Ghrelin-containing neurons in the olfactory bulb send collateralized projections into medial amygdaloid and arcuate hypothalamic nuclei: neuroanatomical study

Abstract

Ghrelin, a gastrointestinal hormone, is a modulator of the sense of smell. The main source of ghrelin in the central nervous system has been mainly observed in specific populations of hypothalamic neurons. An increasing number of studies have reported ghrelin synthesis and its effect on neurons outside the hypothalamus. Ghrelin and its receptors are expressed in the olfactory bulbs and in other centres of the brain, such as the amygdala, for processing olfactory signals, pyramidal neurons of the cerebral cortex and the dorsal vagal complex of the medulla oblongata. It is known that ghrelin is involved in cognitive mechanisms and eating behaviours, in fact, its expression increases in anticipation of food intake. In order to identify the existence of centrifugal direct afferents from the main olfactory bulb to the medial amygdala and the hypothalamus arcuate nucleus, in this work we used two retrograde tracers, Dil and Fluoro Gold, and immunohistochemical procedure to visualize positive ghrelin neurons. Our paper provides neuroanatomic support for the ghrelin modulation of smell. Our results show that ghrelin neuron projections from mitral cells of bulbs can transmit olfactory information via branching connections to the amygdala and the hypothalamus. This pathway could play an important role in regulating feeding behaviour in response to odours.

Reduced Olfactory Bulb Volume in Obesity and Its Relation to Metabolic Health Status

“…It has recently been shown that hormones whose homeostatic signaling may be impaired in obesity (Baly et al, 2007;Aime et al, 2012;Russo et al, 2018), modulate olfactory performance in humans. More specifically, intranasally applied insulin as well as intravenously applied ghrelin improve olfactory function (Tong et al, 2011;Thanarajah et al, 2019).…”

Potential Role of Hypothalamic and Plasma Ghrelin in the Feeding Behavior of Obese Type 2 Diabetic Rats with Intraventricular Glucagon-Like Peptide-1 Receptor Agonist Intervention

“…Therefore, our results can lead to at least two different interpretations. On the one hand, ICV Ex-4 administration could activate ghrelin-producing neurons adjacent to the 3rd ventricle to induce feeding, and then Ex-4 may permeate the blood-brain barrier to further stimulate ghrelin-producing cells in the stomach to subsequently regulate feeding [30, 31]. On the other hand, central Ex-4 administration may regulate gastric ghrelin expression directly through the neural signals transmitted by the vagal nerve, which in turn regulates feeding [32-34].…”

Ghrelin as a prominent endocrine factor in stress-induced obesity

“…The ghrelin receptor GHS-R1a is expressed in hypothalamic neuropeptide Y-(NPY) and agouti-related peptide-(AgRP) expressing neurons (NPY/AgRP neurons), somatotropic cells and luteinising hormone (LH)-, thyroid-stimulating hormone (TSH)-, adrenocorticotropic hormone (ACTH)-and prolactin-(PRL) releasing cells in the anterior pituitary [26][27][28][29]. A lower expression of GHS-R1a is found in other brain regions such as the cingulate gyrus [30][31][32], amygdala, olfactory bulb and in hypothalamic ghrelin-receptive neurons adjoining the dorsal vagal complex (DVC) [33]. The expression of GHS-R1a is found across three distinct brain areas: pituitary gland (i.a.…”