The Pineal Hypothesis for Drug Dependence

The pineal gland constitutes a major neuroendocrine organ in the brain. By mean of its neurohormone melatonin it transduces exogenous signals such as circadian and seasonal variations of light and temperature into proper hormonal changes which adjust and adapt internal endocrine functions. Alteration of circadian rhythms has been associated with affective disorders, psychosomatic diseases and cancer. It has been observed that light deprivation, which stimulates (the enzymes responsible for) melatonin production in the pineal, enhances the animal's ethanol preference. Similarly, administration of the pineal hormone to rats maintained under normal conditions of constant photoperiod also induced ethanol drinking. Our hypothesis is that in normal conditions melatonin might be acting as a cerebral "pacemaker", sensitive to endogenous as well as exogenous stimuli in the attempt to maintain an equilibrate circadian interaction between the cerebral activities of endogenous aminergic and opiates systems. Abnormal states (i.e. drug abuse) could result in altered pineal activity, then in rhythmically altered functions of cerebral opiates and/or monoamine neurotransmitters. This may led to the development of a “reward - urge for drug rhythm” resulting in craving, ending in addiction.

Pineal Gland—A Spiritual Third Eye: An Odyssey of Antiquity to Modern Chronomedicine

Pineal gland or “spiritual third eye” is regarded as the gateway of spiritual life as per ancient concepts about the soul. Recently, modern neuroscience has proven that pineal gland is not only the melatonin-secreting neuroendocrine organ which controls the circardian rhythm, but it also has mystical and energetic associations with spirituality. It acts as a tremendous coordinator between molecular, hormonal, physiological, and chemical rhythmic orchestra. Thus, in this article, by highlighting the relation between ancient Indian methodology and modern chronomedicine, the author describes the odyssey of antiquity to modern science.

Identification of peptides from sinus gland extracts in the red swampcrayfish Procambarus clarkii by mass spectrometry

Crustacean sinus gland (SG) is a well-defined neuroendocrine organ that controls the secretion of various neuropeptides which regulate many physiological activities. The red swamp crayfish Procambarus clarkii is a decapod crustacean with both high economic and scientific importance in China. To facilitate physiological investigations of SG peptide/hormone function in this species, we have been employed tissue extract fractionation by HPLC to obtain a complete description of neuropeptidome and used Electrospray ionization-Fourier transform mass spectrometry (ESI-FTMS) to detect the peptidome present in its organ. In total, 48 peptide sequences belonging to several known neuropeptide families including crustacean cardioactive peptide, CHH precursor-related peptides (CPRPs), orcokinins and pigment dispersing hormones were identified. Among these 48 sequences, 26 are novel peptides and 22 are previously identified. Overall, the results give a stimulus for future physiological studies of SG neuropeptides in P. clarkii and other crustaceans.

Adrenal Neoplasia

The adrenal glands are composed of two distinct tissue types: the cortex, which serves as a factory for adrenal steroidogenesis, and the medulla, which produces catecholamines as a neuroendocrine organ. Neoplasia of the adrenal is approached by considering both whether the tumor is benign or malignant and whether it may represent a hormonally active tumor that can contribute to cardiometabolic disease or a hormonally silent tumor. Adrenal neoplasia is rarely malignant. This module discusses the approach to an incidentally discovered adrenal mass, with emphasis on the clinical determination as to whether it is benign or malignant and hormonally functional or nonfunctional. The pathogenesis and genetics of hyperaldosteronism and pheochromocytoma-paraganglioma are reviewed, as are the pathogenesis and management of adrenocortical carcinoma. Tables describe the differential diagnosis and diagnostic approach for an incidentally discovered adrenal mass; suggested biochemical screening tests for incidentally discovered adrenal masses; radiographic features of adrenal masses to determine benign or malignant potential; and the genetics of primary hyperaldosteronism, pheochromocytoma, and paraganglioma syndromes. A drawing shows the genetic mechanisms of hyperaldosteronism in familial hyperaldosteronism type III. Algorithms outline the suggested management approach for the incidentally discovered adrenal mass, genetic counseling and testing for patients with pheochromocytoma or paraganglioma, testing for family members of patients with pheochromocytoma and positive genetic testing, patients with stage I–III adrenocortical carcinoma, and patients with advanced adrenocortical carcinoma. This module contains 6 highly rendered figures, 6 tables, 55 references, and 5 MCQs.