Search

The effects of posttraining excitotoxic lesions of the pedunculopontine tegmental nucleus (PPTg) on two-way active avoidance after changing the conditioned stimulus (CS) used during prelesion training were examined. Prelesion training was carried out with either a tone or a light as the CS, and this CS was changed during postlesion training. Replacing the tone with a light reduced the performance of control and lesioned rats, but the degree of reduction was higher in the latter. Replacing the light with a tone had slight detrimental effects in lesioned rats but not in controls. Thus, posttraining PPTg lesions slowed down the reacquisition of shuttle-box avoidance under conditions of CS transfer, an effect that may be attributable to disruption of attention and/or gating of sensory stimuli. Keywords: pedunculopontine tegmental nucleus, conditioned stimulus transfer, conditioned stimulus modality, two-way active avoidance

Effects of posttraining epinephrine on retention of a massed (1 session, 30 trials) 2-way active avoidance task were studied in rats. Immediately after the training session rats received an injection of 0.05 or 0.01 mg/kg ip epinephrine, or distilled water. Retention was tested 11, 20, or 45 days after training, in independent groups of rats. The 20- and 45-day retention was improved in poor-learning rats and disrupted in good-learning rats. It was concluded that the effect (facilitatory or disruptive) of posttraining epinephrine on memory consolidation depends on the basic learning capacity of rats for this task and needs a long time to be expressed.

Effects of posttraining epinephrine (EPI) on retention of a massed (1 session, 30 trials) 2-way active avoidance task in rats were studied. The rats received an injection (ip) of 0.05 mg/kg EPI, 0.01 mg/kg EPI, or distilled water immediately after the training session. EPI did not improve retention 24 hr after the training session (Experiment 1) but enhanced retention 20 days after the training session (Experiment 2). The group receiving the smaller dose of EPI had better retention than the group receiving the larger dose, indicating dose dependency. The authors suggest that the process of consolidation of massed 2-way active avoidance conditioning is long and elaborative. Posttraining EPI would facilitate this active process of consolidation, improving performance as consolidation goes on. This facilitation needs, at least under certain conditions, more than 24 hr to be expressed as a higher level of performance on the retention test.

The present experiments determined the consequences of blocking muscarinic cholinergic receptors of the prelimbic (PL) cortex in the acquisition and retention of an odor-reward associative task. Rats underwent a training test (five trials) and a 24-h retention test (two retention trials and two relearning trials). In the first experiment, rats were bilaterally infused with scopolamine (20 or 5 microg/site) prior to training. Although scopolamine rats showed acquisition equivalent to PBS-injected controls, they exhibited weakened performance in the 24-h retention test measured by number of errors. In the second experiment, rats were injected with scopolamine (20 microg/site) immediately or 1 h after training and tested 24 h later. Scopolamine rats injected immediately showed severe amnesia detected in two performance measures (errors and latencies), demonstrating deficits in retention and relearning, whereas those injected 1 h later showed good 24-h test performance, similar to controls. These results suggest that muscarinic transmission in the PL cortex is essential for early memory formation, but not for acquisition, of a rapidly learned odor discrimination task. Findings corroborate the role of acetylcholine in consolidation processes and the participation of muscarinic receptors in olfactory associative tasks.

A rapidly learned odor discrimination task based on spontaneous foraging behavior of the rat was used to evaluate the role of N-methyl-D-aspartate (NMDA) receptors (NMDARs) in ongoing memory consolidation. Rats were trained in a single session to discriminate among three odors, one of which was associated with palatable food reward. Previous experiments showed that the NMDAR antagonist DL-APV induced amnesia for this task when injected immediately after training. In the present study, memory was reactivated 24 h after training by exposure to the rewarded odor within the experimental context after which rats received an intracerebroventricular injection of APV. Combined reactivation-drug treatment induced profound amnesia when tested 48 h later. Animals receiving drug alone, in absence of reactivation, showed perfect retention. It is concluded that NMDARs support a consolidation process taking place after memory reactivation.

Abstract: Rats received bilateral stria terminalis (ST) lesions or were sham-operated. Five days later, the animals were trained in a two-way active avoidance task (one session, 30 trials) and, immediately after the training session, received 0.01 mg/kg i.p. epinephrine or distilled water. Retention was tested 20 days after the acquisition session. In sham-operated groups, epinephrine improved retention in rats that were poor learners and impaired it in rats that were good learners. In poor learners with posttraining epinephrine, lesions of the ST not only blocked the facilitatory effect of epinephrine but also disrupted performance throughout the retention session. In good learners, ST lesions attenuated the disruptive effect of epinephrine. Lesions per se did not affect either acquisition or retention. We conclude that ST is involved in the modulatory effect of posttraining epinephrine on memory consolidation. In addition and considering the results observed in rats that were poor learners, we suggest that emotional factors and/or other amygdaloid pathways different from the ST could participate in the effects of posttraining epinephrine, along with the ST.

A 28-year-old otherwise healthy man presented twice with a peroneal nerve palsy, first on the left and 4 months later on the right side. Both palsies occurred after sitting on a chair for a few hours. Personal and family history were unremarkable. Electrophysiologic examinations revealed conduction blocks of the peroneal nerves slightly above the fibular head and signs of acute denervation in the anterior tibial muscles. Bilateral fabellas (sesamoid bones) within the tendon of the lateral head of gastrocnemius muscles detected by ultrasound and MRI (figure) caused these unusual pressure palsies.1Surgical excision of the fabellae resulted in full recovery.