P < 0.05). Western blots of fodrin on the ligated side also showed that AA significantly suppressed 150/145-kDa bands of fodrin breakdown products, which suggested that AA suppressed activation of calpain. Neuropathological quantitative analysis of cell death revealed that 1 mg/kg of AA injection significantly reduced the number of necrotic cells in cortex, caudate putamen, thalamus and hippocampus CA1, whereas that of apoptotic cells was only reduced in cortex. These findings show that intraventricular AA injection is neuroprotective after HI in immature rats.

Analysis of Variance↗
PubMed1998

Adenovirus-mediated gene transfer results in decreased lysosomal storage in brain and total correction in liver of aspartylglucosaminuria (AGU) mouse.

Aspartylglucosaminuria (AGU) is a lysosomal storage disease leading to mental retardation, which is caused by deficiency of aspartylglucosaminidase (AGA). AGU is strongly enriched in the Finnish population in which one major mutation called AGU(Fin) has been identified. The molecular pathogenesis of AGU as well as the biology of the AGA enzyme have been extensively studied, thus giving a profound basis for therapeutic interventions. In this study we have performed adenovirus-mediated gene transfer to the recently produced mouse model of AGU, which exhibits similar pathophysiology as that in humans. Recombinant adenovirus vectors encoding for the human AGA and AGU(Fin) polypeptides were first applied in primary neurons of AGU mouse to demonstrate wild-type and mutant AGA expression in vitro. In vivo, both of the adenovirus vectors were injected into the tail vein of AGU mice and the expression of AGA was demonstrated in the liver. The adenovirus vectors were also injected intraventricularly into the brain of AGU mice resulting in AGA expression in the ependymal cells lining the ventricles and further, diffusion of AGA into the neighbouring neurons. Also, AGA enzyme injected intraventricularly was shown to transfer across the ependymal cell layer. One month after administration of the wild-type Ad-AGA, a total correction of lysosomal storage in the liver and a partial correction in brain tissue surrounding the ventricles was observed. After administration of the Ad-AGU virus the lysosomal storage vacuoles in liver or brain remained unchanged. These data demonstrate that the lysosomal storage in AGU can be biologically corrected and furthermore, in the brain a limited number of transduced cells can distribute AGA enzyme to the surrounding areas.

Adenoviridae↗