No description available.

No description available.

No description available.

In teleost fishes the neurochemicals involved in sensing and responding to hypoxia are unresolved. Serotonergic branchial neuroepithelial cells (NECs) are putative O2 chemoreceptors believed to be homologous to the neural crest (NC) derived APUD (amine-precursor uptake and decarboxylation) pulmonary NECs and carotid body type-1 glomus cells. Branchial NECs contain serotonin (5-HT), thought to be central to the induction of the hypoxic cardioventilatory reflexes. However, application of 5-HT in vivo does not elicit cardioventilatory reflexes similar to those elicited by hypoxia. But previous in vitro neural recordings from glossopharyngeal (IX) afferents innervating O2 chemoreceptors in the trout gill show the same discharge response to hypoxic conditions as does that of acetylcholine (ACh) application. This evidence strongly supports the cholinergic hypothesis of chemoreceptor impulse origin rather than a serotonergic-induced impulse origin model. We therefore hypothesized that NECs contain ACh among other neurochemicals in cells belonging to the APUD series. Although serotonergic branchial NECs did not colocalize with ACh using immunohistochemical methods, several populations of ACh and/or tyrosine hydroxylase (TH) (catecholaminergic) positive, dopamine (DA) negative, cells were found throughout the second gill arch of the channel catfish Ictalurus punctatus. In addition, the NC derivation marker zn-12 labelled the HNK-1-like epitope (Human natural killer) expressed by lamellar pillar cells’ collagen column-associated pillar cell adhesion molecules (CC-PCAMs), evidence confirming their hypothesized NC origin.

Thesis (Ph. D.)--Ohio State University, 2003. / Title from first page of PDF file. Document formatted into pages; contains xii, 120 p.; also includes graphics. Includes bibliographical references (p. 110-120).

Thesis (Ph. D.)--University of Chicago. / Includes bibliographical references. Also available on the Internet.

Thesis (M.S.)--Texas State University-San Marcos, 2006. / Vita. Appendix: leaves 31-35. Includes bibliographical references (leaves 36-39).

Thesis (M.S.)--Texas State University-San Marcos, 2006. / Vita. Appendix: leaves 31-35. Includes bibliographical references (leaves 36-39).

Proefschrift Universiteit Maastricht. / Met bibliogr., lit. opg. - Met samenvatting in het Nederlands.

The mammalian pineal gland is mainly innervated by the sympathetic nervous system which modulates the activity of indole pathway enzymes and the secretion of pineal hormones. Recently researchers have demonstrated and characterized the presence of muscarinic cholinergic receptors in the pineal gland. However the role of these receptors remains unclear. In an attempt to investigate the role of cholinergic receptors in the pineal gland, a number of studies were carried out on the various steps in the indole metabolic pathway, using various agents which act on the cholinergic system. Investigations using pineal organ cultures showed that stimulation of these muscarinic cholinergic receptor sites with a parasympathomimetic agent, a rise in levels of aHT occurred without a concomitant increase in aMT levels. Further organ culture experiments using the cholinergic agonist acetylcholine and anticholinesterase agent physostigmine, produced a similar rise in aHT without altering aMT levels. This acetylcholine-induced rise in aHT levels were not altered by the ganglion blocking agent hexamethonium whilst the antimuscarinic agent atropine prevented the acetylcholine-induced rise in aHT levels. Thesefindings suggest that cholinergic agents may play a role in regulating indoleamine synthesis in the pineal gland. Cyclic-AMP assay studies showed that acetylcholine increases pineal cAMP levels significantly and does not influence the isoproterenol-induced cAMP rise in the pineal gland. The cAMP regulator cAMP-phosphodiesterase (cAMP-PDE) was found to increase significantly in the presence of the anticholinesterase agent physostigmine. NAT enzyme studies revealed that physostigmine does not affect NAT enzyme levels significantly and HIOMT studies showed that this agent does not inhibit HIOMT activity. The mechanism by which acetylcholine and physostigmine are able to cause a increase in aHT and not aMT levels needs to be researched further. Acetylcholinesterase enzyme assay studies revealed that the AChE enzyme undergoes a diurnal rhythm in the pineal gland with activity being higher during the day and lower at night. Investigations using the drug reserpine showed that this rhythm is not under the control of the sympathetic nervous system. Further research needs to be done however, in determining whether or not this enzyme is present in the pineal gland to regulate the levels of acetylcholine interacting with muscarinic receptors in the gland, or for some other reason. Choline acetyltransferase studies demonstrate the presence of the enzyme in the rat brain cerebral cortex as well as showing that melatonin increases ChAT enzyme activity in this tissue. This suggests that melatonin plays a role in cholinergic transmission there. ChAT activity could not be measured in the pineal gland however. Muscarinic receptor binding studies also carried out on rat brain cerebral cortex show that melatonin enhances cholinergic receptor affinity and receptor number in this tissue. In summary, data presented herein concur with proposals that: i) the cholinergic system affects the indole metabolic pathway by causing a rise in aRT but not aMT levels. ii) cholinergic agonist acetylcholine causes cAMP levels to rise with a concomitant increase in cAMP-PDE levels. iii) the enzyme acetylcholinesterase undergoes a diurnal rhythm in the pineal gland which is not under the control of the sympathetic nervous system. iv) the activity of the enzyme choline acetyltransferase is increased by melatonin in the rat brain cerebral cortex suggesting that melatonin facilitates cholinergic transmission in this tissue. v) melatonin enhances cholinergic receptor affinity and receptor number in the cerebral cortex of rat brain.