Database of diseases - Practical psychiatry and psychogeriatry

  In recent years, neuropharmacologists have associated the emergence of anxiety among others with increased galanin production. . Galanin is a neuropeptide of 29- or 30 amino acids. Its wide range of functions include modulation of feeding behavior, gastrointestinal motility, perception of pain, memory and learning, work of the cardiovascular system as well as mood and anxiety. The physiological effects of galanin are relieved by three subtypes (Gal1, Gal2, Gal3) of receptors that signal via G proteins (G-protein-coupled receptors, GPCR), with wide distribution through the central nervous system and nerves. Of these three subtypes, the dense placement of GAL3 in areas of the brain responsible for emotions, such as the hypothalamus and brainstem nucleus (dorsal suture and locus coeruleus) make this the most attractive pharmacological goal. Selected GAL3 antagonists (SNAP 37889 and SNAP 398299) have been shown to have both potent and long-lasting anxiolytic and anti-depressant properties in several animal models. This is due to the partial weakening of the inhibitory effect of galanin on 5-HT transmission on the dorsal nucleus. Recently, a non-specific galanin receptor antagonist, galnon, has been found to have an anxiolytic effect in several groups of rodents. The clinical potential of galanin modulation has been noticed in both severe stress and chronic anxiety. Neuropeptide Y and anxiety   . NPY is the most potent physiological stimulus of anxiety behavior. This neuropeptide, the most abundant peptide in the mammalian brain, is a 36-amino acid polypeptide, rich in tyrosine deposits, with a molecular weight of 4.272 Da. There are six recognized NPY receptor subtypes (Y1-Y5) present in the brain and other tissues. It is co-localized along with norepinephrine in sympathetic nerve fibers and present in noradrenergic, intestinal, cardiac parasympathetic and parasympathetic nerves. It is characterized by sympathetic hyperactivity and is of great importance for anxiety disorders, NPY is released from cardiac sympathetic nerves and appears in marked amounts in the blood in the coronary sinus. In the brain, the main NPY sites are the cerebral cortex, the locus coeruleus, the hippocampus, the brainstem, and the hypothalamus, where its highest concentrations are present. NPY is of interest because of its potential role in modulating mood and anxiety. The basic levels of NPY in war veterans with PTSD were limited compared to healthy people. Another study showed that repetitive stress was associated with the reduction of NPY levels. It was also found that decreased NPY levels in CSF occur in patients with treatment-resistant unipolar acute depression. The anxiolytic action of NPY has also been observed in the work on animal models of these behaviors. (test of the elevated cross maze. Upregulation of NPY mRNA levels in the amygdalae nucleus after chronic stress suggests a potential involvement in adaptive stress responses. According to this view, elevated NPY levels were observed in war veterans with no current PTSD, compared to soldiers who did not take part in combat, and an increase in NPY was associated with the disappearance of previous PTSD symptoms. (Sanjay J. Mathew, Rebecca B. Prince, Dennis S. Charney: Recent advances in the neurobiology of anxiety disorders: the consequences of new therapies in: Difficult problems in psychiatric practice. (edited by J. Krzyżowski). Medic. 2009.) .
Doctor of Medicine Janusz Krzyżowski
Psychiatrist
Private office tel. 22 833 18 68
00-774Warszawa, Dolna 4 lok. 15 .   Neuroanatomy of anxiety The basic area of ​​the brain involved in creating the sense of fear is the amygdala, which coordinates the immediate reaction of the threat, integrating information from sensory elements, context and previous experience, through cortical inflow and subcortical stimuli. In a typical response to mammalian fear, sensory information reaches the amygdala via the anterior part of the thalamus, inducing in the nucleus the onset of behavioral and autonomous reactions of the nervous system through projection to motor parts and brainstem nuclei. A meta-analysis of neuroimaging studies showed that, according to literature, the fear stimulus specifically activates the amygdala in healthy people. Human models of Neurodulation suggest that amygdala is regulated by top-down management of central prefrontal areas, including the orbita-frontal cortex and anterior cortex, as well as the hippocampus, allow specific information such as context, explicit memories, and conscious self-regulation to influence to respond to a threat. Mutual communication between the amygdala and the prefrontal cortex is established as a mechanism to alleviate fear. In patients with anxiety disorders, the characteristic pattern of increased amygdalental reactivity to the threat has been documented in a wide range of disorders and can be observed at very early stages of processing, including the moment when the masked stimulus design prevents the conscious knowledge of the stimulus.

     Neurochemistry of anxiety  

The task of determining the clear neurochemical basis of anxiety is complicated by the high level of comorbidity of anxiety disorders and mood disorders and the overlapping of many other symptoms. The significant role of monoamine neurotransmitters in anxiety (e.g., serotonin, norepinephrine), well-known for their role in mood disorders, is analyzed in many works. However, the most important goals of drug neurochemistry are three aspects of anxiety neurochemistry, which may be very promising as new targets for pharmacotherapy: corticotropin releasing factor (CRF) and hypothalamic-pituitary-adrenal axis; glutaminerganic system; neuropeptides (substance P, neuropeptide Y, oxytocin, orexin, and galanin).

 

Sanjay J. Mathew, Rebecca B. Prince, Dennis S. Charney: Recent advances in the neurobiology of anxiety disorders: the consequences of new therapies. In: Difficult problems in psychiatric practice (ed. J. Krzyżowski). Medic. 2009.)

 

 

.
Doctor of Medicine Janusz Krzyżowski
Psychiatrist
Private office tel. 22 833 18 68
00-774Warszawa, Dolna 4 lok. 15