Article

Reversible reduction in dendritic spines in CA1 of rat and ground squirrel subjected to hypothermia-normothermia in vivo: A three-dimensional electron microscope study.

The Open University, Department of Biological Sciences, Faculty of Sciences, Walton Hall, Milton Keynes MK7 6AA, UK.
Neuroscience (Impact Factor: 3.12). 12/2007; 149(3):549-60. DOI: 10.1016/j.neuroscience.2007.07.059
Source: PubMed

ABSTRACT A study was made at electron microscope level of changes in the three-dimensional (3-D) morphology of dendritic spines and postsynaptic densities (PSDs) in CA1 of the hippocampus in ground squirrels, taken either at low temperature during hibernation (brain temperature 2-4 degrees C), or after warming and recovery to the normothermic state (34 degrees C). In addition, the morphology of PSDs and spines was measured in a non-hibernating mammal, rat, subjected to cooling at 2 degrees C at which time core rectal temperature was 15 degrees C, and then after warming to normothermic conditions. Significant differences were found in the proportion of thin and stubby spines, and shaft synapses in CA1 for rats and ground squirrels for normothermia compared with cooling or hibernation. Hypothermia induced a decrease in the proportion of thin spines, and an increase in stubby and shaft spines, but no change in the proportion of mushroom spines. The changes in redistribution of these three categories of spines in ground squirrel are more prominent than in rat. There were no significant differences in synapse density determined for ground squirrels or rats at normal compared with low temperature. Measurement of spine and PSD volume (for mushroom and thin spines) also showed no significant differences between the two functional states in either rats or ground squirrels, nor were there any differences in distances between neighboring synapses. Spinules on dendritic shafts were notable qualitatively during hibernation, but absent in normothermia. These data show that hypothermia results in morphological changes which are essentially similar in both a hibernating and a non-hibernating animal.

0 Bookmarks
 · 
72 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: We examined the structural plasticity of excitatory synapses from corticostriatal and thalamostriatal pathways and their postsynaptic targets in adult Sprague-Dawley rats to understand how these striatal circuits change in l-DOPA-induced dyskinesias (LIDs). We present here detailed electron and light microscopic analyses that provide new insight into the nature of the structural and synaptic remodeling of medium spiny neurons in response to LIDs. Numerous studies have implicated enhanced glutamate signaling and persistent long-term potentiation as central to the behavioral sensitization phenomenon of LIDs. Moreover, experience-dependent alterations in behavior are thought to involve structural modifications, specifically alterations in patterns of synaptic connectivity. Thus, we hypothesized that in the striatum of rats with LIDs, one of two major glutamatergic pathways would form new or altered contacts, especially onto the spines of medium spiny neuron (MSNs). Our data provide compelling evidence for a dramatic rewiring of the striatum of dyskinetic rats and that this rewiring involves corticostriatal but not thalamostriatal contacts onto MSNs. There is a dramatic increase in corticostriatal contacts onto spines and dendrites that appear to be directly linked to dyskinetic behaviors, since they were not seen in the striatum of animals that did not develop dyskinesia. There is also an aberrant increase in spines receiving more than one excitatory contact(i.e., multisynaptic spines) in the dyskinetic animals compared with the 6-hydroxydopamine-treated and control rats. Such alterations could substantially impair the ability of striatal neurons to gate cortically driven signals and contribute to the loss of bidirectional synaptic plasticity.
    Journal of Neuroscience 07/2013; 33(28):11655-11667. · 6.91 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Synapses are the building blocks of neuronal networks. Spines, the postsynaptic elements, are morphologically the most plastic part of the synapse. It is thought that spine plasticity underlies learning and memory processes, driven by kinases and cytoskeleton protein reorganization. Spine strength depends primarily on the number of incorporated glutamatergic receptors, which are more numerous in larger spines. Intrinsic and circadian fluctuations, occurring independently of presynaptic stimulation, demonstrate the native instability of spines. Despite innate spine instability some spines remain intact lifelong. Threats to spine survival are reduced by physical and mental activity, and declining sensory input, conditions characteristic for aging. Large spines are considered less vulnerable than thin spines, and in the older brain large spines are more abundant, whereas the thin spines are functionally weaker. It can be speculated that this shift towards memory spines contributes to enhanced retention of remote memories typically seen in the elderly. Gaining further insight in spine plasticity regulation, its homeostatic nature and how to maintain spine health will be important future research topics in Neuroscience.
    Neuroscience & Biobehavioral Reviews 01/2014; · 10.28 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Why do neurons have dendritic spines? This question-the heart of what Yuste calls "the spine problem"-presupposes that why-questions of this sort have scientific answers: that empirical findings can favor or count against claims about why neurons have spines. Here we show how such questions can receive empirical answers. We construe such why-questions as questions about how spines make a difference to the behavior of some mechanism that we take to be significant. Why-questions are driven fundamentally by the effort to understand how some item, such as the dendritic spine, is situated in the causal structure of the world (the causal nexus). They ask for a filter on that busy world that allows us to see a part's individual contribution to a mechanism, independent of everything else going on. So understood, answers to why-questions can be assessed by testing the claims these answers make about the causal structure of a mechanism. We distinguish four ways of making a difference to a mechanism (necessary, modulatory, component, background condition), and we sketch their evidential requirements. One consequence of our analysis is that there are many spine problems and that any given spine problem might have many acceptable answers.
    Frontiers in Neuroanatomy 09/2014; 8:95. · 4.06 Impact Factor