Biomedical subjects

Vasco Galhardo

Publications and source records attributed to Vasco Galhardo.

3 recordsLinked to original sources

PubMed2006

Recent advances in basic neurosciences and brain disease: from synapses to behavior.

Understanding basic neuronal mechanisms hold the hope for future treatment of brain disease. The 1st international conference on synapse, memory, drug addiction and pain was held in beautiful downtown Toronto, Canada on August 21-23, 2006. Unlike other traditional conferences, this new meeting focused on three major aims: (1) to promote new and cutting edge research in neuroscience; (2) to encourage international information exchange and scientific collaborations; and (3) to provide a platform for active scientists to discuss new findings. Up to 64 investigators presented their recent discoveries, from basic synaptic mechanisms to genes related to human brain disease. This meeting was in part sponsored by Molecular Pain, together with University of Toronto (Faculty of Medicine, Department of Physiology as well as Center for the Study of Pain). Our goal for this meeting is to promote future active scientific collaborations and improve human health through fundamental basic neuroscience researches. The second international meeting on Neurons and Brain Disease will be held in Toronto (August 29-31, 2007).

Behavior↗

PubMed2006

Switching-on and -off of bistable spontaneous discharges in rat spinal deep dorsal horn neurons.

Somatosensory deep dorsal horn spinal neurons were previously shown to present in vitro a bistable state of activity in which a fixed firing rate is maintained over prolonged periods in the absence of stimulation. Those periods of enhanced spinal spontaneous discharge may play a role in the genesis or maintenance of hyperalgesic states, where episodes of durable spontaneous pain are commonly reported. Here we show in vivo that a small percentage of deep spinal neurons (4% of the recorded population) are capable of rapidly shifting between low-frequency and high-frequency levels of spontaneous activity. At least one of the transitions between the two states was induced by stimulation of the receptive field, making this an interesting and unique case in which stable firing rates are switched-on or -off by somatosensory stimuli.

Action Potentials↗

PubMed2002

Peripheral inflammation increases the functional coherency of spinal responses to tactile but not nociceptive stimulation.

Reorganization of central networks and plasticity of neuronal representations have been implicated in recent years in the dynamic expression of somatosensory responses. The functional properties of spinal cells were shown to change in the scale of minutes after peripheral high-intensity stimulations and to undergo profound alterations in their responses in experimental models of chronic pain. These observations, however, are restricted to recordings from individual cells, and no information exists on how these changes may be reflected on the activity of somatosensory neuronal networks involved in pain processing. To understand how spinal cord networks may be altered after the onset of hyperalgesia, we extracellularly recorded from groups of five to nine neighboring neurons in the hindlimb representation area of the dorsal horn. The multineuronal activity evoked by cutaneous innocuous and noxious stimulation was compared before and for 3 h after the subcutaneous injection of diluted formalin. Formalin caused immediate changes in response properties and mechanical threshold of activation for the majority of the neurons and induced the incorporation of previously unresponsive neighboring neurons to the functional network. Analysis of the temporal correlation within the neuronal population revealed that formalin-induced inflammation increased the functional coherence of the network to the nonnociceptive stimulation but not to the painful stimuli. This increase in the tactile acuity of populations of nociceptive neurons may be a basis for the emergence of touch-evoked pain.

Animals↗