Disease relevance of Avoidance Learning

• Females exhibited hyperactivity in the open field but developed impaired avoidance learning only when exposed prenatally to both propranolol and hypoxia [1].
• RESULTS: Toluene exposure during brain growth spurt reduced behavioral responses including locomotor activity, motor incoordination, and hypnosis to MK-801 and/or ketamine, while leaving cognitive deficits in inhibitory avoidance learning tasks unaffected [2].
• The purpose of the present study was to examine if progesterone, a hormone known for its effectiveness at reducing cerebral edema, could protect against secondary neuronal death and facilitate the acquisition of an avoidance learning task in an ablation model of cortical injury [3].
• Animals prenatally exposed to ethanol had lower birth weights and impaired passive avoidance learning at 17 days of age [4].

Psychiatry related information on Avoidance Learning

• Intracerebral injection of large amounts of glutamate between 5 min and 2.5 min after passive avoidance learning in young chicks inhibits short-term memory, which occurs between 0 and 10 min post-learning in a three-stage model of memory formation first established by Gibbs and Ng(25) [Physiol. Behav. 23:369-375; 1979] [5].
• Pre-administration of docosahexaenoic acid had a profoundly beneficial effect on the decline in avoidance learning ability in the Alzheimer's disease model rats, associated with an increase in the cortico-hippocampal docosahexaenoic acid/arachidonic acid molar ratio, and a decrease in neuronal apoptotic products [6].
• These abnormalities were characterized by a reduction in spontaneous locomotor activity, blockade of methamphetamine-induced hyperactivity, cataleptic behavior, and defects in active avoidance learning [7].
• Lesions of the basolateral amygdala complex block propofol-induced amnesia for inhibitory avoidance learning in rats [8].
• Intra-amygdala injections of corticotropin releasing factor facilitate inhibitory avoidance learning and reduce exploratory behavior in rats [9].

High impact information on Avoidance Learning

• Abnormal avoidance learning in mice lacking functional high-affinity nicotine receptor in the brain [10].
• Chloramphenicol administration during brain development: impairment of avoidance learning in adulthood [11].
• The MAOA-deficient mice exhibited significantly enhanced classical fear conditioning (freezing to both tone and contextual stimuli) and step-down inhibitory avoidance learning [12].
• We used the GABA(A) agonist muscimol to functionally inactivate these nuclei immediately after single-trial Pavlovian fear conditioning or single-trial inhibitory avoidance learning [13].
• We have previously demonstrated that the extent of the IIP-MF subfield is positively correlated with the capacity to perform a spatial radial-maze task and that an experimentally induced enlargement of the IIP-MFs, by means of postnatal thyroxine treatment, predicted the ability of adult two-way avoidance learning [14].

Chemical compound and disease context of Avoidance Learning

• Since the lesion of this brain area selectivity lowers the forebrain concentration of 5-hydroxytryptamine (5-HT), implications of the role of brain 5-HT in avoidance-learning acquisition are discussed [15].
• Subcutaneous DDAVP 20 micrograms/rat or LVP 1 microgram/rat improved conditioned avoidance learning in the 6-OH DA-treated rats at least as much as in control rats [16].
• This paper summarizes results of a series of experiments dealing with the effects of the neuropeptide substance P (SP) on avoidance learning and habituation [17].
• Shuttle box avoidance learning in rats was impaired in animals rendered thiamin deficient but not in animals fed control or alcohol-containing liquid diets [18].
• Active and passive avoidance learning in controls and schizophrenic patients on racemic propranolol and neuroleptics [19].

Biological context of Avoidance Learning

• Differential patterns of extracellular signal-regulated kinase-1 and -2 phosphorylation in rat limbic brain regions after short-term and long-term inhibitory avoidance learning [20].
• Effects of nicotine on active avoidance learning in rats: sex differences [21].
• The acute effects of p-chloroamphetamine (PCA) on one-way active avoidance learning and on central monoamine concentrations were examined in the male rat [22].
• Chronic intermittent ethyl alcohol inhalation and avoidance learning [23].
• Two rat models of memory impairment in passive avoidance learning induced by cerebrovascular disturbance, were established to estimate the effects of a cerebral metabolic enhancer, idebenone [24].

Anatomical context of Avoidance Learning

• In semithin, Toluidine Blue-stained plastic coronal sections, we have observed hyperchromatic granule cells in the dorsal crest of the adult rat dentate gyrus following passive avoidance learning [25].
• The effect of unilateral injection of the neurokinin substance P (SP) and of certain N- or C-terminal SP-fragments into the region of the nucleus basalis magnocellularis (NBM) on inhibitory avoidance learning was investigated [26].
• Taken together, these results indicate that cGMP-regulated processes in the hippocampus play an important role in the early stages of memory consolidation and that cAMP signalling pathways are involved in the late post-training memory processing of inhibitory avoidance learning [27].
• Blockade of cholinergic receptors by an irreversible antagonist, propylbenzilylcholine mustard (PrBCM), in the rat cerebral cortex causes deficits in passive avoidance learning [28].
• Reduced dopamine turnover in the nucleus accumbens may underlie, at least in part, age-related deficits in conditioned avoidance learning and retention [29].

Gene context of Avoidance Learning

• This does not appear to be due to a learning deficit because mice lacking both DARPP-32 and I-1 show normal passive avoidance learning [30].
• Thus, our results indicate that endogenous BDNF is required for both STM and LTM formation of inhibitory avoidance learning, possibly involving CREB activation-dependent mechanisms [31].
• On the other hand, CRF (1.0 microg) consistently and markedly improved retention performance in rats in an inhibitory avoidance learning task [32].
• The aim of the present study was to investigate the different neural substrates underlying short- and long-term inhibitory avoidance learning and memory in rats using phosphorylated extracellular signal-regulated kinase-1 and -2 labeling as an index of plasticity [20].
• An administration of [Leu(13)-(psi-CH(2)NH)-Leu(14)]BN (antagonizes GRP-R>neuromedin B receptor (NMB-R)) impaired the performance of inhibitory avoidance learning in all doses (16, 32, 64 nmol/kg) [33].

Analytical, diagnostic and therapeutic context of Avoidance Learning

• Drugs known to improve memory, including physostigmine, pramiracetam and the muscarinic agonists, oxotremorine and RS 86, selectively induced analgesia in rats subjected to test before the shock plus the shock, thereby supporting a hypothesis of avoidance learning [34].
• Microinjection of serotonin but not noradrenaline into the amygdala improves passive avoidance learning by bulbectomised rats [35].
• Intraperitoneal injection of 1-oleoyl-2-docosahexaenoyl phosphatidylcholine enhances discriminatory shock avoidance learning in rats [36].
• Using the polymerase chain reaction (PCR) differential display directed to cloning transcripts related to retention performance for the inhibitory avoidance learning task, we have isolated two rat cDNA fragments homologous to the 3' untranslated region (3'UTR) of glial fibrillary acid protein (GFAP) cDNA [37].
• Intraventricular injections of 192-saporin destroyed the CBF and impaired passive avoidance learning [38].

References