| dc.contributor.author | Bina, K. G. | en_US |
| dc.date.accessioned | 2014-10-21T12:38:49Z | |
| dc.date.available | 1992 | |
| dc.date.issued | 1992 | en_US |
| dc.identifier.other | AAINN76701 | en_US |
| dc.identifier.uri | http://hdl.handle.net/10222/55301 | |
| dc.description | In mammals, the generation of circadian rhythms and their synchronization to environmental cues are under the control of the suprachiasmatic nucleus (SCN) of the hypothalamus. Brief light exposure of an animal maintained in otherwise constant darkness is capable of causing a shift in the phase of its circadian rhythms, the direction and amplitude of which depend on the time of administration of the light pulse. A plot of such shifts is called a phase response curve (PRC). Daily repetition of such pulses ultimately entrains the circadian system. | en_US |
| dc.description | Retinal ganglion cells convey photic information necessary for rhythm entrainment to the SCN, where they release neurotransmitters to initiate the phase shifting process. Various agonists of putative transmitters at these terminals have been injected into the SCN to test for their capacity to mimic the effects of light. A PRC for carbachol, a non-specific cholinergic agonist, partially mimics the PRC for light, implicating the involvement of acetylcholine (ACh) in photic transmission. This study was aimed at investigating the potential roles of ACh and the neurotrophic factor for central cholinergic neurons, nerve growth factor (NGF), in the process of entrainment of activity rhythms in rodents, using several anatomical and behavioural approaches. | en_US |
| dc.description | Receptor binding studies in hamsters revealed the presence of muscarinic receptors in the SCN, suggesting that cells there are responsive to ACh. Fibers and fiber terminals immunoreactive for choline acetyltransferase (ChAT), the synthetic enzyme for ACh, are found in the rat SCN, suggesting that ACh is released from the terminals of neurons located elsewhere in the brain that project to the SCN. Anterograde tracing studies and a combination of retrograde tracing techniques and immunocytochemistry for ChAT showed that the cholinergic fibers in the SCN arise from cholinergic cells located in the basal forebrain and mesopontine tegmentum. | en_US |
| dc.description | The ventrolateral SCN shows strong immunoreactivity for receptors for NGF (NGF-R). Retrograde tracing techniques combined with immunocytochemistry for NGF-R and ChAT revealed that some of these receptors are located on the terminals of cholinergic cells in the basal forebrain that project into the SCN. Studies involving optic nerve transection and a combination of retrograde tracing techniques and immunochemistry for NGF-R showed that NGF-R are also located on the terminals of retinal ganglion cells in the SCN. | en_US |
| dc.description | Carbachol, administered through indwelling cannulae in the SCN of hamsters, produces phase advances during late subjective night (circadian time (CT) 22) and subjective day (CT6), whereas it produces phase delays during the early subjective night (CT14). Carbachol-induced phase shifts at all three phases were blocked by atropine, a muscarinic antagonist, and not by mecamylamine, a nicotinic antagonist, suggesting that carbachol mediates its phase shifting effects through muscarinic receptors. | en_US |
| dc.description | NGF administered in the same way caused phase advances at CT22 and CT6 and phase delays at CT14. NGF-induced phase shifts at CT6 and CT22 were blocked by an antibody to NGF or by the muscarinic antagonist atropine, indicating that its effects are mediated by a cholinergic mechanism. The failure of both anti-NGF and atropine to block such shifts at CT14, and the induction of phase shifts by Cytochrome-c (biochemically similar to NGF without its receptor binding capabilities) at that phase, suggest that phase shifts induced by NGF at this phase are non-specific. | en_US |
| dc.description | Taken together, these findings suggest that ACh released from the terminals of cholinergic cells that project into the SCN acts on muscarinic receptors, and NGF released from cells in the SCN acts on NGF-R to contribute to phase shifting of the rodent circadian pacemaker. | en_US |
| dc.description | Thesis (Ph.D.)--Dalhousie University (Canada), 1992. | en_US |
| dc.language | eng | en_US |
| dc.publisher | Dalhousie University | en_US |
| dc.publisher | | en_US |
| dc.subject | Biology, Anatomy. | en_US |
| dc.subject | Biology, Animal Physiology. | en_US |
| dc.subject | Biology, Zoology. | en_US |
| dc.title | Anatomical and behavioural analysis of the role of acetylcholine and nerve growth factor in the mammalian circadian system. | en_US |
| dc.type | text | en_US |
| dc.contributor.degree | Ph.D. | en_US |
