An Experimental ‘Dissection’ of the Septal Syndrome

Abstract

I present evidence from several different lines of investigation (including partial lesions, intraseptal and intrahippocampal drug injections, and surgical transections of the major fibre systems that enter, leave, or traverse the area) which indicates that individual components of the septal syndrome in the rat and cat reflect an interruption of different neural elements. The 'disinhibitory' effects of septal lesions on behaviour that is suppressed as a consequence of non-reward are due to an interruption of septo-hippocampal (or hippocampo-septal) connections that do not have a cholinergic synapse in the septum but do have one in the hippocampus. The inhibitory effects of punishment are not mediated by the same pathways but involve amygdalo-septal (no directionality intended) projections that have a cholinergic synapse in the septal area. This component of the septum may communicate with the hippocampus via entorhinal and periamygdaloid projections. This pathway does not appear to have a cholinergic synapse in the hippocampus. The effects of septal lesions on active avoidance are related to an interruption of at least two pathways. The facilitated shuttle box conditioned avoidance response acquisition is related mainly to an interruption of ventral connections of the septum with the lower brainstem. The impaired acquisition of most other avoidance problems seems to be due to an interruption of components of the stria medullaris. Both pathways have a cholinergic synapse in the septal area. The hyperdipsia, finickiness, and sudden weight loss are related to an interruption of pathways that interconnect the septum with the lower brainstem.