Montana Green River Ordinances

Green River Ordinance

Inhibition of alpha7 nicotinic receptors in the ventral hippocampus selectively attenuates reinstatement of morphine‐conditioned place preference and associated changes in AMPA receptor binding

Recurrent relapse is a major problem in treating opiate addiction. Pavlovian conditioning plays a role in recurrent relapse whereby exposure to cues learned during drug intake can precipitate relapse to drug taking. α7 nicotinic acetylcholine receptors (nAChRs) have been implicated in attentional aspects of cognition and mechanisms of learning and memory. In this study we have investigated the role of α7 nAChRs in morphine‐conditioned place preference (morphine‐CPP). CPP provides a model of associative learning that is pertinent to associative aspects of drug dependence. The α7 nAChR antagonist methyllycaconitine (MLA; 4 mg/kg s.c.) had no effect on the acquisition, maintenance, reconsolidation or extinction of morphine‐CPP but selectively attenuated morphine‐primed reinstatement of CPP, in both mice and rats. Reinstatement of morphine‐CPP in mice was accompanied by a selective increase in [3H]‐AMPA binding (but not in [3H]‐MK801 binding) in the ventral hippocampus that was prevented by prior treatment with MLA. Administration of MLA (6.7 μg) directly into the ventral hippocampus of rats prior to a systemic priming dose of morphine abolished reinstatement of morphine‐CPP, whereas MLA delivered into the dorsal hippocampus or prefrontal cortex was without effect. These results suggest that α7 nAChRs in the ventral hippocampus play a specific role in the retrieval of associative drug memories following a period of extinction, making them potential targets for the prevention of relapse

Projections from the brain to the spinal cord in the mouse

The cells that project from the brain to the spinal cord have previously been mapped in a wide range of mammalian species, but have not been comprehensively studied in the mouse. We have mapped these cells in the mouse using retrograde tracing after large unilateral Fluoro-Gold (FG) and horseradish peroxidase (HRP) injections in the C1 and C2 spinal cord segments. We have identified over 30 cell groups that project to the spinal cord, and have confirmed that the pattern of major projections from the cortex, diencephalon, midbrain, and hindbrain in the mouse is typically mammalian, and very similar to that found in the rat. However, we report two novel findings: we found labeled neurons in the precuneiform area (an area which has been associated with the midbrain locomotor center in other species), and the epirubrospinal nucleus. We also found labeled cells in the medial division of central nucleus of the amygdala in a small number of cases. Our findings should be of value to researchers engaged in evaluating the impact of spinal cord injury and other spinal cord pathologies on the centers which give rise to descending pathways

Technical aspects of an impact acceleration traumatic brain injury rat model with potential suitability for both microdialysis and PtiO2 monitoring

This report describes technical adaptations of a traumatic brain injury (TBI) model-largely inspired by Marmarou-in order to monitor microdialysis data and PtiO2 (brain tissue oxygen) before, during and after injury. We particularly focalize on our model requirements which allows us to re-create some drastic pathological characteristics experienced by severely head-injured patients: impact on a closed skull, no ventilation immediately after impact, presence of diffuse axonal injuries and secondary brain insults from systemic origin...We notably give priority to minimize anaesthesia duration in order to tend to banish any neuroprotection. Our new model will henceforth allow a better understanding of neurochemical and biochemical alterations resulting from traumatic brain injury, using microdialysis and PtiO2 techniques already monitored in our Intensive Care Unit. Studies on efficiency and therapeutic window of neuroprotective pharmacological molecules are now conceivable to ameliorate severe head-injury treatment

The spinal precerebellar nuclei: Calcium binding proteins and gene expression profile in the mouse

We have localized the spinocerebellar neuron groups in C57BL/6J mice by injecting the retrograde neuronal tracer Fluoro-Gold into the cerebellum and examined the distribution of SMI 32 and the calcium-binding proteins (CBPs), calbindin-D-28K (Cb), calretinin (Cr), and parvalbumin (Pv) in the spinal precerebellar nuclei. The spinal precerebellar neuron clusters identified were the dorsal nucleus, central cervical nucleus, lumbar border precerebellar nucleus, lumbar precerebellar nucleus, and sacral precerebellar nucleus. Some dispersed neurons in the deep dorsal horn and spinal laminae 6–8 also projected to the cerebellum. Cb, Cr, Pv, and SMI 32 were present in all major spinal precerebellar nuclei and Pv was the most commonly observed CBP. A number of genes expressed in hindbrain precerebellar nuclei are also expressed in spinal precerebellar groups, but there were some differences in gene expression profile between the different spinal precerebellar nuclei, pointing to functional diversity amongst them

On-Off Intermittency in Time Series of Spontaneous Paroxysmal Activity in Rats with Genetic Absence Epilepsy

Dynamic behavior of complex neuronal ensembles is a topic comprising a streamline of current researches worldwide. In this article we study the behavior manifested by epileptic brain, in the case of spontaneous non-convulsive paroxysmal activity. For this purpose we analyzed archived long-term recording of paroxysmal activity in animals genetically susceptible to absence epilepsy, namely WAG/Rij rats. We first report that the brain activity alternated between normal states and epilepsy paroxysms is the on-off intermittency phenomenon which has been observed and studied earlier in the different nonlinear systems.Comment: 11 pages, 6 figure

Using a Panel of Immunomarkers to Define Homologies in Mammalian Brains

Brain mapping has relied on a small number of routine chemical stains for many decades. The advent of immunomarkers has had a major impact on the ability to define homologous nuclei from one species to another. The first atlas to present a panel of immunomarkers was that of Paxinos et al. (1999a,b) in the adult rat brain. The markers used were parvalbumin, calbindin, calretinin, SMI32, tyrosine hydroxylase, and NADPH diaphorase (plus nissl and acetylcholinesterase). The ‘signature’ of a nucleus of interest in a new species can be tested against the findings in the rat. Since the pattern of immunomarkers seems to be conserved in mammalian evolution, such extrapolations can be made with reasonable confidence. A marmoset brain stained with a comprehensive set of immunomarkers has recently been published on the internet (Tokuno et al., 2009) and we are in the process of defining nuclear homologies in this brain by comparison with the same markers in the rat. In this article, we present an example (mapping the amygdala in the marmoset) which demonstrates the application of this immunomarker panel in defining homologies. The technique is particularly valuable in situations where little data on hodology or electrophysiology are available

The Number of Stem Cells in the Subependymal Zone of the Adult Rodent Brain is Correlated with the Number of Ependymal Cells and Not with the Volume of the Niche

The mammalian subependymal zone (SEZ; often called subventricular) situated at the lateral walls of the lateral ventricles of the brain contains a pool of relatively quiescent adult neural stem cells whose neurogenic activity persists throughout life. These stem cells are positioned in close proximity both to the ependymal cells that provide the cerebrospinal fluid interface and to the blood vessel endothelial cells, but the relative contribution of these 2 cell types to stem cell regulation remains undetermined. Here, we address this question by analyzing a naturally occurring example of volumetric scaling of the SEZ in a comparison of the mouse SEZ with the larger rat SEZ. Our analysis reveals that the number of stem cells in the SEZ niche is correlated with the number of ependymal cells rather than with the volume, thereby indicating the importance of ependymal-derived factors in the formation and function of the SEZ. The elucidation of the factors generated by ependymal cells that regulate stem cell numbers within the SEZ is, therefore, of importance for stem cell biology and regenerative neuroscience

Acute Ethanol Administration Rapidly Increases Phosphorylation of Conventional Protein Kinase C in Specific Mammalian Brain Regions in Vivo

Background Protein kinase C (PKC) is a family of isoenzymes that regulate a variety of functions in the central nervous system including neurotransmitter release, ion channel activity, and cell differentiation. Growing evidence suggests that specific isoforms of PKC influence a variety of behavioral, biochemical, and physiological effects of ethanol in mammals. The purpose of this study was to determine whether acute ethanol exposure alters phosphorylation of conventional PKC isoforms at a threonine 674 (p-cPKC) site in the hydrophobic domain of the kinase, which is required for its catalytic activity. Methods Male rats were administered a dose range of ethanol (0, 0.5, 1, or 2 g/kg, intragastric) and brain tissue was removed 10 minutes later for evaluation of changes in p-cPKC expression using immunohistochemistry and Western blot methods. Results Immunohistochemical data show that the highest dose of ethanol (2 g/kg) rapidly increases p-cPKC immunoreactivity specifically in the nucleus accumbens (core and shell), lateral septum, and hippocampus (CA3 and dentate gyrus). Western blot analysis further showed that ethanol (2 g/kg) increased p-cPKC expression in the P2 membrane fraction of tissue from the nucleus accumbens and hippocampus. Although p-cPKC was expressed in numerous other brain regions, including the caudate nucleus, amygdala, and cortex, no changes were observed in response to acute ethanol. Total PKC? immunoreactivity was surveyed throughout the brain and showed no change following acute ethanol injection