Lateral septal lesions enhance conditioned bradycardia in the rabbit.

Abstract

albino rabbits received sham lesions or complete, medial, lateral, or posterior septal lesions and were subjected to differential conditioning in which tones of different frequencies served as conditioned stimuli and paraorbital electric shock was the unconditioned stimulus. Electromyographic (EMG), heart rate (HR), and blood pressure (BP) conditioned responses (CRs) as well as hippocampal rhythmic slow wave activity (RSA) were recorded. Lateral or complete septal lesions enhanced the bradycardiac HR CR but had no effect on the BP depressor response. Both unconditioned and conditioned EMG responses occurred infrequently and were unaffected by any lesion. Unconditioned HR responses and somatomotor threshold determinations to unsignaled electric shock were also unaffected by the lesions. Complete septal lesions increased locomotor activity relative to sham or other septal lesions. Little hippocampal RSA was detected in animals with medial lesions, but the HR CR was unimpaired in these animals. These data implicate the septo-hippocampal circuit in classical conditioning of cardiovascular changes and further suggest that diencephalic forebrain structures may modulate forebrain processing of sensory stimulation, perhaps in terms of assessing its biological significance.

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

“…In the present experiment, it was also found that the animals that received scopolamine application to the medial septal nucleus, which presumably disrupted function in this nucleus, had a larger magnitude HR CR. Although the present findings appear to replicate those of Powell et al (1982), it should be noted that damage to the medial septal nucleus in the latter study had no effect on bradycardiac conditioned HR responding whereas damage to the lateral septal nucleus did. In the present experiment, scopolamine applied to the medial septal nucleus had the same effect as damage to the lateral septal nucleus in the prior study.…”

“…These data thus suggest that limbic system substrates for classical conditioning are different, depending upon the response system assessed. In a previous article, Powell et al (1982) reported that radio-frequency lesions of the medial septal nucleus did not impair the Pavlovian conditioned HR response. In that study, however, it was found that lesions that damaged the lateral septal nu-cleus but left the medial septal nucleus intact exaggerated the magnitude of the bradycardiac response.…”

“…Lacey &Lacey, 1980, andPribram &McGuiness, 1975, in this regard). Acquisition of somatomotor behaviors (e.g., eye blink CRs), on the other hand, may represent processes associated with longterm information storage and retrieval mechanisms (Powell et al, 1982).…”

Dissociation of autonomic and behavioral components of conditioned fear during development in the rat.

“…The inference is that extrapyramidal motor structures are necessary for somatomotor conditioning but that HR conditioning is dependent on other structures, such as those of the limbic system. This argument has been advanced most recently by Powell and colleagues in numerous articles (Buchanan & Powell, 1982;Powell, Milligan, & Mull, 1982), which show that certain limbic system structures, such as the anterior cingulate cortex, may participate in Pavlovian autonomic conditioning in the rabbit. If such is the case, the following assumptions may be made.…”

Further implications of a computational model of septohippocampal cholinergic modulation in eyeblink conditioning

“…Further, the choice of injection site clearly affects different preparations differently. For example, scopolamine injected directly into the medial septum impairs eyeblink conditioning but not heartrate conditioning (Powell, Hernandez, & Buchanan, 1985)-probably only reflecting the fact that heartrate conditioning does not depend on the medial septum (Powell, Milligan, & Mull, 1982)-whereas medial septal lesions, which disrupt septohippocampal cholinergic pathways, devastate eyeblink conditioning (Berry & Thompson, 1979).…”