Brain amygdala

In REM sleep we see this reciprocity at the brain function level. The emotional brain (amygdala) is hyperactive. The executive brain (frontal cortex) is hypoactive. Result emotion is in the saddle. Rational thought is struggling—and failing—to get control of the runaway horse that is the dream. "Don t lose your temper, you say to yourself. This mantra says it all. If you can t maintain top-down control, your emotional brain will get the better of you. 

The following section explores the five areas most consistently found to be abnormal in postmortem studies of autistic brains - amygdala, septal nucleus, hippocampus, anterior cingulate cortex, and cerebellum - and discusses their hypothetical relationship to emotional and interpersonal psychopathology in autism. Note that other brain areas, which are inconsistently abnormal in neuropathological studies, may express inconsistent associated symptoms, variations in psychopathological subtypes, or inconsequential anomalies and are not discussed in this section. 

A mathematical relationship between the components of brain limbic system was proposed by Moren and Balkenius (2000) from the descriptive physical model of the limbic system that provides a qualitative sense of the overall functioning of the system. Figure 2 shows the structure of the Moren-Balkenius computational BEL model. As depicted in the figure, the BEL model has four components of the so-called limbic system of the brain amygdala, orbitofrontal cortex, sensory cortex and thalamus. Of them, amygdala and orbitofrontal cortex perform an important function in emotional processing (Moren and Balkenius 2000). 

Thyroid hormone receptors (THRs) are subdivided intoa and P types, each having two isoforms. In rat brain, THR, mRNA is present in hippocampus, hypothalmus, cortex, cerebellum, and amygdala. Thyroxine (l-T (284) and triiodothyronine (l-T ) (285) are endogenous ligands for the THRs. TRIAC (286) is a THR antagonist. Selective ligands for PPARs have yet to be identified (Table 16). 

Arousal is a state of vigilance regulated by subcortical parts of the nervous system, especially connections between the nuclei of the amygdala, the hypothalamus and the brain stem. These unconscious responses prepare the body for action. 

CRH (Corticotropin releasing hormone) is expressed in the nucleus paraventricularis of the hypothalamus and drives the stress hormone system by activating synthesis and release of corticotropin at the pituitary and in turn corticosteroid from the adrenal cortex. CRH is also expressed at many other brain locations not involved in neuroendocrine regulation, e.g. the prefrontal cortex and the amygdala. Preclinical studies have shown that CRH also coordinates the behavioral adaptation to stress (e.g. anxiety, loss of appetite, decreased sleepiness, autonomic changes, loss of libido). 

Collection of interconnected subcortical and cortical brain structures (including hypothalamus, amygdala, and hippocampus) integrating multimodal intero- and exteroceptive information to produce coherent neuroendocrine and behavioral output, and to support memory functions. 

Extrahypothalamic OX-B-like immunoreactivity, reminiscent to that of CRF, has been described in clustered GABAergic neuronal populations, in the lateral division of central nucleus ofthe amygdala, the bednucleus of the stria terminalis, and in the hippocampus. Moreover, ectopic expression of preproorexin mRNA in the gut, ependymal cells, neuroblastomas, and of orexin receptors in adrenal gland, cancer and hematopietic stem cells suggests yet unexplored roles of orexins as paracrine factors controlling blood-brain barrier, and tumor or stem cell function. 

Although the distribution of these receptors is widespread in the brain, they are found postsynaptically in high concentrations in the hippocampus, septum and amygdala and also on cell bodies of 5-HT neurons in the Raphe nuclei. They are negatively coupled, via Gj/o/z proteins, to adenylyl cyclase such that their activation reduces production of cAMP. In turn, this leads to an increase in K+ conductance and hyperpolarisation of... 

The use of labelled antibodies suggests their presence in the amygdala, septum, hypothalamus and cerebellum. However, little is known about these receptors, mainly because of the shortage, until recently, of selective ligands, their low density and the limited distribution of their mRNA in the brain. 

If a subconvulsive stimulus is applied, generally in rats, at regular intervals, e.g. daily for some two weeks to a specific brain area, especially the amygdala or hippocampus, then eventually full localised (partial) or secondary generalised seizures develop. A similar effect can be obtained by the repeated localised injection of subconvulsive doses of some convulsants. The ability of a drug to reduce the kindled seizure itself may be indicative of value in partial seizure but if it slows the actual development of kindling that may indicate some ability to retard epileptogenesis. 

There is no evidence of a general overactivity in DA function in schizophrenic patients. Plasma prolactin is not reduced, so the DA inhibitory control of its release is normal there is no recorded increase in DA turnover as CSF and plasma levels of its major metabolite HVA are normal and dyskinesias, which would reflect increased DA activity, are rare. PM studies have shown no consistent increases in DA brain levels, although some reports show an increase in the left amygdala, or in the activity of enzymes involved in its synthesis (tyrosine hydroxylase) or metabolism (MAO). For a review of the neurochemistry see Reynolds (1995). 

Lehman M.N. and Winans S.S. (1982). Vomeronasal and olfactory pathways to the amygdala controlling male hamster sexual behavior — autoradiographic and behavioral analyses. Brain Res 240, 27-41. 

Licht G. and Meredith M. (1987). Convergence of main and accessory olfactory pathways onto single neurons in the hamster amygdala. Exp Brain Res 69, 7-18. 

Luiten G.M., Koolhaas J.M., de Boer S. and Koopmans S.J. (1985). The cortico-medial amygdala in the central nervous system organisation of agonistic behaviour. Brain Res 332, 283-297. 

Raisman G. (1972). An experimental study of the projection of the amygdala to the accessory olfactory bulb and its relationship to the concept of a dual olfactory system. Exp Brain Res 14, 395-404. 

The pathologic hallmarks of the disease in the brain include neurofibrillary tangles and neuritic plaques made up of various proteins, which result in a shortage of the neurotransmitter acetylcholine. These are primarily located in brain regions involved in learning, memory, and emotional behaviors such as the cerebral cortex, hippocampus, basal forebrain, and amygdala.11... 

O Virtually all abused substances appear to activate the same brain reward pathway. Key components of the reward pathway are the dopamine (DA) mesocorticolimbic system that projects from the ventral tegmental area (VTA) and the nucleus accumbens (NA) to the prefrontal cortex, the amygdala, and the olfactory tubercle (Figs. 33-3 and 33-4).5 Animal studies... 

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