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Purpose: Non-human primate models of deep brain stimulation (DBS) play an increasingly important role in the exploration of DBS mechanisms. The establishment and recognized usefulness of such models depend on the precise positioning of the stimulating targets and electrode implants. The optimal method of targeting remains controversial. Materials and methods: This paper described an improved stereotactic procedure that uses a self-developed adaptor to improve accuracy. This involved: (1) connecting clinical stereotactic devices with the skull of primates using a self-developed adaptor; (2) pre-operation targeting via magnetic resonance imaging (MRI); (3) target re-checking by microelectrode recording (MER); (4) DBS electrode implantation; (5) post-operative MRI verification of electrode placement and (6) positioning confirmation by DBS programming. Results: Use of the adaptor enabled clinical stereotactic surgery, pre-operative MRI targeting, microelectrode mapping and post-operative verification in primate DBS operations. Discrepancies between achieved and predetermined electrode position were around 0.6 mm. DBS programming improved the motor function of the hemiparkinsonism animals and decreased the numbers of rotation induced by apomorphine, indicating the precise positioning of the stimulating target and successful implanting of electrode using this method. Conclusions: An improved stereotactic procedure was performed during a non-human primate DBS operation using a self-developed adaptor. The accuracy of DBS electrode implantation in non-human primates was improved with this method. [ABSTRACT FROM AUTHOR]

This study evaluated the role of gastrocnemius-derived brain-derived neurotrophic factor (BDNF) and possible mechanism in motor improvement in T10 spinal cord transection (SCT) rats. There was complete paralysis in hindlimbs immediately after SCT, followed by partial functional restoration with time going. The level of BDNF but not its mRNA gradually increased in caudal stump after SCT, whereas a significant increase in both BDNF and its mRNA was simultaneously seen in gastrocnemius. Injection of BDNF antibody into the gastrocnemius significantly decreased hindlimb locomotor function, downregulated the level of BDNF and its mRNA together with extracellular signal-regulated kinase 1/2 (Erk1/2). Moreover, ventral root ligation led to decrease both BDNF and Erk in caudal stump, indicating BDNF transportation from gastrocnemius into the spinal cord. We concluded that gastrocnemius-derived BDNF reduced motor functional deficits in SCT rats through Erk signaling pathway. These novel findings suggested the usage of BDNF in muscle for the treatment of spinal cord injury in clinic. [ABSTRACT FROM AUTHOR]