Publications by authors named "Nicole Kerr"

8 Publications

  • Page 1 of 1

Hippocampal modulation of cardiorespiratory function.

Respir Physiol Neurobiol 2018 06 14;252-253:18-27. Epub 2018 Mar 14.

The Department of Anatomy and Neuroscience, The University of Melbourne, Parkville, VIC, 3010, Australia. Electronic address:

Changes in cardiorespiratory control accompany the expression of complex emotions, indicative of limbic brain inputs onto bulbar autonomic pathways. Previous studies have focussed on the role of the prefrontal cortex in autonomic regulation. However, the role of the hippocampus, also important in limbic processing, has not been addressed in detail. Anaesthetised, instrumented rats were used to map the location of hippocampal sites capable of evoking changes in cardiorespiratory control showing that stimulation of discrete regions within the CA1 fields of both the dorsal and ventral hippocampus potently alter breathing and cardiovascular activity. Additionally, tracing of the neuroanatomical tracts and pharmacological inactivation studies were used to demonstrate a role of the basomedial amygdala in hippocampal evoked responses. Collectively, these data support the existence of a hippocampal-amygdala neural circuit capable of modulating bulbar cardiorespiratory control networks and may suggest a role for this circuit in the top-down regulation of breathing and autonomic outflow necessary for the expression of complex emotions.
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http://dx.doi.org/10.1016/j.resp.2018.03.004DOI Listing
June 2018

Evidence that central pathways that mediate defecation utilize ghrelin receptors but do not require endogenous ghrelin.

Physiol Rep 2017 Aug;5(15)

Department of Anatomy & Neuroscience, University of Melbourne, Parkville, Victoria, Australia

In laboratory animals and in human, centrally penetrant ghrelin receptor agonists, given systemically or orally, cause defecation. Animal studies show that the effect is due to activation of ghrelin receptors in the spinal lumbosacral defecation centers. However, it is not known whether there is a physiological role of ghrelin or the ghrelin receptor in the control of defecation. Using immunohistochemistry and immunoassay, we detected and measured ghrelin in the stomach, but were unable to detect ghrelin by either method in the lumbosacral spinal cord, or other regions of the CNS In rats in which the thoracic spinal cord was transected 5 weeks before, the effects of a ghrelin agonist on colorectal propulsion were significantly enhanced, but defecation caused by water avoidance stress (WAS) was reduced. In knockout rats that expressed no ghrelin and in wild-type rats, WAS-induced defecation was reduced by a ghrelin receptor antagonist, to similar extents. We conclude that the ghrelin receptors of the lumbosacral defecation centers have a physiological role in the control of defecation, but that their role is not dependent on ghrelin. This implies that a transmitter other than ghrelin engages the ghrelin receptor or a ghrelin receptor complex.
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http://dx.doi.org/10.14814/phy2.13385DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5555902PMC
August 2017

Corticospinal tract sprouting in the injured rat spinal cord stimulated by Schwann cell preconditioning of the motor cortex.

Neurol Res 2013 Sep 12;35(7):763-72. Epub 2013 Apr 12.

University of Melbourne, Australia.

Unlabelled: Peripheral nerve preconditioning lesions have been shown to consistently enhance sensory nerve regeneration in the injured spinal cord.

Objective: The aim of this study was to determine if the rat motor cortex could be preconditioned through the implantation of Schwann cells (SC), thereby stimulating sprouting and regeneration of the corticospinal tract (CST).

Methods: Schwann cells (cultured in vitro) were injected into the motor cortex and seven days post-surgery rats underwent a dorsal spinal hemisection injury. Eight weeks following spinal injury animals were perfused and the CST visualised by Avidin-peroxidase histochemistry for dextran-biotin.

Results: Results demonstrate substantially enhanced CST collateral sprouting in both the rostral grey and white matter of the injured spinal cord in animals with SC implanted into the motor cortex compared to control animals with and without cortical vehicle injections. Corticospinal tract peri-wound regenerative sprouting was also enhanced in animals implanted with cortical SC compared to controls, however, only a small degree of CST axonal regeneration was present in the grey matter beneath the injury site. In all groups, CST peri-lesional regenerative sprouting occurred in close proximity to macrophages. Complicated and intimate relationships between CST fibres and these cells were evident.

Discussion: Overall, our data demonstrates that preconditioning the motor cortex with SC prior to spinal injury results in greatly enhanced CST sprouting and that CST peri-wound sprouting takes place in juxtaposition to macrophages.
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http://dx.doi.org/10.1179/1743132813Y.0000000199DOI Listing
September 2013

A Report on the development of the Hawai'i Pediatric Weight Management Toolkit.

Hawaii Med J 2011 Jul;70(7 Suppl 1):49-51

Deer Kerr Consulting, LLC, Honolulu, HI, USA.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3158458PMC
July 2011

Intracanal pressure in compressive spinal cord injury: reduction with hypothermia.

J Neurotrauma 2011 May 24;28(5):809-20. Epub 2011 Mar 24.

Department of Medicine, National Stroke Research Institute and University of Melbourne, Austin Health, Heidelberg, Victoria, Australia.

Most cases of human spinal cord injury (SCI) are accompanied by continuing cord compression. Experimentally, compression results in rapid neurological decline over hours, suggesting a rise in intracanal pressure local to the site of injury. The aim of this study was to measure the rise in local intracanal pressure accompanying progressive canal occlusion and to determine the relationship between raised intracanal pressure and neurological outcome. We also aimed to establish whether hypothermia was able to reduce raised intracanal pressure. We demonstrate that, following SCI in F344 rats, local intracanal pressure remains near normal until canal occlusion exceeds 30% of diameter, whereupon a rapid increase in pressure occurs. Intracanal pressure appears to be an important determinant of neurological recovery, with poor long-term behavioural and histological outcomes in animals subject to 8 h of 45% canal occlusion, in which intracanal pressure is significantly elevated. In contrast, good neurological recovery occurs in animals with near normal intracanal pressure (animals undergoing 8 h of 30% canal occlusion or those undergoing immediate decompression). We further demonstrate that hypothermia is an effective therapy to control raised intracanal pressure, rapidly reducing elevated intracanal pressure accompanying critical (45%) canal occlusion to near normal. Overall these data indicate that following SCI only limited canal narrowing is tolerated before local intracanal pressure rapidly rises, inducing a sharp decline in neurological outcome. Raised intracanal pressure can be controlled with hypothermia, which may be a useful therapy to emergently decompress the spinal cord prior to surgical decompression.
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http://dx.doi.org/10.1089/neu.2010.1622DOI Listing
May 2011

Hypothermia prior to decompression: buying time for treatment of acute spinal cord injury.

J Neurotrauma 2010 Aug;27(8):1357-68

National Stroke Research Institute and University of Melbourne, Department of Medicine, Heidelberg, Victoria, Australia.

Human spinal cord injury (SCI) is usually accompanied by persistent cord compression. Experimental data demonstrate that compression of the traumatized cord results in rapid neurological decline over hours. Undertaking decompression in humans within this time frame has proved impractical, with the time to surgery in studies of urgent decompression averaging between 10 and 24 h. There is, therefore, an important need for a therapy to prevent the neurological deterioration of patients prior to decompressive surgery. The aim of this study was to determine if hypothermia prevents compressive SCI, thereby limiting neurological decline. Rats were subjected to a moderate mid-thoracic SCI and spacers were inserted to compress the spinal cord by 45%. Decompression, by removal of the spacer, was performed immediately, and at 2 or 8 h post-injury. Hypothermia (33 degrees C) was commenced in half the animals at 30 mins post-injury and maintained for 7.5 h, with the other half remaining normothermic (37.3 degrees C). Motor recovery was assessed weekly, and the volume and area of tissue damage determined at the end of the 8-week study period. The results demonstrate that hypothermia significantly improves the behavioral and histological outcome of animals undergoing 8 h of compressive injury (the primary outcome measure). The hypothermia-treated group regained weight-supported locomotion (Basso-Beattie-Bresnahan [BBB] locomotor assessment score 9.5 +/- 0.9), while the normothermic group remained severely paraparetic (BBB score 5.3 +/- 0.6; p
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http://dx.doi.org/10.1089/neu.2010.1360DOI Listing
August 2010

Increasing stair use in a worksite through environmental changes.

Am J Health Promot 2004 Mar-Apr;18(4):312-5

Centers for Disease Control and Prevention, Division of Nutrition and Physical Activity, Atlanta, Georgia 30341, USA.

Purpose: This study assessed the impact on stair use of four sequential environmental interventions: (1) installing new carpet and painting the walls, (2) adding framed art-work on stair landings, (3) displaying motivational signs throughout the building, and (4) adding a stereo system and playing various types of music in the stairwell.

Methods: We conducted a longitudinal study with no comparison group to evaluate the impact of environmental changes on stairway use. The setting was the main stairwell in the Centers for Disease Control and Prevention's (CDC) Rhodes Building in Atlanta, Georgia. Proximity sensors were installed in each stairwell entry to monitor traffic. The subjects were 554 permanent CDC employees and 110 temporary employees. Changes in stairwell use by intervention were evaluated.

Results: Both motivational signs and music significantly increased stair use by 8.9% over baseline (p < .05). The increase in sign use occurred in the first 3 months of the intervention, whereas the increase in music occurred after the first 3 months.

Discussion: These data suggest that physical improvements to a stairwell, signage that encourages stair use, and music may increase physical activity among building occupants.
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http://dx.doi.org/10.4278/0890-1171-18.4.312DOI Listing
April 2004

Prevention of diabetes-induced albuminuria in transgenic rats overexpressing human aldose reductase.

Endocrine 2002 Jun;18(1):47-56

University of Melbourne Department of Medicine, Royal Melbourne Hospital, Parkville, VIC, Australia.

Studies using pharmacologic inhibitors have implicated the enzyme aldose reductase in the pathogenesis of albuminuria and diabetic renal disease. However, a clear conclusion is not easily drawn from such studies since these pharmacologic inhibitors have nonspecific properties. To examine further the role of aldose reductase, we have overexpressed the human enzyme in a transgenic rat model. Transgene expression in the kidney was predominantly localized to the outer stripe of the outer medulla, compatible with the histotopography of the straight (S3) proximal tubule. The effect of enzyme overexpression on diabetes-induced renal function and structure was then investigated. Contrary to what may have been anticipated from the previous enzyme inhibition studies, diabetes-induced albuminuria was completely prevented by the overexpression of aldose reductase. No effect of overexpression of aldose reductase on renal structure nor on urinary excretion of beta2-microglobulin and N-acetyl-beta-D-glucosaminidase was observed in this transgenic rat model. In conclusion, our study strongly suggests that multiple roles for aldose reductase may give it a more complex place in diabetic nephropathy than is currently recognized.
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http://dx.doi.org/10.1385/ENDO:18:1:47DOI Listing
June 2002