ABSTRACT
It has been known that the Alzheimer's disease(AD)is related closely with a synaptic failure,and the p21-activated kinase(PAK)is well documented to play an important role in the regulation of the synaptie functions.However,the relationship between thePAK and the pathology of AD is unclear.In the present study,we examined the expressions of the PAK3(one subtype ofPAK),phospho-rylated-PAK(pPAK) and β-amyloid42(Aβ42,β-amyloid with 42 peptides)in an APP/PS1 double transgenie mouse model of AD andthe morphologies of geurOtlS in the hippocampus at different ages.The Western Blot results showed that the expression of PAK remainedunchanged,while,the expression of pPAK decreased largely at the age of 32 weeks and further decreased significantly with aging in thehippocampus of the APP/PS1 transgenic mouse.A1342 levels in the hippocampus were detected to increase as early as the age of 22 weeks,and kept the increase to continue with aging.The morphological results showed no obvious neuron loss in the sections of Nissl staining,while serious distonion and disorder of the dendrites of the hippocampal neurons were observed on the sections of Gelgi staining in theAPP/PS1 transgenic mouse.The present results suggested that it seemed something wrong in the processes of phospholization of PAK,butnot in the expression of the PAK itself;the toxic Aβ42 might affect the PAK in its phospholization,which in turn directly influence thedendritic development in the hippocampal neurons and cause the dendrites distorting and disordering.
ABSTRACT
It has been reported that the small type of neurons in the dorsal root ganglion (DRG) play an important role in pain regulation by a presynaptic mechanism via the metabotropic type-B γ-aminobutyric acid receptors ( GABABR ). In order to understand whether the 2populations of the small type of the neurons, peptidergic and nonpeptidergic, in DRG share the same role, immunoflourescent histochemical methods and confocal laser scanning microscope were employed to investigate the expression of the GABABR in the peptidergic and nonpeptidergic small DRG neurons. The results revealed that 92% of the peptidergic and 90% of nonpeptidergic small DRG neurons express GABABR in their perikarya and central processes, which distribute in the various laminae of the spinal dorsal horn. These results suggest both the peptidergic and nonpeptidergic populations of the small neurons in the DRG share similar role in pain modulation via presynaptic mechanisms but in given laminae of the spinal dorsal horn.
ABSTRACT
Amygdala (AM) plays crucial roles in emotional learning, memory and behavior. These functions of AM are carried out by three main subnuclei (lateral nucleus, basolateral nucleus and central nucleus) in AM and closely related with a transcription factor, cAMP- responsive element binding protein (CREB) in the neurons of the AM. CREB can be phosphorylated (pCREB) in many kinds of neuronal processes to regulate the synthesis of proteins for the formation of memory processes. In order to identify what neuronal types express pCREB and how the pCREB levels changed at different time intervals after an emotional stress stimulation, the present study is designed to investigate pCREB-, glutamate (Glu)- and parvalbumin (PV)- immunoreactive (IR) profiles in AM and the levels of pCREB in AM after a stress of forced swimming (FS). The results showed that the pCREB expressed in the Glu-IR neurons but not in the PV-IR neurons, and the expression level of the pCREB increased dramatically after the stress. The present results suggested that pCREB modulates the emotional processes through the Glu-IR neurons and that the pCREB greatly upregulated to response to the emotional stimuli.
ABSTRACT
As the elements of local neuronal circuits, parvalbumin (PV)-containing interneurons in the basolateral nucleus (BL) of the amygdala play an important role in the amygdaloid functions of emotion, learning and memory. In order to investigate how the PV-containing interneurons in the BL are controlled, the synapses established on PV- containing interneurons in the BL of the rat amygdala were examined under immunoelectron microscopy using the double labeling methods with anti-PV and anti-dopamine (DA) antibodies for a reference of dopaminergic axon terminals. The results show that the PV immunoreactive (IR) neurons formed the synapses mainly on the dendritic structures from shafts of the dendrites to median and small dendritic branches. 68% of the synapses on the PV-IR profiles were formed by unlabeled axon terminals, and 32 % of them were formed by DA- (21 % ) and PV- (11 % )IR axon terminals. Majority of the synapses on the PV-IR neurons formed by unlabeled axon terminals were symmetric type, and only a small a mount of them were asymmetric that were observed between the PV-IR spines and unlabeled axon terminals and in the serial synapses in which an unlabeled axon terminal symmetrically contacted to another unlabeled axon terminal that, in turn, synapsed asymmetrically to the PV-IR dendritic profiles. The synapses formed between the PV-IR profiles and DA- or PV-IR axon terminals were exclusively symmetric. The present results suggest that the PV-containing interneurons in the BL of the rat amygdala were controlled by an inhibitory network formed by the symmetric synapses around them, among which the DA system was included.
ABSTRACT
It is proposed that following peripheral nerve injury abnormal sprouting of Aβ fiber primary afferent neurons in the spinal cord contributes to the allodynia that often occurs with such injury. The present investigation is to determine whether this sprouting is reversal after compression of peripheral nerve was relieved. In a rat model of neuropathic pain made by rat sciatic nerve compression,chorela toxin B subunit conjugated horseradish peroxidase (CB-HRP) was used to trace the termination of Afiber primary afferents and sections were reacted for using tetramethylbenzidine (TMB) as the chromagen. We demonstrated that the compression to the sciatic nerve also results in hyperalgesia and novel transganglionic CB-HRP staining in laminae Ⅱ, and this sprouting can not be reversed by decompression. This structural reorganization in central nervous system and its irreversible character may contribute to the development and maintenance of neuropathic pain.
ABSTRACT
The relationships between cholinergic neurons and SP terminals were examined in the rat sacral ventral horn at the light and electron microscopic levels by means of double immunostaining methods. Cholinergic neurons were labeled by a monoclonal antibody to choline acetyltransferase (CHAT) with the avidin-biotin technique and stained bluish-green by indolyl-?-galactoside reaction products with ?-galactosidase as a marker. On the same sections, SP fibers were labeled by polyclonal antisera to SP after application of the peroxidase-antiperoxidase (PAP) method and stained brown by diaminobenzidine (DAB)reaction. At the light microscopic level CHAT-I neurons stained bluish-green and SP- I fibers Stained brown were found in the ventral horn. At the electron microscopic level, many asymmetrical axodendritic synapses(type I of Gray)were observed between CHAT-I dendrites and SP-I terminals in the ventral horn, but axosomatic synapses and symmetrical synapses (type I of Gray) were hardly detected. These results indicate that SP-I terminals make direct synapses with CHAT-I motoneurons of sacral ventral horn. These synapses may be predominantly excitatory and have importance in the control of muscular constriction.