This chapter describes how loss of synapses on dendrites of particular neurons can lead to PTSD and its dissociative subtype. In this context, cortical layer 5 pyramidal neurons (L5PNs), together with their apical tuft, oblique and basal dendrites, which respectively receive non-specific thalamic, cortico-cortical and specific sensory synaptic inputs, are highlighted. Using dendritic integration theory (DIT), the model shows how coincident apical tuft and basal activation, facilitated by synapses on oblique dendrites, generates somatic action potential bursting. It is this dendro-somatic electrical coupling of L5PNs that mediates intransitive and transitive consciousness. In contrast, loss of apical synapses and their dendrites, under chronic stress as in PTSD, reduces tuft depolarization and decreases burst firing, thereby producing dissociative symptoms, like derealization and depersonalization. The model is further used to show how integration of optogenetic and anaesthetic studies, together with biophysical network modelling of DIT, can reveal how thalamocortical non-specific inputs regulate coupling and spatial correlation to shape states of consciousness, in particular intransitive and transitive consciousness. DIT can then provide an explanation for how stress-induced synaptic spine loss and apical dendritic retraction can give rise to distortions of consciousness as can occur in PTSD.