Neuroscience letters
-
Neuroscience letters · Aug 2005
Comparative StudyThe effect of acupuncture on motor cortex excitability and plasticity.
Acupuncture has been used extensively in facilitating motor recovery after stroke. Its mechanism of action remains uncertain. In this sham-controlled study, we demonstrate for the first time that acupuncture has a real and enduring effect on motor cortex functional changes, in terms of cortical excitability and output mapping using transcranial magnetic stimulation.
-
Neuroscience letters · Aug 2005
Comparative StudyLong-lasting recovery of locomotor function in chronic spinal rat following chronic combined pharmacological stimulation of serotonergic receptors with 8-OHDPAT and quipazine.
In chronic spinal rats, long-term stimulation of 5-HT receptors with quipazine or 8-OHDPAT by means of daily injection, promotes robust locomotor recovery. The question of a possible potentiation between treatments when applied together was addressed. Daily injections of both 8-OHDPAT and quipazine, were performed for a month in spinal animals. ⋯ Motor performances were significantly better after combined injection of both drugs than when the agonists were used separately. But, the most significant and new result is that the locomotor scores did not decrease during the weeks that followed the end of the treatment. These results suggests a long-lasting and 5-HT-dependent reorganisation of spinal networks.
-
Neuroscience letters · Aug 2005
Comparative StudyUpregulation of the phosphorylated form of CREB in spinothalamic tract cells following spinal cord injury: relation to central neuropathic pain.
Spinal cord injury (SCI) often leads to the generation of chronic intractable neuropathic pain. The mechanisms that lead to chronic central neuropathic pain (CNP) following SCI are not well understood, resulting in ineffective treatments for pain relief. Studies have demonstrated persistent hyperexcitability of dorsal horn neurons which may provide a substrate for CNP. ⋯ This study determined that, in animals experiencing at-level allodynia 35 days after SCI, pCREB was upregulated in the spinal cord segment rostral to the injury. In addition, pCREB was found to be upregulated specifically in STT cells in the rostral segment 35 days after SCI. These findings suggest one mechanism of maintained central neuropathic pain following SCI involves persistent upregulation of pCREB expression within STT cells.
-
Neuroscience letters · Aug 2005
Comparative StudyDegradation of response modulation of visual cortical cells in cats with chronic exposure to morphine.
The primary visual cortex (V1) plays an important role in vision and visual perception. Studies in many brain regions demonstrate that opiate abuse can change excitatory and inhibitory neurotransmission. To investigate the effect of chronic morphine exposure on the response modulation of V1 simple and complex neurons, we carried out in vivo extracellular recordings in V1 of morphine- and saline-treated (control) cats. ⋯ The decrease of response modulation was caused by an increase of F0. Further, morphine re-exposure significantly improved the response properties of V1 neurons in morphine-treated cats. These results suggest that chronic morphine treatment leads to a significant degradation of response modulation of V1 neurons and a morphine dependence of primary visual cortical function.
-
Neuroscience letters · Aug 2005
Comparative StudyIschemic tolerance induction in organotypic hippocampal slices: role for the GABA(A) receptor?
Ischemic preconditioning (IPC) refers to sublethal ischemic insults rendering brain tissue tolerant against subsequent ischemic insults. We investigated the role of the GABA(A) receptor (GABA(A)R) upon IPC induction. Rat organotypic hippocampal slices were subjected to IPC by 15 min of oxygen-glucose deprivation (OGD) followed by 40 min of OGD 48 h later, resulting in robust cell death reduction as assessed by the propidium iodide fluorescence method ('late' or 'second window' IPC). ⋯ However, temporary administration of bicuculline 48 h prior to ischemic challenge was not neuroprotective. In another approach, we tested whether preconditioning with the GABA(A)R agonist, 4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP) mediated ischemic tolerance and found no significant neuroprotection. The results are discussed in light of the intrinsic excitatory-inhibitory balance of glutamate and GABA.