Specific neuronal populations are known to express calcium binding proteins (CBP) such as calbindin (CB), parvalbumin (PV) and calretinin (CR). These CBP can act as calcium buffers that modify spatiotemporal characteristics of intracellular calcium transients and affect calcium homeostasis in neurons. It was recently shown that changes in neuronal CBP expression can have significant modulatory effect on synaptic transmission. Spinothalamic tract (STT) neurons form a major nociceptive pathway and they become sensitized after peripheral inflammation. In our experiments, expression of CBP in STT neurons was studied in a model of unilateral acute knee joint arthritis in rats. Altogether 377, 374 and 358 STT neurons in the segments L3-4 were evaluated for the presence of CB, PV and CR. On the contralateral (control) side 11 %, 9 % and 47 % of the retrogradely labeled STT ne urons expressed CB, PV and CR, respectively. On the ipsilateral (arthritic) side there was significantly more CB (23 %) and PV (25 %) expressing STT neurons, while the number of CR positive neurons (50 %) did not differ. Our results show increased expression of fast (CB) and slow (PV) calcium binding proteins in STT neurons after induction of experimental arthritis. This suggests that change in CBP expression could have a significant effect on calcium homeostasis and possibly modulation of synaptic activity in STT neurons., D. Sojka, G. Zacharova, D. Spicarova, J. Palecek., and Obsahuje bibliografii
Repetitive transcranial magnetic stimulation (rTMS) was shown to
have therapeutic potential for some neurological and psychiatric
disorders. Previous studies reported that low-frequency rTMS
(≤1 Hz) affected synaptic plasticity in rats, however, there were
few investigations to examine the possible effects of rTMS on
structural synaptic plasticity changes in rats, which included the
effects on synaptic morphology in the hippocampus, synaptic
protein markers and Ca2+/calmodulin-dependent protein II
(CaMKII). Sprague-Dawley rats were subject to 500 pulses of
0.5 Hz rTMS for 15 days, or sham stimulation. After last
stimulation, transmission electron microscope (TEM) and
real-time PCR were used to determine the effects of rTMS on
synaptic plasticity. Results showed that rTMS could cause the
change of structural synaptic plasticity, increase the expression of
synaptic protein markers: synaptophysin (SYN) and increase the
expression of CaMKII, relative to normal rats. suggesting
a modulatory effect of chronic rTMS on synaptic plasticity that
may be attributed to the increased expression of CaMKII in rats.
Fragile X syndrome (FXS) is the most frequently inherited form of intellectual disability and prevalent single-gene cause of autism. A priority of FXS research is to determine the molecular mechanisms underlying the cognitive and social functioning impairments in humans and the FXS mouse model. Glutamate ionotropic alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors (AMPARs) mediate a majority of fast excitatory neurotransmission in the central nervous system and are critically important for nearly all aspects of brain function, including neuronal development, synaptic plasticity, and learning and memory. Both preclinical and clinical studies have indicated that expression, trafficking, and functions of AMPARs are altered and result in altered synapse development and plasticity, cognitive impairment, and poor mental health in FXS. In this review, we discuss the contribution of AMPARs to disorders of FXS by highlighting recent research advances with a specific focus on change in AMPARs expression, trafficking, and dependent synaptic plasticity. Since changes in synaptic strength underlie the basis of learning, development, and disease, we suggest that the current knowledge base of AMPARs has reached a unique point to permit a comprehensive re-evaluation of their roles in FXS.