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At least 379 records · Page 21Linked to original sources
PubMed1997

Tail-flick test: II. The role of supraspinal systems and avoidance learning.

It is held that the tail-flick test of pain depends on a spinal reflex because a similar response is observed in spinally transected rats. But when subjects were manually held and a cool heat setting was used, supraspinal systems facilitated the response (Experiment 1). This effect did not depend on the rate at which the tail was heated (Experiment 2) but rather on the co-occurrence of visual, auditory, and tactile cues that predict impending pain (Experiments 3 and 4). Subjects rapidly learned to exhibit a tail movement during these co-occurring cues, and this avoidance response was instrumental in nature (Experiment 5). Optimal learning was observed when the visual signal was presented 8-12 s before a heat-elicited response is normally observed (Experiment 6), and a low dose of morphine inhibited the performance of the instrumental response (Experiment 7).

Acoustic Stimulation↗
PubMed1999

Adenosine-amino acid interactions in the chick brain: a role in passive avoidance learning.

The present work describes interactions between adenosine and the amino acids glutamate and GABA in slices of intermediate medial hyperstriatum ventrale (IMHV), an area of the chick brain known to be involved in learning and memory events associated with a one-trial passive avoidance task. In slices derived from the IMHV of untrained chicks, the A(1) receptor agonist N(6)-cyclohexyladenosine (CHA; 10 microM) specifically inhibited glutamate release. Conversely, cyclopentyltheophylline (CPT; 100 microM an A(1) antagonist) increased glutamate release from the slices and blocked the CHA-induced inhibition of glutamate. The A(2) receptor agonist 2-p-(2-carboxylethyl)-phenylamino-5'-N-ethylcarboxamido adenosine hydrochloride (CGS 21680) selectively increased glutamate release when applied at 5 microM while it selectively inhibited GABA release at a lower concentration (10 nM). The addition of NMDA to the medium, resulted in increased adenosine release equivalent to that found following stimulation with 50 mM KCl. Both the NMDA and the KCl-induced increases were eliminated by addition of D-2-amino-5 phosphopentanoic acid (D-AP5), an NMDA-receptor antagonist. Slices prepared from the IMHV of chicks following successful training on the task showed enhanced adenosine release 30 min, 1, 3 and 6.5 h after training compared to chicks trained to peck a water-coated bead. The results show that changes in adenosine release from the IMHV accompany memory formation in the chick. We suggest that adenosine-amino acid transmitter interactions potentially via the activation of NMDA receptors, a necessary step in long-term memory formation for the task, may modulate the formation of memory for the one-trial passive avoidance task.

Adenosine↗
PubMed1985

Involvement of spinal serotonergic pathways in nociception but not in avoidance learning.

The effects of selective lesions of the descending serotonergic (5-HT) pathways on analgesia and avoidance deficit induced by the 5-HT releasing compound p-chloroamphetamine (PCA, 2.5 mg/kg) were investigated in male rats. Intrathecal injection of 5,6-DHT (20 micrograms/rat) reduced the uptake of labelled 5-HT into spinal synaptosomes by approximately 85% but did not significantly affect the uptake of noradrenaline. The lesions produced a significant hyperalgesia and strongly attenuated the analgesic effect of PCA in the hot-plate test. In the flinch-jump test 5,6-DHT lesioned rats receiving PCA did not differ from the saline control group. Spinal lesioning did not, however, affect one-way active avoidance performance and did not prevent the marked impairment of avoidance performance induced by PCA. Thus, the avoidance deficit caused by PCA is independent of the descending serotonergic pathways and of the analgesia induced by PCA. These results support the view of a differential involvement of the ascending and descending serotonergic projections in behavioural processes controlled by aversive stimuli.

5,6-Dihydroxytryptamine↗
PubMed1981

Avoidance learning and mechanism of the protective effect of apomorphine against hypoxia.

We have analyzed a conditioned avoidance response (CAR) in rats, under both normoxia and hypobaric hypoxia (300 torr), to try to elucidate the mechanism of apomorphine's protective effect against hypoxia. The resistance to hypoxia is markedly increased by apomorphine (1 mg/kg i.p.) and, to a lesser degree, by an alpha-adrenergic pre-synaptic (yohimbine 1 mg/kg i.p.) or post-synaptic (phenoxybenzamine 1 mg/kg i.p.) blocker. The anti-hypoxic property of apomorphine is not altered when associated with domperidone (0.5 mg/kg i.p.), a peripheral blocker of the dopaminergic receptors. Resistance to hypoxia is decreased by propranolol (1 mg/kg i.p.) and pimozide (1 mg/kg i.p.). It is not modified by tylciprine (2 mg/kg i.p.) or by metergoline (2.5 mg/kg i.p.), a blocker of the 5-hydroxytryptamine (5 H T) receptors. However, the association of any of the above pharmacological agents with apomorphine destroys apomorphine's anti-hypoxic effect. There has even been shown a positive potentialisation ( i.e. an increase of the inhibitory effect) between apomorphine, hypoxia, and the added drug. This potentialisation is already noticeable under normoxia for the association of each of the drugs with apomorphine. Free alpha, beta adrenergic, cerebral dopaminergic, and serotoninergic receptors and an intact amine metabolic pathway therefore seem required for apomorphine to develop its anti-hypoxic activity.

Animals↗
PubMed1976

The development of passive and active avoidance learning in the cat.

Kittens of 25 and 50 days of age were tested on a passive avoidance task in a 2-compartment black-white shuttle box. Latency to enter the dark side of the box was the same for both groups on Day 1, but the latency to enter the dark side on Day 2 was much shorter for the younger kittens. Other kittens were trained in a step-up active avoidance task also at 25 and 50 days of age. No differences were found in active avoidance performance between the younger and older animals, indicating that active and passive avoidance tasks may possibly reflect separate developmental processes that mature at different rates in the cat.

Age Factors↗
PubMed1994

Differential recovery of inhibitory avoidance learning by striatal, cortical, and mesencephalic fetal grafts.

Four groups of male Wistar rats showing disrupted inhibitory avoidance conditioning due to striatal lesions were studied. Three groups received striatal, cortical, or ventral mesencephalic brain grafts and the fourth group remained as a lesioned control. Sixty days postgraft the animals were retrained in an inhibitory avoidance task. The striatal-grafted animals were the only group that significantly improved in the ability to acquire the inhibitory avoidance task. Acetylcholinesterase histochemistry revealed positive patches of cells in the striatal grafts. Cortical grafts showed less reactivity, without patches. Immunocytochemical analyses for tyrosine hydroxylase revealed positive cell reactivity in the mesencephalic grafts and few positive fibers were detected in the border between the striatal grafts and the host tissue. These results demonstrate that striatal but not cortical or mesencephalic brain grafts can promote the restoration of the ability to acquire an inhibitory avoidance task and suggest that the acetylcholine tissue content is involved in the behavioral recovery.

Acetylcholine↗
PubMed1988

Age differences in acquisition and retention of one-way avoidance learning in C57BL/6NNia and autoimmune mice.

Acquisition and 48-h retention of a step-up active avoidance response were studied in separate age groups of C57BL/6NNia mice (aged 1.5, 3.5, 6, 12, or 26 months) and five strains of genetically autoimmune mice differing in life span. The C57BL/6NNia mice showed no change in ability to acquire the avoidance response between 1.5 and 3.5 months, but showed a steady decline in that ability thereafter. Mouse strains with early-onset autoimmune disorder (NZB/B1NJ, MRL/MpJ-lpr, and BXSB/MpJ) showed declines in acquisition capability between 1.5 and 3.5 months of age, whereas mouse strains with mild, late-onset autoimmune disorder (MRL/MpJ- + and NZBWF1/J) showed stable or improved acquisition during that period. Both the C57BL/6NNia and NZB/B1NJ mice showed age-dependent declines in 48-h retention performance by 12 months of age. These findings suggested that while 48-h retention performance deficits were most related to chronological age, avoidance acquisition deficits were related to development of autoimmunity.

Aging↗
PubMedDate not supplied

[Effect of consumption of sucrose and saccharin on passive avoidance learning in female Wistar rats].

Influence of consumption of 32% sucrose or 0.1% saccharin solutions on passive avoidance acquisition in female Wistar rats was studied at different stages of estrous cycle. Under conditions of weak electrical shock, rats of the control and saccharin groups showed no acquisition at any stage of estrous cycle. Under the same conditions females of the sucrose group acquired the avoidance behavior if trained on the first day of diestrous and metestrous but not proestrous and estrous. The stage of estrous cycle on the second day did not influence the latency during testing session.

Animals↗
PubMed2004

The effect of reversible inactivation of the supramammillary nucleus on passive avoidance learning in rats.

Previous studies have shown that the presence of hippocampal theta activity is important for learning and memory, and that the medial supramammillary nucleus (mSuM) is involved in the control of the frequency of theta rhythm. It has also been shown that the depression of mSuM activity by chlordiazepoxide causes modest impairment of spatial learning. On the other hand, the lateral supramammillary nucleus (lSum) increases long-term potentiation (LTP) of hippocampal population spikes. However, to our knowledge, no reports exist concerning the role of the supramammillary area (SuM) in passive avoidance (PA) learning. In the present study, rats were chronically implanted with a cannula aimed at SuM and were trained on a step-through PA task. They received intra-SuM injection of lidocaine or saline at the following intervals: 5 min before training, 5, 90, and 360 min after the acquisition trial, or 5 min before the retrieval test. When lidocaine was injected 5 min before training there was no effect on acquisition of PA but retrieval was significantly poorer than the control group injected with saline. Lidocaine injection 5 min after the acquisition trial impaired PA retention, but reversible inactivation of SuM at 90 and 360 min after training and 5 min before the retrieval test showed no significant effect on PA retention. It can be concluded that SuM contributes to PA consolidation at least 5 min after the acquisition trial and that this effect may be accomplished through SuM projections to the septal and/or hippocampal areas participating in the PA memorization processes.

Analysis of Variance↗