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Biomedical subjects

G Jonsson

Publications and source records attributed to G Jonsson.

At least 19 recordsLinked to original sources
PubMed1991

Production and characterization of monoclonal antibodies to Vibrio cholerae soluble haemagglutinin.

Monoclonal antibodies (MAbs) against a protease of Vibrio cholerae, the soluble haemagglutinin (sHA), have been prepared and characterized with regard to their ability to inhibit different biological properties of sHA and to protect against experimental V. cholerae infection. Four fusion experiments yielded two specific immunoglobulin G1 MAbs that reacted with sHA produced by different V. cholerae O1 and non-O1 strains but that differed in their antigen-binding capacity. Both MAbs were capable of inhibiting the haemagglutinating and protease activities of sHA as well as its ability to nick the enterotoxin A subunit, but neither of them had any effect on the mucinase activity of sHA. One of the MAbs significantly inhibited experimental cholera infection induced by sHA-producing V. cholerae O1 in rabbit small intestine.

Animals↗
PubMed1990

GM1 ganglioside reduces edema and monoaminergic neuronal changes following experimental focal ischemia in rat brain.

Seventy-two hours following a middle cerebral artery occlusion, the associated increase in water content on the ischemic side was significantly reduced by the exogenous administration of monosialoganglioside GM1 (30 mg/kg, i.p.). The levels of dopamine and serotonin on the ischemic side were approximately 50% and 80% of those on the contralateral non-ischemic side, respectively. Treatment with GM1 (5 times during the first 48 h after occlusion) produced a significant reduction in the levels of dopamine and serotonin loss. The present findings are compatible with the observed protective action of the exogenously administered GM1 following ischemic brain injury.

Animals↗
PubMed1990

Structural and neurochemical effects in mouse cerebellum following neonatal methylazoxymethanol and 6-hydroxydopamine treatment.

The effects of neonatal treatment with the antimitotic agent methylazoxymethanol and the catecholamine neurotoxin 6-hydroxydopamine on cerebellar morphology and monoamine innervation in the N.M.R.I. mouse has been studied. Methylazoxymethanol (25 mg/kg s.c.) treatment induced a cerebellar weight reduction of 40% as observed in the adult stage, while other CNS regions analysed were unaffected. An obvious atrophy of the cerebellar cortex was found, with an irregular distribution of the Purkinje cells, while Bergmann glia fibers deviated from their normal radial configuration and showed a tendency to form clusters. A 65% increase of tyrosine hydroxylase immunoreactive fiber density was found in the cerebellar cortex and 3H-5-hydroxytryptamine in vitro synaptosomal uptake was increased by 55%. Noradrenaline and 5-hydroxytryptamine concentrations in the cerebellum increased by 50 and 30%, respectively, whereas the total content of both neurotransmitters in cerebellum was approximately unchanged after methylazoxymethanol treatment. A significant reduction in total cerebellar in vitro binding of 3H-WB-4101 and 3H-dihydroalprenolol was also found, indicating compensatory receptor alterations following methylazoxymethanol treatment. The effect of combined treatment of methylazoxymethanol and the neurotoxin 6-hydroxydopamine (50 mg/kg s.c., day 1) showed a very pronounced reduction of noradrenaline concentration in cortex cerebri, while the noradrenaline concentration in cerebellum was increased by 185% and the tyrosine hydroxylase immunoreactive fiber density by 125%, indicating an additional relative hyperinnervation of cerebellar noradrenaline fiber due to a "pruning effect" of the 6-hydroxydopamine treatment. The results imply a relatively rigid development of terminal arborization of central nervous system monoamine neurons, relatively independent of neuronal and glial arrangement in the target area.

Animals↗
PubMed1990

MPTP-induced hypoactivity in mice: reversal by L-dopa.

Three experiments were performed to study the subchronic effects of treatment with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 2 x 40 mg/kg subcutaneously two weeks before testing) in C57 BL/6 mice upon spontaneous motor activity and the reversal of the long-term behavioural changes by acute treatment with L-Dopa. Mice treated with MPTP showed a drastic reduction of striatal dopamine levels (-88%) associated with reductions of all three parameters of spontaneous motor activity, i.e. locomotion, rearing and total activity, during both the initial, exploratory, stage (first 90 min), and later stages of the 3- or 4-hr test periods. L-Dopa (5-80 mg/kg subcutaneously) injected 60 min. after the start of testing dose-dependently improved all three parameters studied in MPTP treated mice with 10 mg/kg being the lowest dose causing a significant effect, while doses above 20 mg/kg caused hyperactivity. During the initial period, rearing activity in MPTP mice was to a variable degree suppressed by the L-Dopa treatment (20-80 mg/kg); these reductions were followed by enormous increases in motor activity by the 40 mg/kg (locomotion) and 80 mg/kg (total activity) L-Dopa groups. Both the degree and duration of the L-Dopa-induced hypoactivity for locomotor behaviour increased dose-dependently in control mice. No suppressive effects of L-Dopa were obtained for total activity in control mice, although the 80 mg/kg L-Dopa doses evoked hyperactivity for up to 90 min. following treatment for both locomotion and total activity.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1989

Selective lesion of central dopamine or noradrenaline neuron systems in the neonatal rat: motor behavior and monoamine alterations at adult stage.

Different parameters of motor behavior (locomotion, rearing and total activity counts) were studied in the adult rat following neonatal intracisternal 6-hydroxydopamine (6-OHDA, 50 micrograms) treatment combined with noradrenaline (NA) uptake blocker (desipramine) or dopamine (DA) uptake blockers (amfolenic acid or GBR 12909) to obtain selective DA or NA lesions respectively. At 61-65 days of age, selective DA-lesioned animals showed an initial decrease in spontaneous motor behavior at test days 1 and/or 2, while at test days 4 and 5 hyperactivity was observed. However, following amfolenic acid or GBR 12909 pretreatment leading to a selective NA lesion, no difference in spontaneous motor behavior was seen on any of the 5 test days. Determination of regional brain levels of NA and DA confirmed the type of lesion predicted from the various pretreatments with selective uptake blockers. These data suggest that changes in motor behavior in the adult rats, following neonatal 6-OHDA treatment, are specifically related to a DA-denervation, whereas an NA lesion does not seem to influence the spontaneous motor behavior. However, following the selective DA lesion, significant increases of serotonin levels in striatum and cerebellum were observed, while following selective NA lesions an increase of cerebellar NA levels was found concomitant with drastic reductions of NA levels in frontal cortex and spinal cord.

Aging↗
PubMed1989

Saccadic reaction times, eye-arm coordination and spontaneous eye movements in normal and MPTP-treated monkeys.

The oculomotor performance of monkeys was investigated before and after destruction of nigrostriatal dopamine neurons by MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine). Stimulus-triggered saccades and their relationships to arm movements were measured in a reaction time task. Spontaneous eye movements were recorded while monkeys sat in a primate chair and looked around the laboratory without performing any task. In the reaction time task, saccades and arm movements were commonly triggered by the rapid, visible and audible opening of a small food-containing box which was located at a constant position in front of the animal at eye level. Median saccadic latencies ranged from 68 to 118 ms in intact animals. Saccades were followed by onset of electromyographic (EMG) activity in the extensor digitorum communis and the biceps brachii, the prime mover muscles for the following arm reaching movement. Latencies of stimulus-triggered saccades showed an absence of linear relationship to EMG or arm movement reaction time in intact animals (correlation coefficients of 0.15-0.56). This suggests that eye and arm movements were initiated independently from each other in this experimental situation. Treatment with MPTP resulted in 98-99.5% loss of striatal dopamine in both monkeys. This induced a 29-93% increase in saccadic latency in the reaction time task. The sequential occurrence of saccade, EMG activity and arm movement in each trial was preserved, although intervals between onset of saccades and onsets of EMGs and arm movements were prolonged by 53-173% and 33-679% respectively. Onsets of individual saccades remained uncorrelated with onsets of EMG activity or arm movement. Spontaneous eye movements were strongly reduced in frequency and amplitude after MPTP. Administration of the dopamine precursor L-Dopa increased spontaneous eye movements for less than two hours. The severe deficits in stimulus-triggered and spontaneous saccadic eye movements are oculomotor components of hypokinesia arising after MPTP-induced lesions of the nigrostriatal dopamine system in primates. The data are further evidence for a role of midbrain dopamine neurons in behavioral responsiveness and spontaneous activity.

Animals↗
PubMed1989

Immunohistochemical and behavioral analysis of spinal lesions induced by a substance P antagonist and protection by thyrotropin releasing hormone.

Using behavioural, morphological and immunohistochemical analysis, the effect of intrathecal administration of a substance P antagonist, Spantide [D-Arg1, D-Trp7,9, Leu11)-SP), was studied. Antisera raised against markers for motoneurons, local spinal neurons, descending bulbospinal systems and primary afferents were used. The effect of some drugs, including thyrotropin releasing hormone (TRH), on Spantide-induced effects were also analyzed. After injection of 2 micrograms of Spantide at the lumbar level, a marked necrosis of the spinal cord was observed extending for about 5-6 segments, affecting mostly the ventral horns. Thus, calcitonin gene related peptide (CGRP)-like immunoreactivity (LI) in motoneurons completely disappeared and no motoneurons could be seen in cresyl violet-stained sections. The first changes were observed 6 h after Spantide injection and at 24 h a complete necrosis was seen. Marked reductions in the number of 5-hydroxytryptamine (5-HT)- and substance P-positive fibers were also observed. The effects were less dramatic in the dorsal horns, but at the site of maximal effects there was a disturbance also of CGRP-, substance P-, and neuropeptide tyrosine (NPY)-positive fibers in the superficial layers of the dorsal horn. These effects could be completely counteracted by multiple intravenous injections of TRH as well as with 5-methoxy-N, N-dimethyltryptamine (5-MeDMT), a 5-HT agonist. The behavioural analysis showed parallel changes, with permanent motor impairment after Spantide-treatment and complete absence of these symptoms when TRH or 5-MeDMT was given in addition. Finally, the effect of Spantide on 5-HT, noradrenaline, substance P and CGRP levels was measured biochemically. The present results are discussed in the light of recent findings that Spantide can cause a dramatic reduction in spinal blood flow.

Animals↗
PubMed1989

Effects of d-amphetamine and methylphenidate on hyperactivity produced by neonatal 6-hydroxydopamine treatment.

Neonatal intracisternal administration of 6-hydroxydopamine (6-OHDA, 50 micrograms on day 1 after birth) caused a marked hyperactivity when the rats were tested as adults. These rats also showed severe DA depletions in striatum and nucleus accumbens. Pretreatment with the noradrenaline (NA) uptake inhibitor desipramine provided protection against NA depletion in frontal cortex and nucleus accumbens. Pretreatment with DA uptake inhibitors, amfolenic acid or GBR 12909, before 6-OHDA, provided full protection against DA depletion but produced marked NA depletion in frontal cortex. These rats did not demonstrate any degree of hyperactivity. Low doses of d-amphetamine (0.25 mg/kg SC) or methylphenidate (1 mg/kg SC) reversed the hyperactivity in DA-depleted rats but increased motor activity in vehicle-treated and NA-depleted rats. Higher doses of d-amphetamine (1 mg/kg) or methylphenidate (4 mg/kg) produced potentiated levels of locomotion but attenuated levels of rearing in DA-depleted animals. The results further suggest the utility of the neonatal DA lesion in rats as a potential animal model for derivation of therapeutic agents that may be efficacious in the treatment of the hyperkinetic syndrome.

Animals↗
PubMed1989

Capsaicin treatment to developing rats induces increase of noradrenaline levels in the iris without affecting the adrenergic terminal density.

The effects of administration of capsaicin to developing and adult Sprague-Dawley rats on substance P-containing primary afferent and peripheral adrenergic nerves were analysed by histochemical and neurochemical techniques. In control rats a relatively dense innervation with substance P-immunoreactive fibers was seen in the iris, while 10 weeks after a single neonatal injection of capsaicin (50 mg/kg s.c.) a moderate loss of substance P-immunoreactive nerve fibers was observed. The substance P level was decreased by 60%, while the noradrenaline level, 3H-noradrenaline uptake in vitro and the noradrenaline nerve density were unaltered. Repeated injections of capsaicin (2 x 50 mg/kg, 3 x 20 mg/kg s.c.) for 5 weeks to developing rats led to a very marked decrease of the substance P level and an almost complete disappearance of substance P-immunoreactive fibers in the iris, when analysed at 10 weeks of age. The noradrenaline level in the iris was significantly increased (+42%), while no significant changes in noradrenaline level were observed in heart auricula or superior cervical ganglion. The uptake in vitro of 3H-noradrenaline in irides and heart auriculae, as well as the noradrenaline terminal density in the dilator plate and surrounding blood vessels in the iris, were unaffected by repeated capsaicin treatment to developing rats. Capsaicin administration to adult rats (50 mg/kg s.c.), leading to a profound decrease in substance P, did not affect the noradrenaline levels at 24 hr after the injections. The results indicate that an extensive sensory denervation with capsaicin during development can induce an increase of noradrenaline levels in sympathetic nerve terminals in a target area (rat iris) with a rich SP-ergic sensory innervation, although the sympathetic terminal density is not influenced. Furthermore the increase in noradrenaline seems to require an extensive loss of SP-immunoreactive fibers and not solely a reduction of SP levels.

Adrenergic Fibers↗
PubMed1989

Synthesis and release of dopamine in rat brain: comparison between substantia nigra pars compacts, pars reticulata, and striatum.

Dopamine (DA) is synthesized and released not only from the terminals of the nigrostriatal dopaminergic neuronal pathway, but also from the dendrites in the substantia nigra. We have investigated the regulation of the DA turnover, the DA synthesis rate, and the DA release in the substantia nigra pars compacts (SNpc) and pars reticulata (SNpr) in vivo. As a measure of DA turnover, we have assessed the concentrations of 3,4-dihydroxyphenylacetic acid and homovanillic acid. As a measure of the DA synthesis rate, we have determined the 3,4-dihydroxyphenylalanine accumulation after inhibition of aromatic L-amino acid decarboxylase by 3-hydroxybenzylhydrazine. As a measure of DA release, we have investigated the disappearance rate of DA after inhibition of its synthesis by alpha-methyl-p-tyrosine and the 3-methoxytyramine accumulation following monoamine oxidase inhibition by pargyline. Both the DA turnover and the DA synthesis rate increased following treatment with the DA receptor antagonist haloperidol and decreased following treatment with the DA receptor agonist apomorphine in the SNpc and in the SNpr, but the effects of the drugs were less pronounced than in the striatum. gamma-Butyrolactone treatment, which suppresses the firing of the dopaminergic neurons, increased the DA synthesis rate in the striatum (165%), but had no such effect in the SNpc or SNpr. Haloperidol, apomorphine, and gamma-butyrolactone increased, decreased, and abolished, respectively, the DA release in the striatum, but the drugs had no or only slight effects on the alpha-methyl-p-tyrosine-induced DA disappearance and on the pargyline-induced 3-methoxytyramine accumulation in the SNpc or SNpr. Taken together, these results indicate that the DA synthesis rate, but not the DA release, are influenced by DA receptor activity and neuronal firing in the SNpc and SNpr. This is in contrast to the situation in the striatum, where both the DA synthesis rate and the DA release are under such control.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1989

Adaptive changes in alpha-2 adrenoceptor mediated responses: analgesia, hypothermia and hypoactivity.

The acute effects of the alpha-2 adrenoceptor agonists, clonidine and guanfacine, upon antinociception, hypothermia and motor activity were compared under conditions of receptor antagonism, denervation, and chronic administration of a tricyclic antidepressant compound. The analgesic actions of clonidine and guanfacine were antagonised by idazoxan, an alpha-2 receptor antagonist, but potentiated by pretreatment with the noradrenaline neurotoxin DSP4, and attenuated by chronic treatment with desipramine (DMI). Clonidine- and guanfacine-induced hypothermia was antagonised by idazoxan, potentiated by prior treatment with DSP4 and attenuated by chronic administration with DMI. Both clonidine and guanfacine produced decreases in motor activity that were attenuated by idazoxan but unaffected by prior DSP-4 treatment. Chronic DMI administration also attenuated clonidine-induced hypoactivity but potentiated guanfacine-induced hypoactivity. These diverse results describe both similar and differential adaptive mechanisms modulating the functional effect of alpha-2 receptor systems in the central nervous system.

Adaptation, Physiological↗
PubMed1989

Deficits in reaction times and movement times as correlates of hypokinesia in monkeys with MPTP-induced striatal dopamine depletion.

1. We quantitatively assessed deficits in the initiation and execution of arm movements occurring after destruction of nigrostriatal dopamine neurons by systemic administration of MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) (Sigma). Three monkeys performed a reaction time task in which they reached toward a single and constant target for food reward. 2. After administration of MPTP, all three monkeys showed hypokinesia necessitating dopamine precursor or receptor agonist treatment. The partial recovery of one animal from initial akinesia after 19 days permitted discontinuation of dopaminergic drug therapy, although marked hypokinesia remained present. The two other animals displayed additional, intermittent phases of rigidity and activation tremor and needed continuous dopaminergic drug therapy for most of the postlesion period. 3. Administration of MPTP significantly prolonged EMG reaction time in prime mover muscles and arm movement reaction time by 47-225% and 18-129%, respectively, on the six sides of the three animals, compared with control measurements before the lesion. EMG and arm movement reaction time increased over consecutive trials in most sessions comprising 110-130 movements, the first 20 movements showing almost normal values. The delay time between onsets of EMG and arm movement showed unsystematic changes. These deficits in movement initiation were observed both with and without dopamine precursor therapy. They lasted during the whole testing period of several months. 4. Linear correlations between arm movement onset and EMG onset in the two prime mover muscles, the extensor digitorum communis and the biceps, showed coefficients of mostly 0.7-0.9, both before and after MPTP. These data suggest that the temporal relationship between onsets of arm movement and EMG were not substantially affected by MPTP. 5. Arm movement time was divided into two phases. The duration of movement between the resting key and the target, a small food-containing box located ahead of the animal, was denoted as reaching movement time. The following hand manipulation inside the food box was measured as box movement time. After MPTP, both measures were significantly prolonged by 10-103% and 12-251%, respectively, on the six sides of the three monkeys. These deficits in movement execution were observed both with and without dopaminergic drug therapy and during the whole testing period. 6. Task performance after MPTP treatment was studied in one monkey in the absence of dopaminergic drug therapy. EMG and arm movement reaction times recovered partially over several weeks, while the prolongations in reaching and box movement times remained unchanged.(ABSTRACT TRUNCATED AT 400 WORDS)

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1989

Food and nutrient intakes in Swedish diabetic children.

Food and energy intakes in diabetic children, 7-9 and 12-14 years of age, were studied by the 7-d record method. The mean duration of diabetes in the younger group was 3.0 years and in the older group 4.2. The children had 3 main meals and 3.4 light meals daily. The median daily number of sandwiches was 7, often offered as snacks. All children used a low-fat margarine, low-fat cheese and low-fat milk. Sweets and diabetic food were seldom used. Of the energy intake protein contributed 18 per cent, fat 32 per cent and carbohydrates 50 per cent, including sucrose 2 per cent. Mean daily intake of fibre was 20 g. Compared to healthy children of the same age and from the same areas of Sweden the diabetics had a more regular meal pattern, their energy intakes did not differ, but the diet of diabetics was lower in fat and sucrose and higher in protein. The mean height, weight and BMI did not differ from healthy children.

Adolescent↗
PubMed1988

Intrathecal noradrenaline restores 5-methoxy-N,N-dimethyltryptamine induced antinociception abolished by intrathecal 6-hydroxydopamine.

Intrathecal administration of 6-hydroxydopamine (6-OHDA) abolished the antinociceptive effects of acute administration of 5-methoxy-N,N-dimethyltryptamine (5-MeODMT, 1 mg/kg, s.c.) in the hot-plate, tail-flick and shock titration tests of nociception. The antinociceptive effects of 5-MeODMT, abolished by the prior intrathecal 6-OHDA treatment, were restored by intrathecal administration (2 or 1 microgram) of noradrenaline (NA), immediately prior to 5-MeODMT, in all three tests of nociception. Biochemical analysis confirmed severe NA depletions (95 percent loss) in the lumbar and thoracic regions of the spinal and much lesser dopamine depletions (25-35 percent loss). Intrathecal 5,7-dihydroxytryptamine (5,7-DHT) attenuated 5-MeODMT induced antinociception in the tail-flick test and combined NA + 5-MeODMT induced antinociception in the hot-plate and tail-flick tests. Intrathecal administration of 5,7-DHT caused a severe depletion of 5-hydroxytryptamine in the lumbar region of the spinal cord. The present findings demonstrate further the modulatory role of NA upon serotonergic systems in nociception and indicate the necessity of NA availability for induction of 5-MeODMT analgesia.

5,7-Dihydroxytryptamine↗
PubMed1988

Exogenous GM1 ganglioside and thyrotropin-releasing hormone do not affect survival rate of spinal motorneurons and number of ventral root myelinated fibers following early postnatal sciatic nerve transection.

Treatment with gangliosides or thyrotropin-releasing hormone has been shown to stimulate structural and functional recovery that follows mechanical or chemical lesions in the nervous system. We studied the possible effects of the ganglioside GM1 and thyrotropin-releasing hormone on the survival rate of spinal motorneurons after sciatic nerve transection at the age of 1 week in the rat. GM1 (30 mg/kg body weight, i.p.) was administered 24 and 1 h before and once daily for 2 weeks after transection. TRH (2 mg/kg body weight, i.p.) was administered 1 h before, at 2, 16, and 24 h, and thereafter once daily for 7 days after transection. Nine weeks postlesion, the number of motorneuron profiles labeled by retrograde transport from the proximal stump of the sciatic nerve was counted and measured using a computerized image analysis system, and the number of myelinated axons in ventral roots L4 and L5 was estimated. Compared with controls, no significant effects of GM1 or hormone treatment were observed with regard to the number, diameter, and area of motorneuron profiles and the number of ventral root myelinated axons ipsilateral to sciatic nerve injury. The results may indicate principal differences between various lesions and/or metabolic reactions following a lesion of developing and adult neurons. The present lesion model with an intense axon reaction and extensive nerve cell death does not seem to respond to administration of exogenous GM1 or thyrotropin-releasing hormone.

Animals↗
PubMed1988

Acute electrophysiological and neurochemical effects of administration of MPTP in mice.

The changes occurring during the first few hours after subcutaneous administration of the catecholaminergic neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) were investigated. Injections of MPTP (30-60 mg/kg s.c.) reduced the impulse rate by 12-45% in all dopaminergic neurones tested in the pars compacta of the substantia nigra. Depressions were maximal at 11 min and remained present for more than 2 hr after injection. This effect was completely abolished by prior administration of the catecholamine uptake inhibitor, nomifensine (13-69 mg/kg s.c.), which prevents the toxic metabolite of MPTP 1-methyl-4-phenylpyridine (MPP+) from entering dopaminergic neurones. These results suggest an intraneuronal mechanism underlying the observed depressions in impulse rate. Levels of dopamine (DA) were decreased at 3 hr after administration of MPTP (50 mg/kg s.c.) by 60% and 54% in the striatum and substantia nigra, respectively. Pretreatment with nomifensine (25 mg/kg, intraperitoneally) prevented the decrease in DA only in the striatum. This suggests an acute DA-releasing effect of MPTP in the striatum, mediated by intracellular accumulation of MPP+, while not explaining the depression of activity of DA neurones occurring with a different time course.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1988

Neonatal 6-hydroxydopamine-induced dopamine depletions: motor activity and performance in maze learning.

Three experiments were performed to study the effect of dopamine (DA) depletions, induced by neonatal intracerebroventricular (ICV) treatment with 6-hydroxydopamine (6-OHDA), upon measures of spontaneous motor activity. Instrumental learning for food reward in an Olton radial arm maze and escape learning from a large, circular water maze were studied also. Motor activity was measured by direct observation of rats in a modified radial arm maze and by use of automated test cages equipped with photocell devices. 6-OHDA-treated rats demonstrated considerable and long-lasting locomotor (ambulation) activity and total activity increases. 6-OHDA-treated rats showed notably less rearing activity than the vehicle-treated rats during the initial 20 min of each 60-min test period. However, over the second half of these 60-min test periods, the 6-OHDA-treated rats demonstrated significantly more rearing activity than the vehicle-treated rats. In the acquisition of the running response, to obtain the 8 food pellets placed in each of the 8 arms of the radial arm maze, 6-OHDA rats showed a retarded acquisition, as measured by the latency and number of arms visited to acquire all eight pellets. 6-OHDA-treated rats failed completely to acquire the Morris-type swim maze task by which they were required to locate a platform just under the water surface in a circular water tank. The neurochemical assays indicated severe DA depletion in several forebrain regions. The present findings add to existing indications of the potential of this DA depletion condition as an animal model of the minimal brain dysfunction syndrome.

Animals↗