Showing 1 - 10 of 22 Items

• Embargo End Date: 2027-05-15

Date: 2024-01-01

Creator: Eliza Schotten

Access: Embargoed

Date: 2024-01-01

Creator: Katrina Carrier

Access: Open access

The ability of nervous systems to maintain function when exposed to global perturbations in temperature and salinity is a non-trivial task. The nervous system of the American lobster (H. americanus), a marine osmoconformer and poikilotherm, must be robust to these stressors, as they frequently experience fluctuations in both. I characterized the effects of temperature on the output of the pyloric circuit, a central pattern generator in the stomatogastric nervous system (STNS) that controls food filtration and established the maximum temperature that neurons in this circuit can withstand without “crashing” (ceasing to function but recovering when returned to normal conditions). I established a range of saline concentrations that did not cause the system to crash, and then determined whether combinatorial changes in temperature and salinity concentrations alter the maximum temperature the system tolerated. Even as burst frequency increased as temperature increased, phase constancy was observed. Interestingly, the system crashed at higher temperatures upon exposure to lower saline concentrations and lower temperatures in higher saline concentrations. I also established the range of saline concentrations that the lobster’s whole heart and cardiac ganglion (CG), the nervous system that controls the lobster’s heartbeat, can withstand. Then, I examined whether exposure to altered salinity and elevated temperature alters the crash temperature of the whole heart and CG. The CG crashed at higher temperatures than the whole heart in each saline concentration. Like the STNS, the whole heart and CG both crashed at higher temperatures in lower saline concentrations and higher temperatures in lower saline concentrations.

Date: 2024-01-01

Creator: Grant Griesman

Access: Open access

Central pattern generators (CPGs) are neuronal networks that produce rhythmic motor output in the absence of sensory stimuli. Invertebrate CPGs are valuable models of neural circuit dynamics and neuromodulation because they continue to generate fictive activity in vitro. For example, the cardiac ganglion (CG) of the Jonah crab (Cancer borealis) and American lobster (Homarus americanus) contains nine electrochemically coupled neurons that fire bursts of action potentials to trigger a heartbeat. The CG is modulated by neuropeptides, amines, small molecule transmitters, gases, and mechanosensory feedback pathways that enable flexibility and constrain output. One such modulator, the SLY neuropeptide family, was previously shown to be expressed in hormonal release sites and within the CG itself and has unusual processing features. However, its physiological effect was unknown. Here, I performed dose-response experiments in the crab and lobster whole heart and isolated CG to determine the threshold concentration of SLY neuropeptides to which these systems respond. The crab isoform had strong, excitatory effects in the crab whole heart and weakly modulated the crab CG. The lobster isoform weakly modulated the lobster whole heart and CG. Surprisingly, the crab isoform exerted large, variable effects on the lobster system, which suggests that SLY neuropeptides, their receptors, and their signaling pathways may be evolutionarily conserved across these two species. This research contributes to our understanding of how neural circuits can generate flexible output in response to modulation. It may also offer insight into processes influenced by peptidergic neurotransmission in the nervous systems of other animals, including mammals.

• Embargo End Date: 2027-05-16

Date: 2024-01-01

Creator: Sam McClelland

Access: Embargoed

Date: 2024-01-01

Creator: Josephine P. Tidmore

Access: Open access

Central pattern generator (CPG) networks produce the rhythmic motor patterns that underlie critical behaviors such as breathing, walking, and heartbeat. The fidelity of these neural circuits in response to fluctuations in environmental conditions is essential for organismal survival. The specific ion channel profile of a neuron dictates its electrophysiological phenotype and is under homeostatic control, as channel proteins are constantly turning over in the membrane in response to internal and external stimuli. Neuronal function depends on ion channels and biophysical processes that are sensitive to external variables such as temperature, pH, and salinity. Nonetheless, the nervous system of the American lobster (Homarus americanus) is robust to global perturbations in these variables. The cardiac ganglion (CG), the CPG that controls the rhythmic activation of the heart in the lobster, has been shown to maintain function across a relatively wide, ecologically-relevant range of saline concentrations in the short-term. This study investigates whether individual neurons of the CG sense and compensate for long-term changes in extracellular ion concentration by controlling their ion channel mRNA abundances. To do this, I bathed the isolated CG in either 0.75x, 1.5x, or 1x (physiological) saline concentrations for 24 h. I then dissected out individual CG motor neurons, the pacemaker neurons, and sections of axonal projections and used single-cell RT-qPCR to measure relative mRNA abundances of several species of ion channels in these cells. I found that the CG maintained stable output with 24 h exposure to altered saline concentrations (0.75x and 1.5x), and that this stability may indeed be enabled by changes in mRNA abundances and correlated channel relationships.

Date: 2024-01-01

Creator: Karin van Hassel

Access: Open access

The cardiac ganglion (CG) is a central pattern generator, a neural network that, when activated, produces patterned motor outputs such as breathing and walking. The CG induces the heart contractions of the American lobster, Homarus americanus, making the lobster heart neurogenic. In the American lobster, the CG is made up of nine neurons: four premotor pacemaker neurons that send signals to five motor neurons, causing bursts of action potentials from the motor neurons. These bursts cause cardiac muscle contractions that vary in strength based on the burst duration, frequency, and pattern. The activity of the CG is modulated by feedback pathways and neuromodulators, allowing for flexibility in the CG’s motor output and appropriate responses to changes in the animal’s environment. Two feedback pathways modulate the CG motor output, the excitatory cardiac muscle stretch and inhibitory nitric oxide feedback pathways. Despite our knowledge of the modulation of the CG by feedback pathways and neuromodulators separately, little is known about how neuromodulators influence the sensory feedback response to cardiac muscle stretch. I found one neuromodulator to modulate each phase of the stretch response differently, one neuromodulator to generally not affect the stretch response, and three neuromodulators to suppress the stretch response. These results suggest neuromodulators can act to produce flexibility in a CPG’s motor output, allowing the system to respond appropriately to changes in an organism’s environment, and allow for variation in CPG responses to different stimuli.

Date: 2024-01-01

Creator: Zackery D. Reynolds

Access: Access restricted to the Bowdoin Community

• Restriction End Date: 2026-06-01

Date: 2023-01-01

Creator: Eliza M. Rhee

Access: Access restricted to the Bowdoin Community

Date: 2023-01-01

Creator: Isabel Stella Petropoulos

Access: Open access

A substantial factor for behavioral flexibility is modulation — largely via neuropeptides — which occurs at multiple sites including neurons, muscles, and the neuromuscular junction (NMJ). Complex modulation distributed across multiple sites provides an interesting question: does modulation at multiple locations lead to greater dynamics than one receptor site alone? The cardiac neuromuscular system of the American lobster (Homarus americanus), driven by a central pattern generator called the cardiac ganglion (CG), is a model system for peptide modulation. The peptide myosuppressin (pQDLDHVFLRFamide) has been shown in the whole heart to decrease contraction frequency, largely due to its effects on the CG, as well as increase contraction amplitude by acting on periphery of the neuromuscular system, either at the cardiac muscle, the NMJ, or both. This set of experiments addresses the location(s) at which myosuppressin exerts its effects at the periphery. To elucidate myosuppressin’s effects on the cardiac muscle, the CG was removed, and muscle contractions were stimulated with L-glutamate while superfusing myosuppressin. Myosuppressin increased glutamate-evoked contraction amplitude in the isolated muscle, suggesting that myosuppressin exerts its peripheral effects directly on the cardiac muscle. To examine effects on the NMJ, excitatory junction potentials were evoked by stimulating of the motor nerve and intracellularly recording a single muscle fiber both in control saline and in the presence of myosuppressin. Myosuppressin did not modulate the amplitude of EJPs suggesting myosuppressin acts at the muscle and not at the NMJ, to cause an increase in contraction amplitude.

• Restriction End Date: 2028-06-01

Date: 2023-01-01

Creator: Jada Scotland

Access: Access restricted to the Bowdoin Community