For example, hypothalamic nuclei project to visceral nuclei in both the medulla oblongata and the spinal cord; in the spinal cord these projections terminate upon cells of the intermediolateral cell column in thoracic, lumbar, and sacral segments.
In Migraine, clear examples of monoaminergic brainstem activation come from both neurophysiology [12, 47] and neuroimaging studies where the dorsal rostral brainstem, which contains state-setting aminergic, including serotonergic, nuclei projecting to the thalamus and cortex, was activated immediately before [48] and during an attack of episodic [49, 50] and chronic [4, 51] migraine.
With respect to the thalamostriatal system, different thalamic nuclei project selectively to either the CN or the Put [71] [77].
In detail, the axons arising in the ventroposterolateral and the ventroposteromedial nuclei project to primary somatosensory cortex in the postcentral gyrus (Brodmann areas 3a, 3b, 1, and 2), to the secondary somatosensory cortex in the parietal operculcum, and to the insula [49], [53].
Conversely, most thalamic nuclei project to more than one cortical area injected in this study.
The anterior thalamic nuclei project directly to the hippocampal formation via the cingulum bundle.
The CL and CM nuclei project to all 6 cortical areas in various proportions, reaching up to 13% for the CL projection to PMd in MK2.
Those injections involving the basal nuclei are of particular interest as there is evidence from retrograde tracers (Buckwalter et al., 2007) that these nuclei project lightly to the retrosplenial cortex.
The anterior thalamic nuclei project via the retrosplenial cortices to the hippocampus [ 51, 52], thus underlying the importance of both these circuits and of PTPH1 in the mnemonic process.
These nuclei project to the pituitary via the median eminence, where they release vasopressin and oxytocin, peptides involved in reproduction, regulation of blood pressure, and control of the hypothalamic-pituitary-adrenal (HPA) axis [reviewed in [ 97]].
