Effects of intracisternal 6-hydroxydopamine treatment on acquisition and performance of rats in a double T-maze.

136 male Sprague-Dawley rats in 4 experiments were subjected to various treatments with 6-hydroxydopamine (6-OHDA) to produce decrements in brain catecholamine content either before or after learning to respond in an appetitively motivated double –T maze task. Intracisternal injections of 6-OHDA not only impaired acquisition of the required behavioral response but also decreased performance of Ss which had previously acquired the task. Although reduced food consumption found in 6-OHDA-treated Ss may contribute to the observed deficits in –T maze responding, the behavioral deficit produced by 6-OHDA injection did not seem to be due only to a simple decrease in food intake. The decrements in acquisition and performance were clearly related to amount of central catecholamine depletion produced by 6-OHDA treatment. Further analysis suggested that the behavioral deficits were more related to the reductions in dopamine than they were to the depletion of brain norepinephrine. (33 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Synthesis of potential hydrazinoamine tuberculostatics. XIV. Reactions of 2-aminoethylhydrazine with ketones

The role of brain catecholaminergic mechanisms in habituation of activity was investigated in rat pups treated with 6-hydroxydopamine (6-OHDA). Intracisternal administration of this agent in the neonatal period resulted in a permanent and significant depletion of brain dopamine to 35.5% of controls while brain norepinephrine remained unchanged. Activity levels in normal developing rat pups increased rapidly between 15-22 days, then declined at maturity (26 days), while activity in 6-OHDA treated animals during this peak period of behavioral arousal increased to a significantly greater degree than that of their littermate controls. Habituation of activity, defined as the decrement of spontaneous activity, was calculated by regression over the first 30 min of observation. At both 5 and 8 days of age 6-OHDA and control rat pups exhibited low levels of activity whose decrease with time did not differ significantly and this pattern continued through 12 days of age. However, by 15 days of age activity in control animals declined by 19% each 10 min period compared to only a 10% decline found in 6-OHDA animals. At 19 days normal rat pups declined by 10% compared to a significantly reduced decrement of 3% found in treated animals, but these differences were no longer apparent by 22, 26, or 29 days of age. Our results are consistent with the notion that habituation of activity is a complex phenomenon mediated in part by catecholaminergic systems.     

Influences of deviations of thyroid functions on the effects of MAOI in rats--changes of 5-HT, 5-HIAA and norepinephrine contents and tyramine uptake by the brain and fluctuation of the rectal temperature]

The drug 6-hydroxydopamine (6-OHDA) has been reported to reduce hypothalamic norepinephrine (NE) content after administration into the lateral ventricle without altering the dopamine content of tubero-infundibular neurons. Serum prolactin levels in male rats injected with 2 X 250 mug 6-OHDA were significantly higher than in untreated control rats. Intraventricular injection of male rats with artificial cerebrospinal fluid resulted in elevated mean prolactin levels similar to those observed in 6-OHDA-treated animals. Further experimentation on animals decapitated at different times after removal from the animal quarters, indicates that prolcatin levels in 6-OHDA-treated rats are continuously elevated whereas they rise from basal levels to extremely high levels in CSF-treated rats, thus resulting in similar mean values. The CSF-treated controls ate hypersensitive to the stress of being removed from their normal environment. Such an effect was not observed in 6-OHDA-treated nor in untreated, and thus stress-inexperienced rats. In a long term study, serum prolactin and luteinizing hormone (LH) levels were followed over a period of 71 days after 6-OHDA treatment. Prolactin levels increased within one day after treatment and stayed at a high level for 15 days. Subnormal prolactin values were measured 37 days after 6-OHDA treatment. Serum LH levels were below normal 3 h and one day and were increased 37 and 71 days after 6-OHDA treatment. These results suggest that NE is important in the transmission of stressful stimuli to hypothalamic prolactin regulating centers. They further suggest functional recovery of LH and prolactin regulating mechanisms after 6-OHDA treatment.     

Differential effects of maternal and sibling presence on hyperactivity of 6-hydroxydopamine-treated developing rats.

Assessed the influence of test environment on the expression of hyperactivity produced by neonatal 6-hydroxydopamine (6-OHDA) administration in Sprague-Dawley rat pups at 15, 19, and 22 days of age in 3 experiments. The 6-OHDA Ss and an equal number of controls were tested in isolation, mixed groupings of 2 treated and 2 control pups, mixed groupings with their anesthetized mothers, mixed groupings with an anesthetized sibling, and homogeneous groupings of all treated and all control siblings. Social factors had differential effects on activity, particularly at 19 days of age: the 6-OHDA Ss were hyperactive relative to controls in isolation, and both treated and control pups were equally active in the mixed grouping and were hyperactive relative to control isolation levels. The addition of an anesthetized mother sharply attenuated the activity of both types of pups. It is concluded that social factors strongly influenced the behavior of rat pups with whole brain dopamine depletion produced by 6-OHDA and, within the confines of this animal model of hyperactivity, exerted greater attenuating effects on their activity than previously observed with stimulant medication. (32 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Monoamine neurotoxins: selective and delayed effects on behavior in colonies of laboratory rats

Male laboratory rats were raised in two colonies, each of 27 rats, and then given intraventricular injections of the norepinephrine neurotoxin 6-hydroxydopamine (6-OHDA) or the serotonin neurotoxin 5,6-dihydroxytryptamine (5,6-DHT) or saline. They were then returned to their enclosure and behavior during the next 50 days was observed. Shortly after neurotoxin injections the 6-OHDA rats spent more time in the burrows than controls and when out were inactive. The 5,6-DHT rats in contrast spent more time in the open than controls, ran more in activity wheels, approached humans, and fought more. Fighting, mounting, and hoarding in the colony gradually increased for 25 days; during this time the status of the 6-OHDA animals fell progressively whereas the 5,6-DHT animals increased in dominance. Social behavior returned to more normal levels after 50 days. Several successive stages of behavioral alterations occur following neurotoxin injections.     

Genetic differences in ethanol drinking of the rat following injection of 6-OHDA, 5,6-DHT or 5,7-DHT into the cerebral ventricles

The preference characteristics for ethanol of four different strains of rats were determined in a two-choice situation by offering water and ethanol in a concentration which was increased from 3 to 30% over a 12-day test sequence. Using stereotaxic procedures, 50 mug 5,6-dihydroxytryptamine (5,6-DHT), 200 mug 6-hydroxydopamine (6-OHDA) or 100 mug 5,7-dihydroxytryptamine (5,7-DHT) were then injected acutely into the lateral cerebral ventricle in a 20 mul volume. Rats of the Sprague-Dawley strain increased their ethanol preference following the lesioning of the serotonergic system by 5,6-DHT, whereas similar destruction of catecholaminergic neurons by 6-OHDA markedly suppressed ethanol intake; Long-Evans rats displayed a similar trend in ethanol drinking patterns. However, animals of the Holtzman strain manifested the increased drinking after 5,6-DHT, but showed no suppression of drinking following 6-OHDA. The preference of rats of the Wistar strain was unaffected by 5,6-DHT but attenuated by 6-OHDA. 5,7-DHT had little or no effect on ethanol consumption in any of these strains. These findings thus suggest that genetic factors are an important determinant in an animal's response to a drug that affects 5-HT or NE systems in the brain, particularly when ethanol selection is investigated.     

Differential effects on body weight of central 6-hydroxydopamine lesions in obese (ob/ob) and diabetes (db/db) mice.

Obese (ob/ob) and diabetes (db/db) mice are genetic mutants that have been shown to have altered levels of central catecholamines (CAs) as well as syndromes of obesity, hyperphagia, and hyperglycemia. Because the CAs, and particularly norepinephrine (NE), are implicated in the control of feeding, levels of central CAs were experimentally reduced in ob/ob and db/db mice to investigate the role of CAs in these cases of spontaneously occurring obesity. Lesions produced by 6-hydroxydopamine (6-OHDA) were used to produce large depletions of NE and dopamine (DA) in both ob/ob and db/db mice and in lean control Ss of the same background strains. In the db/db but not the ob/ob, central CA depletion was accompanied by a significant and persistent weight loss and by a reduction in plasma glucose levels when compared with vehicle-infused controls. Treatment with the NE uptake blocker desipramine (DI) prior to 6-OHDA infusions attenuated NE but not DA depletion. Diabetes Ss that received DI pretreatment showed a weight loss and decrease in plasma glucose proportional to the amount of NE depletion. Lean Ss that received the 6-OHDA treatments showed only a transient weight loss and no significant change in blood glucose. Abnormalities in central noradrenergic systems may account for part of the obesity syndrome in the diabetes mouse. (29 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Restoration of sympathetic noradrenergic nerve fibers in the spleen by low doses of L-deprenyl treatment in young sympathectomized and old Fischer 344 rats

It is well-established that noradrenergic (NA) nerve fibers in spleen and lymph nodes influence cell-mediated immune responses. Such responses are diminished in young animals following chemical sympathectomy and in older animals accompanying an age-related decline in NA nerve fibers in spleen and lymph nodes. The purpose of this study was to determine whether treatment with deprenyl, an irreversible monoamine oxidase-B (MAO-B) inhibitor, would hasten the process of splenic NA reinnervation following chemical sympathectomy in young rats and would reverse the age-related loss of sympathetic NA fibers in the spleen of old rats. To examine the effects of deprenyl in young sympathectomized rats, 3-month-old male Fischer 344 (F344) rats were treated with 6-hydroxydopamine (6-OHDA) and administered 0, 0.25, 1.0, 2.5, or 5.0 mg deprenyl/kg body weight (BW)/day intraperitoneally (i.p.) for 1, 15, or 30 days. In another study, 21-month-old male F344 rats were treated with 0, 0.25, or 1.0 mg deprenyl/kg BW/day i.p. for 9 weeks. At the end of the treatment period, spleens were removed and NA innervation was assessed by fluorescence histochemistry, immunocytochemistry, and quantitation of norepinephrine (NE) by high performance liquid chromatography with electrochemical detection (HPLC-EC). In the spleens of young sympathectomized rats, there was faint fluorescence or absence of fluorescence and tyrosine hydroxylase-positive (TH+) fibers around the central arteriole and in the periarteriolar lymphatic sheath of the white pulp one day after administration of 6-OHDA, indicating a severe loss of NA innervation compared with unlesioned control animals. Treatment of sympathectomized rats with 1.0 mg, 2.5 mg, and 5.0 mg/kg deprenyl for 30 days increased the density of NA innervation estimated by both fluorescence histochemistry and immunocytochemistry compared with vehicle-treated controls recovering spontaneously from 6-OHDA. Splenic NE concentration was increased in the hilar region of sympathectomized rats treated with 2.5 mg and 1.0 mg/kg deprenyl after 15 and 30 days, respectively, compared with untreated and vehicle-treated sympathectomized rats. The spleens of untreated and saline-treated old rats showed a reduction in the density of NA innervation in the white pulp compared with young animals. Treatment of old rats for 9 weeks with 1.0 mg/kg deprenyl induced moderate to intense fluorescent fibers and linear TH+ nerve fibers around the central arteriole and in other compartments of the white pulp, and increased splenic NE concentration in the hilar region and NE content in the whole spleen. Taken together, these results provide strong evidence for a neurorestorative property of deprenyl on sympathetic NA innervation of the spleen, which may lead to an improvement in cell-mediated immune responses.     

The dorsal tegmental noradrenergic projection: An analysis of its role in maze learning.

Evaluated the hypothesis that the noradrenergic projection from the locus coeruleus (LC) to the cerebral cortex and hippocampus is an important neural substrate for learning. Four experiments were conducted with 61 male Wistar rats. Maze performance was studied in Ss receiving either electrolytic lesions of LC or 6-hydroxydopamine (6-OHDA) lesions of the dorsal tegmental noradrenergic projection. The LC lesions did not disrupt the acquisition of a running response for food reinforcement in an L-shaped runway, even though hippocampal-cortical norepinephrine (NE) was reduced to 29%. Greater telencephalic NE depletions (to 6% of control levels) produced by 6-OHDA also failed to disrupt the acquisition of this behavior or to impair the acquisition of a food-reinforced position habit in a 'T'-maze. Neither locomotor activity nor habituation to a novel environment was affected by the 6-OHDA lesions. Ss with such lesions were, however, found to be significantly more distractible than were controls during the performance of a previously trained response. The hypothesis that telencephalic NE is of fundamental importance in learning was not supported. The data suggest that this system may participate in attentional mechanisms. (24 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Increased alcohol drinking in isolate-housed alcohol-preferring rats.

Alcoholism is a complex disorder influenced by interactions between genetic and environmental risk factors. This study examined the influence of isolate housing on ethanol intake in alcohol-preferring (P) and non-alcohol-preferring (NP) rats. Rats were isolate-housed or pair-housed for 8 weeks when between 45 and 96 days old. Ethanol drinking was assessed using a 24-hr preference test (10% ethanol vs. water) and 20-min limited access tests. A behavioral test battery was used to assess anxiety-like, depressive-like, acoustic startle, and motor behavior. Isolate housing increased home cage drinking in both lines and increased limited access drinking selectively in P rats. Isolation also reduced swim test immobility and prepulse inhibition in P rats and increased locomotor stereotypies in NP rats. Taken together, these data demonstrate that Line × Environment interactions influence the effects of isolation. Furthermore, isolation selectively increased ethanol intake in high drinking P rats. This effect was not correlated with changes in other behaviors. Selective enhancement of limited access ethanol drinking in P rats may represent a model whereby genetic liability to excessive drinking is enhanced by specific environmental exposures. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Infarct topography and hemiparesis profiles with cerebral convexity infarction: the Stroke Data Bank

The development of natural killer (NK) cell activity was assessed in Fischer 344 (F344) rats sympathectomized as neonates with the neurotoxin, 6-hydroxydopamine (6-OHDA). No NK cell activity was detected in sympathectomized or vehicle-injected control animals at 7 days of age. At 10 and 14 days of age, NK cell activity was reduced in spleens from sympathectomized male and female rats. At 21 days of age, a reduction in NK cell activity was detected only in sympathectomized male rats. Sympathectomy did not alter NK cell activity at 28 and 42 days of age in either gender. At 56 days of age, NK cell activity was increased in neonatally sympathectomized females; rats of both genders acutely sympathectomized at 56 days of age also showed enhanced NK cell activity. No differences were observed at 90 days of age in neonatally or acutely sympathectomized males of females. Prior treatment with desipramine, which blocks uptake of 6-OHDA into nerve terminals and prevents the destruction of sympathetic nerve terminals, prevented these 6-OHDA-induced effects, suggesting that sympathectomy, and not direct toxic effects of 6-OHDA treatment of NK cells, accounted for the alterations in NK cell activity. Together, these results indicate that the sympathetic nervous system is an integral component of the developing lymphoid and hematopoietic microenvironment.     

Central noradrenergic neurons: Differential effects on body weight of electrolytic and 6-hydroxydopamine lesions in rats.

Compared the effects of bilateral electrolytic and 6-hydroxydopamine (6-OHDA) lesions of the ventral noradrenergic bundle (VB) in 2 experiments with a total of 67 female albino rats. When Ss were fed only a standard laboratory diet, no significant differences were found between groups. When a high-fat diet supplement was introduced, the group with electrolytic lesions became significantly heavier than the control group; however, the 6-OHDA group did not differ from the controls. Norepinephrine depletion was significantly greater following the 6-OHDA than the electrolytic lesions. Both lesions reduced telencephalic dopamine and serotonin only slightly. Exp II, in which both types of lesions were placed at a rostral ventromedial hypothalamic site, yielded the same pattern of results. Diet-dependent increased in body weight were attributed to the destruction of a non-noradrenergic system, which was spared by the relatively selective 6-OHDA lesion but damaged by the nonselective electrolytic lesion. (39 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of 6-hydroxydopamine and pimozide on temperature maintenance by the chicken

Intraventricular implants of pimozide in adult white leghorn hens were used to block dopamine (DA) receptors, and 6-hydroxydopamine (6-OHDA) was injected intraventricularly to destroy the noradrenergic system locally. The hens were exposed to ambient temperatures of 5 and 35 degrees C, and their core temperature was measured. One hundred micrograms of 6-OHDA significantly reduced the norepinephrine (NE) but not the DA content of the hypothalamus and reduced the uptake of [3H]NE but not of [3H]DA by synaptosomes in vitro. Neither of the drug treatments nor their combination affected average core body temperature (Tb) at either 5 or 35 degrees C. Pimozide treatment caused a lower maximum Tb at 35 degrees C and a higher maximum Tb at 5 degrees C than the control treatment. No evidence was obtained that 6-OHDA treatment affected body temperature regulation. It is concluded that neither the DA nor the NE system is essential for normal temperature maintenance in the hen exposed to either 5 or 35 degrees C.     

Depletion of dopamine in the nucleus accumbens prevents the generation of locomotion by metabotropic glutamate receptor activation

The contribution of dopamine (DA) to the locomotion elicited by activation of nucleus accumbens (NAcc) metabotropic glutamate receptors (mGluRs) was investigated in the rat. Different groups of rats were pretreated with bilateral microinjections of either 6-hydroxydopamine (6-OHDA) or its vehicle into the NAcc and, on separate tests starting 10 days later, were tested for locomotion following microinjections (into the same site) of saline, the mGluR agonist, 1-aminocyclopentane-trans-1,3-dicarboxylic acid [(1S, 3R)-ACPD, 0.5 nmol/side] and amphetamine (AMPH, 6.8 nmol/side). DA levels at the microinjection sites were significantly depleted in 6-OHDA-treated rats (42-99% depletions compared to control values obtained in vehicle-treated rats). In contrast to the increased locomotion observed in non-lesioned animals, rats pretreated with 6-OHDA showed no increase in locomotor activity in response to (1S, 3R)-ACPD or AMPH when these were microinjected into the NAcc. The two groups of rats were indistinguishable when tested following NAcc saline. These findings suggest that, as with AMPH, enhanced locomotion produced by NAcc mGluR activation is dependent on intact DA neurotransmission in this site.     

Enhanced frustrative nonreward effect following 6-hydroxydopamine lesions of the lateral septum in the rat.

Tested the effect of local injections of 6-hydroxydopamine (6-OHDA [3 μg/1 μl]) into the lateral septum in a paradigm that leads to an energizing behavior, through a possible frustrative effect, induced by partial or total omission of reward in hungry adult male Sprague-Dawley rats. Biochemical assays in the septum showed that 6-OHDA reduced endogenous dopamine and, to a lesser extent, noradrenaline concentrations and left intact noncatecholaminergic neurons such as serotoninergic terminals. In a double straight alley, Ss were exposed to an acquisition phase, a partially reinforced phase, and an extinction phase. Ss with lesions ran faster for food than controls in the partial reinforcement or extinction situation. The 2 groups also behaved similarly after the 1st 6 trials of the extinction phase. When Ss were tested in a leverpress conditioning task, lesioned and control Ss learned this task equally well, both with respect to the number of leverpresses and the time to obtain a fixed number of food pellets. In the 1st 5 min following the omission of reward, the number of leverpresses increased more for the lesioned Ss than for controls, a difference that disappeared in the later stages of the test. Results indicate that the loss of septal dopaminergic innervation produces behavioral effects similar to those obtained after total destruction of the same areas by electrocoagulation. (30 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Specificity of amphetamine induced release of norepinephrine and serotonin from rat brain in vitro

Incubation of normal rat cortical or brain stem tissue with 3H-NE or 3H-5-HT and subsequent exposure to amphetamine produced a concentration-related release of the transmitters from tissue stores into the incubation media. Although pretreatment with the catecholamine neurotoxin in 6-hydroxydopamine (6-OHDA) reduced the retention of 3H-NE in both of these tissues, the proportion of 3H-NE released by amphetamine was attenuated only in cortical tissue. Pretreatment with the serotonergic neurotoxin, 5,6-dihydroxytryptamine (5,6-DHT) had no effect on the retention or release of 3H-NE in cortical or brain stem tissue. Pretreatment with 5,6-DHT reduced the retention of 3H-5-HT in the cortex and brain stem, but the release of 3H-5-HT was significantly attenuated only in the latter tissue. 6-OHDA pretreatment increased the retention and proportion of cortical 3H-5-HT released by amphetamine but reduced the release of brain stem 3H-5-HT in the absence of an effect on retention. It appears that the in vitro release of 3H-NE from the cerebral cortex occurs primarily from catecholamine and not serotonergic neurons whereas the cortical release of 3H-5-HT is not an event specific to serotonergic nerve terminals. The release of 3H-5-HT from brain stem does not appear to be restricted to the serotonergic cell bodies since its release was attenuated by 5,6-DHT and 6-OHDA.     

Depletion of cortical norepinephrine in rats by 6-hydroxydopamine does not impair performance of a delayed-nonmatching-to-sample task.

Rats were trained on a spatial delayed-nonmatching-to-sample (DNMTS) task, matched for performance, and randomly assigned to treatment with dorsal noradrenergic bundle injections of either 6-hydroxydopamine, to deplete cortical norepinephrine (NE), or vehicle, to control for the effects of surgery. After recovery, there were no significant differences between the groups when retrained on the DNMTS task at retention intervals (RIs) from 0.1 to 15.0 sec. Furthermore, no differences were observed when rats were trained at a 6.0-sec RI filled with distracting stimuli or when dummy information runs were added to increase proactive interference. These results demonstrate that depletion of cortical NE cannot account for the DNMTS performance deficits observed in rats recovered from pyrithiamine-induced thiamine deficiency (R. L. Knoth and R. G. Mair, 1991; J. K. Robinson and Mair, 1992). (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Age-related reduction of reflex bradycardia in conscious rats by catecholaminergic nucleus tractus solitarius lesions

To determine whether catecholaminergic lesions in the nucleus tractus solitarius (NTS) have age-related baroreflex effects, we compared conscious 3-month- and 14-month-old rats pretreated with either 6-hydroxydopamine (6-OHDA) or vehicle injected into the NTS. Body weights fell immediately in both age groups, but after 2 weeks the weight loss persisted only in 14-month-old rats. Mean pressures and heart rates, though diminished after 3 days, were later elevated slightly in 3-month- but not in 14-month-old rats. Two weeks after 6-OHDA pretreatment, reflex tachycardia was reduced in both age groups, but reflex bradycardia was reduced only in 3-month-old and not in 14-month-old rats. Corresponding changes in vehicle-treated rats were not significant. Because 6-OHDA induced lesions in the NTS inhibited reflex bradycardia selectively at 3 but not at 14 months of age, our results suggest that catecholaminergic mechanisms in the NTS for regulating reflex bradycardia become impaired with age.     

In vitro denervation of the portal vein and caudal artery of the rat

The effects of 6-hydroxydopamine (6-OHDA) on the isolated portal vein and caudal artery of the rat were studied to investigate the possibility of producing in vitro adrenergic denervation of these blood vessels. Loss of nerve function was determined by field stimulation of the nerves, using short pulses, and by 3H-norepinephrine (NE) uptake. Addition of 6-OHDA produced contractions of both veins and arteries. Two hours after treatment with 6-OHDA, the contractile responses of the caudal arteries and portal veins to field stimulation were reduced to undetectable levels. At this point, the vessels were unable to take up 3H-NE and incubation of the preparations with l-NE failed to restore the contractile responses to nerve stimulation. Prejunctional supersensitivity to l-NE was observed in the portal vein after 6-OHDA but hot in helically cut strips of caudal artery. Prejunctional supersensitivity of the caudal artery to NE was seen, however, if the vessel geometry was kept intact, suggesting that the uptake mechanism for catecholamines only plays a major role in the termination of action of exgenous NE when norepinephrine is applied through the nerve plexus. We conclude that in vitro treatment with 6-OHDA rapidly produces functional adrenergic denervation of both portal vein and caudal artery of the rat and provides an accurate assessment of the importance of the neuronal uptake mechanism to NE sensitivity.     

Neonatal hemidecortication or frontal cortex ablation produces similar behavioral sparing but opposite effects on morphogenesis of remaining cortex.

Made behavioral comparisons between Long-Evans rats with complete removal of the neocortex of one hemisphere (hemidecorticate) or of the cortex anterior to bregma in both hemispheres (frontal cortex) in adulthood and rats with similar removals at 7 days of age. Neonatal ablation of the frontal cortex produced partial sparing of performance on the Morris water task and reduced the thickness of the remaining neocortex. Neonatal hemidecortication produced similar sparing of function on the water task but increased the thickness of the contralateral neocortex. Results are consistent with hemispherectomy studies done with children and imply that behavioral sparing following neonatal cortical lesions is independent of the gross morphogenesis of the remaining neocortex. (16 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)