The neurotrophin brain-derived neurotrophic factor (BDNF) plays an essential role during development, promoting the survival of specific populations of central and peripheral neurons. During adulthood, BDNF also acts as a synaptic modulator in several areas of the central nervous system (CNS), including the spinal cord, and is involved in short and long term changes of synaptic efficacy. In spinal cord dorsal horn BDNF is expressed in the peptidergic terminals originating from primary afferent fibres, while its high affinity receptor trkB has been detected on both primary afferent terminals and dorsal horn neurons. In superficial dorsal horn, exogenous BDNF modulates fast excitatory (glutamatergic) and inhibitory (GABAergic/glycinergic) signals, as well as slow peptidergic neurotransmission. Conditions of inflammatory and neuropathic pain alter the expression of BDNF and trkB receptors in dorsal horn. In experimental pain models, modulation of synaptic transmission by BDNF plays an important role in the induction and maintenance of central sensitization.
BDNF and TrkB mediated mechanisms in the spinal cord / Bardoni, R., Merighi, A. - In: Synaptic Plasticity in Pain233 SPRING STREET, NEW YORK, NY 10013, UNITED STATES : Springer New York, 2009. - ISBN 9781441902252. - pp. 89-108 [10.1007/978-1-4419-0226-9_5]
BDNF and TrkB mediated mechanisms in the spinal cord
Bardoni R.;
2009
Abstract
The neurotrophin brain-derived neurotrophic factor (BDNF) plays an essential role during development, promoting the survival of specific populations of central and peripheral neurons. During adulthood, BDNF also acts as a synaptic modulator in several areas of the central nervous system (CNS), including the spinal cord, and is involved in short and long term changes of synaptic efficacy. In spinal cord dorsal horn BDNF is expressed in the peptidergic terminals originating from primary afferent fibres, while its high affinity receptor trkB has been detected on both primary afferent terminals and dorsal horn neurons. In superficial dorsal horn, exogenous BDNF modulates fast excitatory (glutamatergic) and inhibitory (GABAergic/glycinergic) signals, as well as slow peptidergic neurotransmission. Conditions of inflammatory and neuropathic pain alter the expression of BDNF and trkB receptors in dorsal horn. In experimental pain models, modulation of synaptic transmission by BDNF plays an important role in the induction and maintenance of central sensitization.
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