PubMed Health⌕ Search

Biomedical subjects

A G Romano

Publications and source records attributed to A G Romano.

29 records · Page 2Linked to original sources

Enhanced learning following a single, acute dose of MDA.

The behavioral effects of a single, acute dose of methylenedioxyamphetamine (MDA) were assessed using the rabbit nictitating membrane (NM) preparation. Acquisition of the classically conditioned NM response was carried out in a single session under MDA at doses of 10 and 20 mumol/kg (1.79 and 3.58 mg/kg, respectively) and retention was assessed during a drug-free state 48 h later. In agreement with previous reports, MDA at a dose of 10 mumol/kg enhanced acquisition of the conditioned NM response and learning was retained in the nondrug state. However, MDA at a dose of 20 mumol/kg failed to affect either acquisition or retention. In further agreement with previous reports, MDA at 10 mumol/kg facilitated the amplitude of the unconditioned response during unpaired stimulus presentations. It is suggested that this enhanced motor response may be due to enhanced neural transmission in the afferent limb of the unconditioned reflex arc.

3,4-Methylenedioxyamphetamine↗

Evidence for an involvement of the mu-type of opioid receptor in the modulation of learning.

Pavlovian conditioning of the rabbit's nictitating membrane response was used to determine whether the retardation of learning produced by enkephalin derivatives was mediated through an action on mu- or delta-opioid receptors. Intraventricular injection of the highly selective mu-agonist, [D-Ala2, MePhe4, Gly-ol5] enkephalin (DAMGO) significantly retarded (2 nmol) or completely blocked (20 nmol) the acquisition of conditioned responses. The retarded or blocked acquisition of conditioned responses produced by DAMGO could still be detected when the rabbits were tested two days after cessation of drug injections, suggesting that DAMGO had affected learning and not simply performance of conditioned responses. Intraventricular injection of a comparable dose (20 nmol) of the highly selective delta-agonist, [D-Pen2,5] enkephalin (DPDPE) did not retard learning. A higher dose of DPDPE (200 nmol), which would be expected to act at both mu- and delta-receptors, did produce a retardation of acquisition that was comparable to the effects of a 2-nmol dose of DAMGO. However, unlike DAMGO, the retardation of learning produced by this dose of DPDPE appeared to be due, at least in part, to a reduction in the aversive properties of the unconditioned stimulus. The retardation of learning produced by 2 nmol of DAMGO and 200 nmol of DPDPE was due to an action on an opioid receptor because this effect was blocked by a subcutaneous injection of naloxone (2.5 mumol/kg), a specific opioid antagonist. The stereoselective effects of the mu-opioid agonist levorphanol further confirmed that the retarded learning was mediated through actions at the mu-opioid receptor. Autoradiographic studies indicated that a 2-nmol, intraventricular dose of DAMGO achieved contents greater than 1 pmol/mg in tissue lying within 2 mm of the lateral ventricle, third ventricle and cerebral aqueduct. These data suggest that enkephalins produce a retardation of learning through an effect on the mu-type of opioid receptor and that at least one locus of their actions is produced at periventricular sites lying within 2 mm of the ventricles.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Harmaline-induced impairment of Pavlovian conditioning in the rabbit.

In this study we examined the effects of harmaline on Pavlovian conditioning of the rabbit's nictitating membrane response. The acquisition of conditioned responses was determined during a single session consisting of 120 pairings of a tone-conditioned stimulus with a corneal air puff unconditioned stimulus. Harmaline severely retarded (5 mg/kg) or completely blocked (10 and 20 mg/kg) acquisition of conditioned responses. The blocked or retarded acquisition of conditioned responses could still be detected when the rabbits were tested 2 d after cessation of drug injections, suggesting that harmaline was affecting acquisition and not the motoric expression of conditioned responses. Control experiments established that harmaline (5 mg/kg) did not affect (1) baseline levels of responding, (2) the level of non-associative responding to the conditioned stimulus, (3) the amplitude or any of the temporal characteristics of the unconditioned response, (4) the development of habituation to the unconditioned stimulus, and (5) the threshold of the unconditioned stimulus for eliciting the unconditioned response. However, harmaline did produce a 12 dB increase in the intensity threshold of the conditioned stimulus for eliciting conditioned responses. We concluded that the primary effect of harmaline was to impair stimulus processing within brainstem circuits such as to reduce the excitatory properties of the conditioned stimulus, thus retarding its entry into associative learning. The results were discussed with respect to the possible role of the inferior olive in associative learning.

Acoustic Stimulation↗

Recoverable and nonrecoverable deficits in conditioned responses after cerebellar cortical lesions.

This study reexamined the effects of unilateral damage to cerebellar hemispheral lobule VI on the rabbit's conditioned nictitating membrane (NM) response. Extensive unilateral removal of hemispheral lobule VI in 11 rabbits impaired ipsilateral conditioned responses as reflected by reductions of 52% in mean frequency and 53% in mean amplitude during test trials on the first postoperative session. The decreases in the amplitude and frequency of conditioned responses were highly correlated (r = 0.82). The frequency of conditioned responses recovered to control levels but their amplitudes remained reduced such that the correlation between these two measures of responding was no longer significant by the 12th postoperative conditioning session. The decrease in the amplitude of conditioned responses was not accompanied by changes in onset latency or rise time. There was no significant impairment of conditioned responses in surgical controls and animals with only partial damage to hemispheral lobule VI. It was concluded that hemispheral lobule VI plays an important role in the regulation of motor centers in the brainstem so as to facilitate the initiation and optimum execution of the conditioned NM reflex. This cortical regulation of the conditioned NM response may contain learned elements; however, these cannot be resolved with lesion methods, nor has their existence been proven in this or other lesion studies. Nevertheless, the results of this study do demonstrate that the cerebellar cortex cannot be considered as the single locus necessary for NM conditioning.

Animals↗

Retention and acquisition of classical trace conditioned responses by rabbits with hippocampal lesions.

The effects of dorsal hippocampal lesions on retention of classical trace conditioned responses were examined using the rabbit nictitating membrane preparation. Animals were trained to criteria and then lesioned either in the cortex or in the hippocampus and the cortex. Hippocampal damage had no effect on the retention of responses but produced significantly longer onset latencies. A control group of hippocampal animals acquired conditioned responses (CRs) at least as quickly as the prelesion subjects, and they also exhibited longer response onset latency. A second experiment evaluated the performance of hippocampal lesioned animals in classical trace conditioning with either a low-intensity periorbital shock or corneal air puff as the unconditioned stimulus (UCS). Hippocampal animals successfully acquired CRs under both conditions but exhibited an alteration of response onset which was dependent on the form of the UCS. Hippocampal animals displayed shorter response onset in the air-puff condition and longer response onset in the shock condition. Cortical animals timed responses consistently regardless of the UCS. These findings strongly suggest that the hippocampus modulates temporal characteristics of learned behavior.

Animals↗

Extinction and retention of a classically conditioned flexor nerve response in acute spinal cat.

These experiments were conducted to examine extinction and retention of a classically conditioned response in acute spinal cats. Conditioning was obtained by pairing a mild electrical stimulus to the superficial peroneal sensory nerve (CS) with a stronger electrical stimulus to the ankle skin (US) of the same leg. Subsequent extinction was produced by presenting CS-alone trials. In the first experiment, animals given massed extinction trials showed response decrements to base levels. Response decrements were not found in animals that received distributed extinction trials. In the second experiment, .5-, 1-, 2-, 3-, or 4-hr intervals between acquisition and extinction produced no significant differences in the extinction data. In the third experiment, animals received extinction trials immediately or 30 min after acquisition trials, followed by 20 additional extinction trials 30 min later. Analyses of these data indicated significant acquisition and extinction in the 10- and 20- acquisition trial groups. As in Experiment 2, varying the interval between acquisition and extinction did not produce any group differences in the extinction data. The results of these experiments demonstrate that response increases produced by paired trials in the spinal preparation do not decay spontaneously over time and are not caused by sensitization effects.

Animals↗

Central and peripheral influences on retention of postural asymmetry in rats.

Four studies were conducted to delineate potential neural processes involved in retention of a peripherally induced postural asymmetry. In the first experiment, dorsal and ventral spinal root section following varying intervals of stimulation successfully abolished peripherally induced hindlimb asymmetry. Experiment 2 revealed that 50 min of ventral root stimulation, in the absence of central connection, was not effective in producing asymmetry persistence. In an attempt to more closely delineate the time parameters involved in peripherally induced asymmetry retention, Experiment 3 was conducted. Asymmetry was found to consistently outlast a spinal transection if 40 min of stimulation was given. Finally, possible modulatory higher brain center influences on the retention processes were demonstrated in Experiment 4. Asymmetry persistence was consistently observed in animals that received 10, 20, 30, 40, or 50 min of hindlimb stimulation if 50 min were allowed to elapse between the onset of stimulation and spinal section. These results, when coupled with the findings of earlier studies, suggest an active involvement of spinal reflex centers in the fixation process. In addition, these studies indicate that the manner in which reflex activity is altered is not crucial as long as underlying time parameters are adhered to. Finally, the present studies demonstrate that higher center influences can modulate retention of a postural asymmetry in a complex manner.

Animals↗

Temporal parameters involved in retention of reflex alterations in spinal rats.

Temporal parameters concerning retention of a stimulation-induced hindlimb flexion were investigated. After spinal transection, 60 rats received 10, 20, 30, 40, 45, or 50 min of hindlimb stimulation. Consistent persistence of flexion following stimulus cessation was observed in rats that were stimulated for at least 30 min. When the results ae compared with previous data, the spinalized rat shows a 10-min reduction in the critical time interval needed to consistently obtain poststimulation persistence of flexion.

Animals↗

Fixation of spinal reflexes in rats by central and peripheral sensory input.

Two methods were used to demonstrate retention of postural asymmetries after spinal cord section in adult rats. In the first preparation, postural asymmetries of the hindlimbs were induced by placing electrolytic lesions in the anterior cerebellum. Asymmetry was found to consistently outlast a spinal cord section if 45 min were allowed between brain lesion and cord section. A certain percentage of rats allowed 35 or 40 min also demonstrated the retention. In the second preparation, postural asymmetries induced by 45 min of direct hindlimb stimulation were also retained after spinal section. Rhizotomy prior to stimulation resulted in a lack of appreciable asymmetry upon termination of the stimulation. Finally, retention of a hindlimb-stimulation-induced asymmetry was observed in animals that underwent a spinal section prior to the stimulation. The present series of studies demonstrates that the "spinal fixation" phenomenon can be obtained by induction of postural alterations from central (cerebellar lesion) and peripheral (hindlimb stimulation) sources. In addition, results obtained from spinal animals indicate that retention of peripherally induced asymmetry is not crucially dependent on higher brain center activity but rather seems to be more dependent on long-term alterations that occur directly in the spinal reflex system.

Animals↗

Unconditional-stimulus locus and interstimulus-interval shift in rabbit (Oryctolagus cuniculus) nictitating membrane conditioning.

The nictitating membrane response of rabbits was conditioned at a 200 msec interstimulus interval (ISI) with either circumorbital (C) or paraorbital (P) shock as the unconditional-stimulus locus. After 3 acquisition days half of each group was shifted to a 700 msec interstimuls interval. Results indicated: (1) more rapid acquisition for Group C, (2) postshift response decrements for both groups, (3) more rapid and stable, as well as complete return to preshift performance levels for Group C. Results were discussed in terms of the response-shaping hypothesis and the contiguity-substitution hypothesis in explaining both conditional response emergence and subsequent modifications of CR topography.

Animals↗