Frequency Of Conditioned Responses Research Articles

Prolonged regulatory effect of thyroliberin on conditioned vegetative responses in hedgehogs.

The neurochemical (neuropeptide) correction of disturbed automatic functions is a topical problem of modern neurophysiology and medicine. Most of the experimental studies on vegetative and motor reactions and the possibilities to compensate for their disturbance have been performed on partially immobilized animals [4, 5, 7, 8]. Only a few complex studies on vegetative and motor reactions under the conditions of free behavior have been conducted. We did not find publications on such studies on insectivores. Thyroliberin (thyrotropin-releasing hormone) is interesting because of its pronounced cardiovascular effect [1, 2]. This hormone attracts special attention as a specific regulator of respiration. Currently, thyroliberin is used in clinical practice to relieve hypoxia and normalize respiration and blood circulation in newborns [1, 2, 11‐13]. Therefore, we studied the role of thyroliberin in the regulation of conditioned motor and vegetative reactions in hedgehogs. The experiments were carried out on 13 hedgehogs Erinaceus europaeus. We used the model of eating behavior with simultaneous recording of the motor, respiratory, and cardiac components of higher nervous activity (HNA) in free-moving animals. An advantage of this method is that it allows the researcher to monitor the ratio between the three components of HNA at different stages of the formation of conditioned reflexes and to study the effects of neuropeptides on these components in animals belonging to lower stages of mammalian evolution. The electrocardiogram (ECG) was recorded with the use of silver cuff-shaped electrodes attached to three limbs (the two fore and the left hind). The respiratory component was recorded with the use of a nipple tube filled with graphite powder and set in a special cuff, which was attached to the hedgehog’s abdomen. To avoid noise when recording the vegetative activity in free-moving animals, we (together with V.P. Ivanov, an engineer at our laboratory) developed and built an operational amplifier with a high input resistance in the cardiograph. The noise caused by the effect of the supply-line frequency on the ECG record was eliminated with the use of special filters and shielded wires. Taking into account that hedgehogs would curl up into a ball, we used the following experimental procedure. Hedgehogs deprived of food (for one or two days) with the cuffs attached to them were taught to receive food reinforcement from the feeder (five to seven days). After this, conditioned reflexes were formed in the animals. A 50-dB, 200-Hz sound above the human hearing threshold served as a conditioned stimulus, and a 50-Hz sound, as a differentiation stimulus. Vegetative parameters were recorded on an N338-6P six-channel automatic recorder. In addition to positive conditioned responses, an internal inhibition of the extinction and differentiation types was formed in hedgehogs. We used an acute extinction, with an absence of motor responses to three consecutive nonreinforcements serving as a criterion for extinction. We measured the background heart rate (HR) and respiration rate (RR), their changes in response to the conditioned stimulus at different stages of the formation of the conditioned reflex, latent periods (LPs) of the motor and vegetative components, intersignal activity, and changes of these parameters after thyroliberin administration. The thyroliberin was prepared at the Department of the Chemistry of Natural Compounds, Faculty of Chemistry, St. Petersburg State University. The preparation was administered subcutaneously at a dose of 35‐40 μ g/kg 10 min before the experiment. We found that conditioned motor food-procuring responses were the first to be formed and reinforced: this took 60‐65 simultaneous applications of the conditioned and unconditioned stimuli. At the stage of reinforced conditioned responses, their latent period was relatively constant; its duration was 2.5 ∠ 0.53 s. Conditioned respiratory responses were formed later, after 75‐80 applications of the stimuli. At the initial stages, there were no constant patterns of conditioned respiratory responses. At the stage of reinforcement, the conditioned-response frequency tended to decrease. It took considerably more time for the cardiac component to PHYSIOLOGY

The NMDA antagonist memantine impairs classical eyeblink conditioning in humans

The present study investigated the effects of a single oral dose (30 mg) of the non-competitive N-methyl- d-aspartate (NMDA) receptor antagonist memantine on memory and learning in human subjects. Sixteen male healthy volunteers participated in a double blind placebo controlled study. There were no significant effects of Memantine on mood, attention or immediate and delayed verbal and visuospatial memory. Memantine did, however, delay the acquisition of classical eyeblink conditioning and reduced the overall frequency of conditioned responses without affecting reflex or spontaneous eyeblinks. These findings are compatible with the higher affinity of memantine to cerebellar as compared to forebrain tissue and demonstrate the dissociability of different memory systems by pharmacological tools.

Projections from the thoracic cord to the cerebellar nuclei in the rat

Kinematic and dynamic analyses were employed to study the effects of cerebellar lesions on conditioned and unconditioned nictitating membrane responses in the rabbit. It was found that conditioned responses acquired to an auditory stimulus accelerated in two bursts as indicated by two distinct peaks of acceleration. The second peak of acceleration was very weak during the early portions of conditioning but became a prominent feature of the conditioned response over 16 sessions of conditioning. The second peak of acceleration in the conditioned response was more sensitive to cerebellar damage than was the first peak. When lesions of the cerebellum permanently reduced the amplitude of conditioned responses, but did not affect their frequency, the second peak of acceleration was nearly abolished while the first peak was unaffected. When cerebellar lesions profoundly impaired both the amplitude and frequency of conditioned responses, large and permanent impairments occurred in both peaks of acceleration. Lesions of the anterior interpositus nucleus most severely impaired both peaks of acceleration in the conditioned response and significantly reduced the acceleration of unconditioned responses across a wide range of intensities of corneal air puff. The deficit in the acceleration of unconditioned responses became manifest only after membrane extension exceeded 0.12 mm. The impairment in the amplitude of the unconditioned response after cerebellar lesions more closely approximated the impairment in the amplitude of the conditioned response when the force-generating properties of the conditioned and unconditioned stimuli were equated. It was hypothesized, therefore, that one reason why conditioned responses are so easily disrupted by cerebellar lesions is because they are of low force and not simply because they are learned.It was proposed that the two peaks of acceleration that characterize the conditioned response represent the function of two distinct anatomical systems. The first, a short-latency system, initiates the response and is most likely mediated by circuits that traverse the pontomedullary reticular formation. The second, a longer-latency system, amplifies response amplitude and its neural basis remains to be elucidated. The two components of the conditioned response may reflect two sequential bursts of activity in the accessory abducens nucleus, the principal site of the motoneurons for the retractor bulbi muscle, or may reflect the synergistic activity of the accessory abducens nucleus and the motor nuclei of the other extraocular muscles. It was concluded that the vulnerability of the second component of the conditioned response to cerebellar damage reflects an important role for the cerebellum in modulating the degree to which long-latency neural systems contribute to the ongoing performance of learned and unlearned behaviors.

1503 Projections from the thoracic cord to the cerebellar nuclei in the rat

Kinematic and dynamic analyses were employed to study the effects of cerebellar lesions on conditioned and unconditioned nictitating membrane responses in the rabbit. It was found that conditioned responses acquired to an auditory stimulus accelerated in two bursts as indicated by two distinct peaks of acceleration. The second peak of acceleration was very weak during the early portions of conditioning but became a prominent feature of the conditioned response over 16 sessions of conditioning. The second peak of acceleration in the conditioned response was more sensitive to cerebellar damage than was the first peak. When lesions of the cerebellum permanently reduced the amplitude of conditioned responses, but did not affect their frequency, the second peak of acceleration was nearly abolished while the first peak was unaffected. When cerebellar lesions profoundly impaired both the amplitude and frequency of conditioned responses, large and permanent impairments occurred in both peaks of acceleration. Lesions of the anterior interpositus nucleus most severely impaired both peaks of acceleration in the conditioned response and significantly reduced the acceleration of unconditioned responses across a wide range of intensities of corneal air puff. The deficit in the acceleration of unconditioned responses became manifest only after membrane extension exceeded 0.12 mm. The impairment in the amplitude of the unconditioned response after cerebellar lesions more closely approximated the impairment in the amplitude of the conditioned response when the force-generating properties of the conditioned and unconditioned stimuli were equated. It was hypothesized, therefore, that one reason why conditioned responses are so easily disrupted by cerebellar lesions is because they are of low force and not simply because they are learned.It was proposed that the two peaks of acceleration that characterize the conditioned response represent the function of two distinct anatomical systems. The first, a short-latency system, initiates the response and is most likely mediated by circuits that traverse the pontomedullary reticular formation. The second, a longer-latency system, amplifies response amplitude and its neural basis remains to be elucidated. The two components of the conditioned response may reflect two sequential bursts of activity in the accessory abducens nucleus, the principal site of the motoneurons for the retractor bulbi muscle, or may reflect the synergistic activity of the accessory abducens nucleus and the motor nuclei of the other extraocular muscles. It was concluded that the vulnerability of the second component of the conditioned response to cerebellar damage reflects an important role for the cerebellum in modulating the degree to which long-latency neural systems contribute to the ongoing performance of learned and unlearned behaviors.

Classical eyeblink conditioning in Parkinson's disease.

Patients with Parkinson's disease (PD) show impairments of a range of motor learning tasks, including tracking or serial reaction time task learning. Our study investigated whether such deficits would also be seen on a simple type of motor learning, classic conditioning of the eyeblink response. Medicated and unmediated patients with PD showed intact unconditioned eyeblink responses and significant learning across acquisition; the learning rates did not differ from those of healthy control subjects. The overall frequency of conditioned responses was significantly higher in the medicated patients with PD relative to control subjects, and there was also some evidence of facilitation in the unmedicated patients with PD. Conditioning of electrodermal and electrocortical responses was comparable in all groups. The findings are discussed in terms of enhanced excitability of brainstem pathways in PD and of the involvement of different neuronal circuits in different types of motor learning.

Changes in the motor pattern of learned and unlearned responses following cerebellar lesions: A kinematic analysis of the nictitating membrane reflex

Kinematic and dynamic analyses were employed to study the effects of cerebellar lesions on conditioned and unconditioned nictitating membrane responses in the rabbit. It was found that conditioned responses acquired to an auditory stimulus accelerated in two bursts as indicated by two distinct peaks of acceleration. The second peak of acceleration was very weak during the early portions of conditioning but became a prominent feature of the conditioned response over 16 sessions of conditioning. The second peak of acceleration in the conditioned response was more sensitive to cerebellar damage than was the first peak. When lesions of the cerebellum permanently reduced the amplitude of conditioned responses, but did not affect their frequency, the second peak of acceleration was nearly abolished while the first peak was unaffected. When cerebellar lesions profoundly impaired both the amplitude and frequency of conditioned responses, large and permanent impairments occurred in both peaks of acceleration. Lesions of the anterior interpositus nucleus most severely impaired both peaks of acceleration in the conditioned response and significantly reduced the acceleration of unconditioned responses across a wide range of intensities of corneal air puff. The deficit in the acceleration of unconditioned responses became manifest only after membrane extension exceeded 0.12 mm. The impairment in the amplitude of the unconditioned response after cerebellar lesions more closely approximated the impairment in the amplitude of the conditioned response when the force-generating properties of the conditioned and unconditioned stimuli were equated. It was hypothesized, therefore, that one reason why conditioned responses are so easily disrupted by cerebellar lesions is because they are of low force and not simply because they are learned. It was proposed that the two peaks of acceleration that characterize the conditioned response represent the function of two distinct anatomical systems. The first, a short-latency system, initiates the response and is most likely mediated by circuits that traverse the pontomedullary reticular formation. The second, a longer-latency system, amplifies response amplitude and its neural basis remains to be elucidated. The two components of the conditioned response may reflect two sequential bursts of activity in the accessory abducens nucleus, the principal site of the motoneurons for the retractor bulbi muscle, or may reflect the synergistic activity of the accessory abducens nucleus and the motor nuclei of the other extraocular muscles. It was concluded that the vulnerability of the second component of the conditioned response to cerebellar damage reflects an important role for the cerebellum in modulating the degree to which long-latency neural systems contribute to the ongoing performance of learned and unlearned behaviors.