Regulation anxiety

Methodological differences may account for discrepant results found with the same neuropeptide. A major weakness of many of the studies mentioned in this review is that they examined only one element of a complex neuropep-tidergic system in a single brain region at a certain time point. Future studies in which multiple components of neuropeptidergic systems are all studied at once and in various brain areas in their dynamics will aid in understanding how the individual elements of this system co-ordinate their activity in regulating anxiety-related behaviour. 

Noradrenergic model. This model suggests that the autonomic nervous system of anxious patients is hypersensitive and overreacts to various stimuli. The locus ceruleus may have a role in regulating anxiety, as it activates norepinephrine release and stimulates the sympathetic and parasympathetic nervous systems. Chronic noradrenergic overactivity down regulates 02-adrenoreceptors in patients with generalized anxiety disorder (GAD) and posttraumatic stress disorder (PTSD). Patients with social anxiety disorder (SAD) appear to have a hyperresponsive adrenocortical response to psychological stress. 

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). 

The evidence outlined so far does little to explain how monoamines or anti-anxiety drugs might influence anxiety states. To achieve this, an integrated view of the relevant brain systems is required, together with an appreciation of how their function is regulated. 

Perturbation of the 5-HT system can elicit changes in a wide variety of behaviors. Furthermore, drugs that act on serotonergic neurons and their receptors are used to treat diseases such as depression, anxiety disorders and schizophrenia. Thus, 5-HT has been implicated in the regulation of many behaviors and physiological processes. The involvement of 5-HT in three areas - neuroendocrine function, circadian rhythms and feeding behavior - will be highlighted for illustrative purposes. 

There are gradients of health status across income and education (referred to as socioecomic status or SES ) that are not explained by access to health care or other simple explanations [40]. Therefore, it may be of great relevance in the future to understand the role of such factors as sense of control, helplessness, persistent fear and anxiety, diet, exercise, and the impact of the living and social (e.g. family and work) environments in regulating the allostatic systems these factors could cause allostatic systems to operate inefficiently and lead to an acceleration of genetic predispositions towards disease. 

Substance P, an undecapeptide, is abundant both in the periphery and in the central nervous system. It is usually co-localized with one of the classical neurotransmitters, most commonly serotonin. Substance P is thought to have a role in the regulation of pain, asthma, psoriasis, inflammatory bowel disease and, in the CNS, emesis, migraine, schizophrenia, depression and anxiety. The substance-P-preferring receptor neurokinin-1 has been focused on most intensively in drug development, and existing... 

Neuropeptide Y (NPY) and its receptors may also be important in the regulation of anxiety and stress. NPY is synthesized in the arcuate nucleus, which receives LC input. In a number of rodent models, NPY administration has anxiolytic and, at somewhat higher doses, sedative effects. Likewise, NPY antagonizes CRH-induced stress responses, and suppresses LC firing when injected... 

Sanders SK, Shekhar A. (1995). Regulation of anxiety by GABAA receptors in the rat amygdala. Pharmacol Blochem Behav. Dec 52(4) 701-6. 

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