Linda L. Hernandez

Lateral hypothalamic lesions: Effects on pavlovian cardiac and eyeblink conditioning in the rabbit

Rabbits received either bilateral lesions of the far lateral hypothalamus (LH), or sham-operate lesions. After recovery from surgery the animals were exposed to Pavlovian conditioning in which eyeblink (EB), electromyographic (EMG), and heart rate (HR) conditioned responses (CRs) were recorded. Adaptation, acquisition and extinction training were studied. Subsequent to conditioning, free-field activity, paraorbital electric shock thresholds, and HR unconditioned responses (URs) were measured. At the end of behavioral testing forebrain norepinephrine (NE), dopamine (DA), an serotonin (5-HT) concentrations were assessed. Animals with LH lesions did not differ from controls on EB responding during either adaptation or acquisition. However, lesioned animals revealed more EB CRs during extinction than control animals. EMG CRs were minimal in both groups of animals. Lesioned animals showed smaller HR changes than control animals during all phases of training, although HR CRs tended to consist of bradycardia in all animals. No differences were observed in either shock thresholds or open field activity as a result of LH lesions. Cortical and hippocampal 5-HT and NE concentrations were significantly depleted in lesioned as compared to control animals. These findings were interpreted within the framework of the phasic control of attention by midbrain modulation of forebrain structures; however, the interruption of downward going fibers which mediate brain stem cardiac control cannot be ruled out.

Age-related changes in pavlovian conditioning: Central nervous system correlates

Two groups of New Zealand Albino rabbits, average age 6 and 40 months, were subjected to Pavlovian conditioning in which eyeblink (EB) and heart rate (HR) responses were assessed. At the end of conditioning biogenic amine content was assessed in several brain areas; dopamine receptor binding was assessed in caudate nucleus. Older animals revealed an impairment in EB conditioning relative to the young animals; the conditioned decelerative HR response was increased in magnitude in the old animals. Significant deficits in cortical norepinephrine and serotonin were observed in the old subjects, but in both old and young animals the magnitude of the bradycardia was positively correlated with forebrain norepinephrine and inversely correlated with serotonin concentration. Receptor binding experiments revealed that 3H-spiroperidol receptor density was decreased in caudate nuclei of old animals; however, receptor affinity was unaffected by age.

An analysis of some perceptual effects of morphine, chlorpromazine, and LSD

Male albino rats were trained to detect either a pure tone or a weak footshock embedded in white noise by utilizing a discrete-trial two-choice, successive discrimination procedure. The effects of morphine, chlorpromazine (CPZ), and lysergic acid diethylamide (LSD) were then analyzed on several measures of performance. Morphine (2.5–10 mg/kg) produced a nonspecific decrease in accuracy of discrimination on trials when the stimulus was presented as well as on trials when no stimulus occurred. Morphine was also followed by dose-dependent decreases in speed to initiate trials and by increases in intersubject variability. CPZ (1.0–4.0 mg/kg) caused a decrease in accuracy only on no-stimulus trials and, like morphine, decreased speed to initiate trials. LSD (0.04–0.16 mg/kg) decreased overall accuracy in a nonspecific manner (i.e., when shock and tone discriminations were considered together) and decreased speed by producing periods of nonresponding.

CLASSICAL (PAVLOVIAN) CONDITIONING MODELS OF AGE-RELATED CHANGES IN ASSOCIATIVE LEARNING AND THEIR NEUROBIOLOGICAL SUBSTRATES

In the present paper, we will evaluate classical conditioning in both human and non-human animals as possible models for assersing the neurobiological mechanisms that underlie the learning and memory changes that occur in senescent organisms

Electrical stimulation of insular cortex elicits cardiac inhibition but insular lesions do not abolish conditioned bradycardia in rabbits

Conscious rabbits received electrical stimulation of insular and more posterior perirhinal cortex through chronically implanted electrodes. Active sites for cardiovascular responses were found in both anterior and posterior insular cortex as well as more posterior perirhinal regions. Although differential response topographies occurred related to anterior versus posterior insular cortex, all heart rate responses consisted of bradycardia. Pharmacological manipulations revealed that this bradycardia was due to a combination of vagal and sympatho-inhibitory mechanisms. Some posterior sites yielded pressor responses, and bradycardia which was sensitive to phentolamine, suggesting that the bradycardia in these instances was due to activation of the baroreceptor reflex. All other blood pressure changes were depressor responses. In a second experiment two different groups of rabbits with lesions of either anterior or posterior agranular insular cortex were compared with a third group of animals with sham lesions in a differential Pavlovian conditioning experiment. No lesion completely abolished the classically conditioned bradycardia associated with tone/shock contingencies. However, anterior insular lesions attenuated the magnitude of the conditioned bradycardia compared to the posterior and sham lesions. Control experiments suggested that this attenuation was due to the lesions effects on the conditioned stimulus/unconditioned stimulus association and not to its effects on unconditioned responding to the conditioned stimulus or unconditioned stimulus alone.

Naloxone induces multiple effects on aversive Pavlovian conditioning in rabbits.

A series of experiments examined the effects of intravenous naloxone treatment on aversive Pavlovian conditioning of eye-blink and heart rate responses, and related unconditioned behaviors, in rabbits. Naloxone treatment before testing attenuated bradycardiac orienting responses to tones used as conditioning stimuli. Naloxone also attenuated conditioned bradycardia when administered either before or after training sessions, but it potentiated conditioned bradycardia during extinction of discriminative conditioning. Naloxone did not influence acquisition or extinction of discriminative eye-blink conditioning or somatic or cardiac responses to shocks used as unconditioned stimuli, but it did decrease locomotor activity. Naloxone treatment immediately after training sessions facilitated acquisition of eye-blink responses. It was concluded that naloxone influences aversive Pavlovian conditioning in more than one way: (a) During training, it appears to alter reception and processing of signals but does not affect subsequent development of somatic responses to the Pavlovian conditioning contingency. (b) After training sessions, naloxone apparently affects consolidation of both somatic and autonomic conditioning. (c) Naloxone also appears to delay extinction of Pavlovian conditioning; this effect may similarly involve changes in a stimulus-processing mechanism or in memory functions, but it apparently does not involve changes in somatomotor responsitivity.

Ethanol enhancement of Pavlovian conditioning

Rabbits were tested for Pavlovian conditioning and extinction of eye blink and heart rate responses, following water or various doses of ethanol (375-1,500 mg/kg, po). The highest dose suppressed both eye blink and heart rate conditioning during training, whereas the lowest dose enhanced heart rate responses during training and increased eye blink responses during later extinction in a symmetrically state-dependent manner. An intermediate dose (750 mg/kg) administered during training enhanced heart rate responses and suppressed eye blink responses but increased eye blink responses during later extinction following either ethanol or water. Ethanol treatments also suppressed unconditioned responses to shock and increased locomotor activity in rabbits; however, these effects differed qualitatively from those that occurred during Pavlovian training and extinction. These results suggest that very low doses of ethanol can enhance the ability of stimuli to elicit Pavlovian conditioned reflexes and impair the ability to adaptively modify these reflexes when stimulus contingencies later change.

Effects of naloxone on pavlovian conditioning of eyeblink and heart rate responses in rabbits

Abstract Albino rabbits were subjected to aversive Pavlovian conditioning and extinction of eyeblink and heart rate responses. Naloxone administration had no effect on acquisition of the eyeblink response but increased responding during extinction. Naloxone also attenuated the bradycardiac heart rate CR, suggesting that endogenous opioids may be involved in mediating this response.

Effects of opiates on the discriminative stimulus properties of dopamine agonists

Two groups of rats were trained to discriminate the dopamine agonists amphetamine (0.75 mg/kg) or apomorphine (0.38 mg/kg) from saline in a two-lever operant task. Various doses of morphine and pentazocine were tested for generalization to and interference with the discriminative stimulus complexes produced by the dopamine agonists. Low doses of morphine appeared to produce a stimulus complex which is similar to that produced by apomorphine, but which differs from the produced by amphetamine. Pentazocine showed no evidence of generalization to either the apomorphine or the amphetamine cue. Neither opiate interfered with discriminative stimuli produced by the dopamine agonists, although decreases in the number of animals responding occurred.

Intraseptal scopolamine has differential effects on Pavlovian eye blink and heart rate conditioning.

The effects of intraseptal scopolamine hydrobromide injections on Pavlovian (classical) conditioning were evaluated, with tones used as the conditioned stimulus (CS) and a periorbital electric shock train as the unconditioned stimulus (UCS). Eye blink (EB) and heart rate (HR) conditioned responses were concomitantly recorded. Although injections of scopolamine into the medial septum impaired the acquisition of the Pavlovian conditioned eyelid reflex, these injections enhanced the magnitude of accompanying Pavlovian conditioned HR decelerations. However, scopolamine applied to the lateral septal area had no effect on EB conditioning, relative to the vehicle, but, like medial injections, enhanced the magnitude of the accompanying HR decelerations. These results are compatible with those of previous investigations: Medial septal dysfunction impairs somatomotor conditioning but leaves autonomic conditioning intact, and septal dysfunction produces a parasympathetic bias of the cardiovascular system.