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PubMed2001

How do animals actually solve the T maze?

Rats were trained on a reinforced, delayed alternation T-maze task in the presence (cue group) or absence (no-cue group) of salient extramaze landmarks. A surprising finding was that the acquisition and memory performance of the 2 groups did not differ. Manipulations of the extramaze landmarks for the cue group suggested that, although landmarks were used to guide behavior, other sources of information were also used normally. The no-cue group was able to perform the task at above-chance levels even when extramaze, intramaze, and inertial sources of orientation were manipulated. These results suggest that memory performance on the T maze does not rely exclusively on the processing of allocentric spatial relationships in the maze environment.

Animals↗
PubMed1996

Genetic variation in the morphology of the septo-hippocampal cholinergic and GABAergic system in mice. I. Cholinergic and GABAergic markers.

In the present study, variations of cholinergic and GABAergic markers in the medial septum/vertical limb of the diagonal band of Broca (MS/vDB) and the hippocampus of eight different inbred mouse strains were investigated. By means of immunocytochemistry against the acetylcholine-synthesizing enzyme choline acetyltransferase (ChAT), the cholinergic neurons were visualized and the number of ChAT-positive neuronal profiles in the MS/vDB was counted. Cholinergic and GABAergic septo-hippocampal projection neurons were detected with a combined retrograde tracing and immunocytochemical approach. In order to quantify the cholinergic innervation of various hippocampal sub-regions, we estimated the density of acetylcholinesterase (AChE)-containing fibers as visualized by AChE histochemistry. Additionally, the densities of muscarinic receptors (mainly the subtypes M1 and M2) in different hippocampal areas of seven inbred strains were measured by means of quantitative receptor autoradiography. We found significant strain differences for the number of ChAT-positive neurons in the MS/vDB; in the numbers of cholinergic septo-hippocampal projection neurons; in the density of cholinergic fibers in hippocampal subfields CA3c, CA1, and in the dentate gyrus; and in the density of muscarinic receptors in the hippocampus. In contrast the GABAergic component of the septo-hippocampal projection did not differ between the strains investigated. The number of ChAT-reactive neurons in the MS/vDB was not correlated with either hippocampal cholinergic markers. This might be attributed to different collateralization of cholinergic neurons or to different projections of these neurons to other brain regions. These results show a strong hereditary variability within the septo-hippocampal cholinergic system in mice. In view of the role of the cholinergic system in learning and memory processes, strain differences in cholinergic markers might be helpful in explaining behavioral variation.

Animals↗
PubMed2003

Dietary fatty acids alter blood pressure, behavior and brain membrane composition of hypertensive rats.

The beneficial effect of dietary n-3 polyunsaturated fatty acids (PUFAs) on developing hypertension has been repeatedly demonstrated. However, related changes in brain membrane composition and its cognitive correlates have remained unclear. Our study aimed at a comprehensive analysis of behavior and cerebral fatty acid concentration in hypertension after long-term PUFA-rich dietary treatment. Hypertensive and normotensive rats were provided a placebo, or one of two PUFA-enriched diets with a reduced (n-6)/(n-3) ratio for 75 weeks. Exploratory behavior and spatial learning capacity were tested. Systolic blood pressure (BP) was repeatedly measured. Finally, brain fatty acid composition was analyzed by gas chromatography. Hypertensive rats exhibited more active exploration but impaired spatial learning compared to normotensives. Both diets reduced BP, increased PUFA and monounsaturated fatty acid (MUFA) concentration, and reduced saturated fatty acid content in brain. The level of cerebral PUFAs and MUFAs was lower in hypertensive than in normotensive rats. Furthermore, BP positively, while spatial learning negatively correlated with cerebral (n-6)/(n-3) PUFA ratio. We concluded that regular n-3 PUFA consumption could prevent the development of hypertension, but reached only a very delicate improvement in spatial learning. Furthermore, we consider a potential role of metabolically generated MUFAs in the beneficial effects of PUFA supplementation.

Animals↗
PubMed2005

Effects of prenatal methylazoxymethanol acetate (MAM) treatment in rats on water maze performance.

Prenatal methylazoxymethanol acetate (MAM) treatment has been shown to induce morphological abnormalities in cortical areas of the offspring. Based on the neuroanatomical and behavioural abnormalities, this treatment has been suggested as a useful animal model for schizophrenia. In a previous study (Jongen-Relo AL, Leng A, Luber M, Pothuizen HHJ, Weber L, Feldon J. The prenatal methylazoxymethanol acetate treatment: a neurodevelopmental animal model for schizophrenia? Behav Brain Res 2004;149:159-81) we have studied MAM-treated animals in a series of behavioural tests related to schizophrenia, such as latent inhibition and pre-pulse inhibition of the acoustic startle response to establish the validity of prenatal MAM treatment (20mg/kg i.p. on gestational days 9-15; MAM 9-MAM 15). We found that, apart from a marginal effect of increased activity in the open field, the MAM treatment on gestational day 15 was behaviourally ineffective. Here, we extended our previous study to a water maze experiment conducted in the same batch of animals as presented previously (MAM 12-MAM 15). MAM-treated animals showed similar water maze performance compared with control animals during the acquisition phase and the probe tests. However, during the reversal phase, MAM 15 animals showed impaired acquisition of the new platform location. This might indicate some cognitive deficits in MAM 15 animals in terms of working memory or behavioural flexibility. However, in combination with the lack of behavioural abnormalities of MAM 12-MAM 15 animals in several other tests related to schizophrenia in the previously reported study, the use of MAM treatment (MAM 12-MAM 15) as a valid model for schizophrenia still remains debatable.

Analysis of Variance↗
PubMed2004

Residual oculomotor and exploratory deficits in patients with recovered hemineglect.

Several studies on hemineglect have reported that patients recover remarkably well when assessed with neuropsychological screening tests, however, they show deficits on novel or complex tasks. We investigated whether such deficits can be revealed with eye movement analysis, applying two basic oculomotor tasks as well as two exploratory tasks. Eye movements were recorded in eight hemineglect patients at least eleven months after right-hemisphere brain damage had occurred. Sixteen healthy volunteers participated in the control group. Regarding the basic oculomotor tasks, only the overlap task revealed residual deficits in patients, suggesting that a directional deficit in disengaging attention persisted during recovery. Further residual deficits were evident in the exploratory tasks. When everyday scenes were explored, patients showed a bias in early orienting towards the ipsilateral hemispace. In a search task, they demonstrated the same orienting bias as well as a non-directional deficit concerning search times. Moreover, patients preferentially fixated in the contralateral hemispace, but did not benefit from this asymmetry in terms of search times, i.e. they did not detect contralateral targets faster than ipsilateral ones. This suggests a dissociation between oculomotor processes and attentional ones. In conclusion, we have identified behavioural aspects that seem to recover slower than others. A disengagement deficit and biases in early orienting have been the most pronounced residual oculomotor deficits.

Adult↗
PubMed2003

Intrahippocampal infusion of a cyclooxygenase-2 inhibitor attenuates memory acquisition in rats.

Cyclooxygenase-2 (COX-2) inhibitors have been shown to block memory retention in rodents following Morris water maze training and in chicks following a passive avoidance task. However, the role of COX-2 in acquisition has not been analyzed. We show that pre-training intrahippocampal infusion of a COX-2 specific inhibitor (celecoxib) attenuated water maze acquisition. These findings, along with previously published reports, implicate COX-2 activity in both memory acquisition and retention.

Animals↗
PubMed2000

Ameliorative effects of tamolarizine on place learning impairment induced by transient forebrain ischemia in rats.

In the present study we investigated the effect of (+/-)-1-(3, 4-dimethoxyphenyl)-2-(4-diphenylmethylpiperazinyl) ethanol dihydrochloride (tamolarizine), a calcium entry blocker, on place learning impairment in rats with damage selective to the hippocampal CA1 subfield induced by transient forebrain ischemia. Tamolarizine was administered (40 mg/kg) immediately after 15-min brain ischemia. Place learning was tested in a task in which the rat was required to alternatively visit two places located diametrically opposite each other in an open field. The ischemia+saline group showed severe learning impairment in this task; their performance level was significantly inferior to that of the sham-operated group through the test period (30 days). Although the ischemia+tamolarizine group showed slight impairment of place learning during the course of this test, they later reached almost the same performance level as the sham-operated group. Selective neuronal loss in the CA1 subfield was much less in the ischemia+tamolarizine group than in the ischemia+saline group. These results indicate that tamolarizine treatment protects the hippocampus from ischemic brain damage and ameliorates place learning impairment.

Animals↗
PubMed1973

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Age Factors↗
PubMed2002

Rewarding effects of the cholinergic agents carbachol and neostigmine in the posterior ventral tegmental area.

Rats learned to lever-press for microinjections of the cholinergic agonist carbachol (30-500 pmol per infusion) or the acetylcholinesterase inhibitor neostigmine (7.5-75 pmol per infusion) into the posterior ventral tegmental area (VTA) of the brain. Intracranial carbachol self-administration was site-specific. Carbachol was not reliably self-administered into a site just dorsal to the VTA or into the adjacent substantia nigra and was self-administered only weakly into the adjacent anterior VTA or interpeduncular nucleus. Carbachol produced conditioned place preferences when injected into the posterior but not into the anterior VTA or sites dorsal to the posterior VTA. Rats self-administered carbachol less when it was co-infused with the muscarinic cholinergic receptor antagonist scopolamine or the nicotinic cholinergic receptor antagonist dihydro-beta-erythroidine, and also when the rats were pretreated with the D1 dopamine antagonist SCH 23390. These findings implicate both nicotinic and muscarinic cholinergic neurotransmission in ventral tegmental reward function and suggest special involvement of the posterior portion of the VTA in cholinergic reward function.

Animals↗
PubMed2003

Kappa opioid receptor antagonism and prodynorphin gene disruption block stress-induced behavioral responses.

Previous studies have demonstrated that stress may increase prodynorphin gene expression, and kappa opioid agonists suppress drug reward. Therefore, we tested the hypothesis that stress-induced release of endogenous dynorphin may mediate behavioral responses to stress and oppose the rewarding effects of cocaine. C57Bl/6 mice subjected to repeated forced swim testing (FST) using a modified Porsolt procedure at 30 degrees C showed a characteristic stress-induced immobility response and a stress-induced analgesia observed with a tail withdrawal latency assay. Pretreatment with the kappa opioid receptor antagonist nor-binaltorphimine (nor-BNI; 10 mg/kg, i.p.) blocked the stress-induced analgesia and significantly reduced the stress-induced immobility. The nor-BNI sensitivity of the behavioral responses suggests an activation of the kappa opioid receptor by a stress-induced release of dynorphin peptides. Supporting this hypothesis, transgenic mice possessing a disrupted prodynorphin gene showed no increase in immobility or stress-induced analgesia after exposure to repeated FST. Because both stress and the kappa opioid system can modulate the response to drugs of abuse, we tested the effects of forced swim stress on cocaine-conditioned place preference (CPP). FST-exposed mice conditioned with cocaine (15 mg/kg, s.c.) showed significant potentiation of place preference for the drug-paired chamber over the responses of unstressed mice. Surprisingly, nor-BNI pretreatment blocked stress-induced potentiation of cocaine CPP. Consistent with this result, mice lacking the prodynorphin gene did not show a stress-induced potentiation of cocaine CPP, whereas wild-type littermates did. The findings suggest that chronic swim stress may activate the kappa opioid system to produce analgesia, immobility, and potentiation of the acute rewarding properties of cocaine in C57Bl/6 mice.

Analgesia↗
PubMed1993

An ACTH/MSH(4-9) analog counteracts the behavioral effects of a mineralocorticoid receptor antagonist.

The ACTH/MSH(4-9) analog Org2766 has been demonstrated to counteract age-related behavioral and morphological parameters especially those related to hippocampal functioning. Hippocampal mineralocorticoid receptors (MRs) are known to decline in the senescent rat. This decrease can be also counteracted by a chronic treatment with an ACTH(4-9) analog. The apparent effect of the peptide on hippocampal functioning prompted us to study a possible interaction between ACTH and MRs at a behavioral level. A chronic treatment with the ACTH(4-9) analog prevented the behavioral alteration induced by a specific MR antagonist (RU28318; 100 ng/microliters, ICV) in the Morris water maze and a step-through avoidance task. A possible role for neuronal excitation, involving MR activation, in peptide-facilitated behavioral recovery as seen in lesion studies and aging is discussed.

Adrenocorticotropic Hormone↗
PubMed2003

Long-term effects of clomethiazole in a model of global ischemia.

The failure of neuroprotective drugs in clinical trials has raised questions about the predictive value of animal models. To address this issue we reexamined the efficacy of clomethiazole using functional and histological outcome measures in combination with long-term survival times. Gerbils were exposed to 5 min of global ischemia and received 400 mg/ml clomethiazole (via osmotic minipump) plus a bolus injection (60 mg/kg) 30 min after ischemia. Brain temperature was maintained at approximately 36.5 degrees C during ischemia and for the first 30 min after ischemia, and was monitored in all groups for 24 h. Subgroups of clomethiazole-treated gerbils had their temperatures regulated in the normothermic range while in other animals temperature was not controlled. Open-field habituation tests were conducted 5, 10, 30, and 60 days after occlusion. CA1 cell counts and CA1 slice recordings were done at the conclusion of behavioral testing. Clomethiazole significantly attenuated CA1 cell loss at 10-, 30-, and 60-day survival. A modest reduction in habituation deficits was evident only on Day 10 (P < 0.05). Similarly, field potential amplitude was not maintained in the rostral CA1 region. Clomethiazole produced mild hypothermia that developed over several hours. Based on short-term CA1 cell counts, clomethiazole provided significant histological protection with limited functional preservation. Neuroprotection disappeared when longer survival times (60 day) were employed and temperature confounds eliminated. These data demonstrate the necessity of utilizing more clinically relevant survival times and carefully monitoring/regulating postischemic temperature when assessing potential neuroprotective compounds.

Animals↗
PubMed2002

Rewarding and psychomotor stimulant effects of endomorphin-1: anteroposterior differences within the ventral tegmental area and lack of effect in nucleus accumbens.

Endomorphin-1 (EM-1) is a recently isolated endogenous peptide having potent analgesic activity and high affinity and selectivity for the mu-opioid receptor. The present study was designed to investigate the rewarding and psychomotor stimulant effects of EM-1 in specific brain regions. We found that rats would learn without priming or response shaping to lever-press for microinjections of EM-1 into the ventral tegmental area (VTA); responding was most vigorous for high-dose injections into the posterior VTA. Rats did not learn to lever-press for microinjections of EM-1 into the nucleus accumbens (NAS) or regions just dorsal to the VTA. Lever-pressing for EM-1 in the VTA was extinguished when vehicle was substituted for the peptide and was reinstated when EM-1 reinforcement was re-established. Conditioned place preference was established by EM-1 injections into the posterior but not the anterior VTA or the NAS. Injection of EM-1 (0.1-1.0 nmol) into the posterior VTA induced robust increases in locomotor activity, whereas injections into the anterior VTA had very weak locomotor-stimulating effects. When injected into the NAS, EM-1 (0.1-10.0 nmol) did not affect locomotor activity. The present findings implicate the posterior VTA as a highly specific and sensitive site for opioid reward and suggest a role for EM-1-containing projections to the posterior VTA in the rewarding effects of other reinforcers.

Animals↗
PubMed1998

Kinematics of goal-directed arm movements in neglect: control of hand velocity.

Do patients with unilateral neglect exhibit direction-specific deficits in the control of movement velocity when performing goal-directed arm movements? Five patients with left-sided neglect performed unrestrained three-dimensional pointing movements to visual targets presented at body midline, the left and right hemispace. A group of healthy adults and a group of patients with right-hemispheric brain damage but no neglect served as controls. Pointing was performed under normal room light or in darkness. Time-position data of the hand were recorded with an opto-electronic camera system. We found that compared to healthy controls, movement times were longer in both patient groups due to prolonged acceleration and deceleration phases. Tangential peak hand velocity was lower in both patient groups, but not significantly different from controls. Single peak, bell-shaped velocity profiles of the hand were preserved in all right hemispheric patients and in three out of five neglect patients. Most important, the velocity profiles of neglect patients to leftward targets did not differ significantly from those to targets in the right hemispace. In summary, we found evidence for general bradykinesia in neglect patients, but not for a direction-specific deficit in the control of hand velocity. We conclude that visual neglect induces characteristic changes in exploratory behavior, but not in the kinematics of goal-directed movements to objects in peripersonal space.

Adolescent↗
PubMed1998

Histological and behavioral protection by (-)-nicotine against quinolinic acid-induced neurodegeneration in the hippocampus.

Injections of quinolinic acid (60, 180, and 600 nmol) in the dorsal hippocampus induced significant neurotoxicity that was evident 1 day after the injection. By day 3, pyramidal as well as granular cells were affected even at the lowest dose of quinolinic acid, an effect that persisted up to 20 days. Consistent with the histological findings, animals with bilateral injections in the dorsal hippocampus were cognitively impaired during acquisition and retention of spatial information in the water maze. A subacute treatment with (-)-nicotine (62 micromol/kg/day) delivered by subcutaneous minipumps prevented the histological and cognitive deficits induced by the bilateral quinolinic acid (60 nmol) injections. These data indicate that quinolinic acid can induce degeneration of both pyramidal as well as granule cells in the hippocampus, leading to cognitive impairments in the rat, and that activation of neuronal nicotinic acetylcholine receptors can prevent the neurodegenerative process induced by quinolinic acid.

Animals↗
PubMedDate not supplied

Potentiation of ischemia-related behavioral alterations by electro-acupuncture in gerbils.

Gerbils subjected to global ischemia or sham-ischemia received electro-acupuncture (EA) or sham EA at points 26 Du (Renzhong) and 8 Du (Junsuo). All animals were then tested for motor activity in an open field, and for spontaneous alternation in a T maze. Results show that EA alone did not affect any behavioral parameter. Ischemia alone increased motor activity without significantly interfering with spontaneous alternation. EA in ischemic gerbils potentiated the increase of motor activity and elicited a decrease in spontaneous alternation. Thus, our data show an interaction between global ischemia and EA applied at specific acupoints which, however, consists of a potentiation rather than an alleviation of the behavioral alterations consecutive to the ischemic insult.

Analysis of Variance↗