Septal area

Berridge, CW (1998) Modulation of forebrain electroencephalographic action and behavioral state by locus coeruleus-noradrenergic system involvement of the medial septal area. Adv. in... 

The neural structures involved in the promotion of the waking (W) state are located in the (1) brainstem [dorsal raphe nucleus (DRN), median raphe nucleus (MRN), locus coeruleus (LC), laterodorsal and pedunculopontine tegmental nuclei (LDT/PPT), and medial-pontine reticular formation (mPRF)] (2) hypothalamus [tuberomammillary nucleus (TMN) and lateral hypothalamus (LH)[ (3) basal forebrain (BFB) (medial septal area, nucleus basalis of Meynert) and (4) midbrain ventral tegmental area (VTA) and substantia nigra pars compacta (SNc) (Pace-Schott Hobson, 2002 Jones, 2003). The following neurotransmitters function to promote W (1) acetylcholine (ACh LDT/PPT, BFB) (2) noradrenaline (NA LC) (3) serotonin (5-HT DRN, MRN) (4) histamine (HA TMN) (5) glutamate (GLU mPRF, BFB, thalamus) (6) orexin (OX LH) and (7) dopamine (DA VTA, SNc) (Zoltoski et al, 1999 Monti, 2004). 

Olds, J. and Milner, P. (1954) Positive reinforcement produced by electrical stimulation of septal area and other regions of rat brain. J. Comp. Physiol. Psychol. 47, 419-427. 

Gorman L, Pang K, Frink K, Givens B, Olton D. 1994. Acetylcholine release in the hippocampus Effects of cholinergic and GABAergic compounds in the medial septal area. Neuroscience Letters 166(2) 199-202. 

Forehmin frontal cortex olfactory nucleus nucleus accumbens septal area amygdala hypothalamus entorhinal cortex caudate nucleus entopeduncular nucleus hippocampus ventral and medial thalamus median forebrain bundle dorsal noradrenergic bundle... 

This neurotransmitter is contained in a few pathways, of which the midbrain raphe nuclei to the limbic-septal area (e.g., hippocampus and amygdala) is probably the most important. Serotonin abnormalities are widely reported in patients with depression, especially those with suicidal behavior, including the following ... 

Medium-high density of D2 receptors was found in the islands of Calleja, ventral pallidum, zona incerta, GP, central amygdala, in some cells of the anterior lobe of the pituitary, and at several sites in the forebrain the laterodorsal septal area, hippocampus, subiculum, lateral habenula, STh, lateral mammillary bodies. D2 receptors were also found with a medium-high density in various cortical fields prefrontal, anterior cingulate, entorhinal and perirhinal cortices. In the brain stem, medium-high density of D2 receptors was found in the VTA, SNc, ventral SNr, parabrachial nucleus, superior and inferior colliculi, dorsal raphe nucleus and locus coeruleus. 

Medium-high density of D3 mRNA was described in the septal area, in the medial division of the bed nucleus of the stria terminalis, in the nuclei of the horizontal and vertical limbs of the diagonal band, in the nucleus gelatinous and paracentral nucleus of the thalamus, in the medial and ventral lateral geniculate nuclei, and in the lateral portion of the SNc. 

Gaspar P, Berger B, Alvarez C, Vigny A, Henry JP (1985) Catecholaminergic innervation of the septal area in man immunocytochemical study using TH and DBH antibodies. J Comp Neurol 247 12-33. 

Meibach RC, Siegel A (1977a) Efferent connecdons of die septal area in die rat An analysis udlizing retrograde and anterograde transport mediods. Brain Res 119 1—20. 

Fig. 32.17 Congenital liver fibrosis onset of drrhotic transformation, pathologically augmented bile-duct aggregates in portal and septal areas (Sirius red)...

Since the high-septal area is depolarised after the first 40 milliseconds, the infarction of this area does not generate vector of infarction that can originate Q waves. In these cases, changes the final portions of the QRS complex may be present. For the typical pattern of this type of infarction to appear, it is required, then, that the infarction involves the middle-low portion of the septum. The other parts may or may not be involved. 

Hartgraves, S.L., Mensah, P.L., and Kelly, P.H., Regional decreases of cortical choline acetyltransferase after lesions of the septal area and in the area of the nucleus basalis magnocellularis. Neuroscience, 7, 2369, 1982. 

ACTH or MSH to the smaller melanocortins such as ACTH 4-9 or ACTH 4-10, although im-munoreactivity to ACTH 4—10 has been demonstrated in the septal area and perimeter of the third ventricle, including the median eminence (Lee et al., 1992). 

In quantitative studies using a radiolabelled MSH tracer, MSH was shown to bind most intensely in the septal area, septohypothalamic nucleus, the bed nucleus of the stria terminalis and the medial preoptic area. Moderate binding was seen in hypothalamic structures including the median eminence, the ventromedial, dorsomedial, arcuate and paraventricular nuclei, and the lateral hypothalamus. These structures are profusely innervated by immunoreactive ct-MSH- and ACTH-containing fibers (Eskay et al., 1979 O Donohue et al., 1979 Guy et al., 1980 Joseph, 1990). The median eminence is also well supplied with MSH receptors, supporting a role for this structure by which peripherally administered neuropeptides may penetrate to exert their central effects (Banks and Kastin, 1988). 

Within the prosencephalon, FGF-1 positive neurons are sparse in the cerebral cortex and hippocampus, but abundant in the septal area, nucleus basalis, and select nuclei of the thalamus (paraventricular, anterodorsal, lateral geniculate) and hypothalamus (lateroanterior). Other areas including pallidum and many thalamic and hypothalamic nuclei contain smaller but still substantial numbers of FGF-1 im-munoreactive neurons (Stock et al., 1992). 

Aggressiveness results from the failure of inhibitory neurochemical processes or exaggeration of stimulatory processes in brain regions, such as the orbito-ffontal cortex, the septal area, hippocampus, amygdala, caudate nucleus, thalamus, ventro-medial and posterior hypothalamus, midbrain tegmentum, pons, and the fastigial nuclei and anterior lobe of the cerebellum. 

Neuropathological examination of the four patients who died indicated neuronal necrosis and astrocytosis, particularly in the hippocampus and the amygdaloid nucleus. All four victims also had lesions in the claustrum, secondary olfactory areas, the septal area, and the nucleus accumbens septi. Two had prominent thalamic damage, especially in the dorsal medial nucleus. The subfrontal cortex was also damaged in three of the patients. The authors noted that the pattern of damage in the hippocampus appeared to parallel that seen in animals that suffered neurotoxic reactions after administration of kainic acid (and domoic acid see above). 

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