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dc.contributor.advisorSillar, Keith T. (Keith Thomas)en
dc.contributor.authorReith, Carolyn A.en
dc.coverage.spatial314pen
dc.date.accessioned2021-04-08T08:59:35Z
dc.date.available2021-04-08T08:59:35Z
dc.date.issued1996
dc.identifier.urihttps://hdl.handle.net/10023/21951
dc.description.abstract1. The role of the inhibitory amino acid, GABA acting at GABAa receptors during embryonic and larval Active swimming in Xenopus laevis has been investigated. 2. Intracellular recordings, under tetrodotoxin, reveal two types of spontaneous inhibitory postsynaptic potential: short duration glycinergic ipsps and longer duration GABAergic ipsps. 3. The neurosteroid, 5β-pregnan-3α-ol-20-one (5β3α), enhances the presynaptic release of GABA and the postsynaptic effects of GABAa receptor activation, without affecting glycinergic ipsps. 4. At embryonic stage 37/8, GABAa receptor activation has an overall inhibitory action on the swimming pattern. 5β3α causes a decrease in the frequency and duration of Active swim episodes. 5. By larval stage 42, GABAa receptor activation influences various parameters of fictive swimming (burst duration, cycle period and rostrocaudal delay) and thus finely tunes the motor output. Bicucullineblockade of GABAa receptors causes swimming frequency and burst durations to increase and rostro-caudal delays to decrease. 6. GABA release from the descending projections of midhindbrain reticulospinal neurons also appears to play a role in the intrinsic termination of larval swimming, as opposed to their previous involvement in a reflex stopping response in the embryo. 7. By stage 42, the dimming response, which elicits swimming following a sudden dimming of the illumination, is declining. GABAergic neurotransmission plays a role in down regulating this sensory reflex. 8. As opposed to embryonic swimming, sustained larval swimming requires a certain level of inhibition since it is abolished when both glycine and GABAa receptors are blocked. 9. When GABAa and glycine receptors are blocked dining NMDA-induced swimming activity, a slow network oscillation is revealed. This appears to result from the enhancement of a pre-existing low amplitude oscillation already present during NMDA-induced rhythmic activity. 10. Pharmacological evidence suggests that the slow network modulation of NMDA-induced swimming results from the expression of intrinsic 5HT-dependent membrane potential oscillations, since both are abolished by a specific 5HTla antagonist, pindobind-5HTla.en
dc.language.isoenen
dc.publisherUniversity of St Andrewsen
dc.subject.lccQL668.E27R3
dc.subject.lcshXenopus laevis--Locomotionen
dc.subject.lcshGABAen
dc.titleGABAergic modulation of locomotor rhythmicity during post-embryonic development in 'Xenopus laevis'en
dc.typeThesisen
dc.type.qualificationlevelDoctoralen
dc.type.qualificationnamePhD Doctor of Philosopyen
dc.publisher.institutionThe University of St Andrewsen


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