Primary afferent-evoked synaptic plasticity in deep dorsal horn neurons from neonatal rat spinal cord in vitro Sandra M. Garraway, Susan Pockett, Shawn Hochman* Department of Physiology, University of Manitoba,Winnipeg, Manitoba, Canada Received 10 February 1997; revised version received 18 June 1997; accepted 20 June 1997 Abstract Whole-cell patch clamp recordings of deep dorsal horn neurons were undertaken in ‘thick’ transverse slices to demonstrate plasticity of primary afferent-evoked synaptic responses following conditioning stimulation. Synaptic plasticity was observed in neurons throughout the age range examined (postnatal days 3–6 and 9–16) but only long-term depression (LTD) was evocable in older animals (P9–16). Both short- and long-latency synaptic responses could undergo long-term potentiation (LTP) and LTD suggesting that AMPA/kainate and NMDA receptor-evoked responses are modifiable.  1997 Elsevier Science Ireland Ltd. Keywords: Long-term potentiation; Long-term depression; Nociception; Development The spinal cord deep dorsal horn (DDH) region contains a heterogeneous population of cells which includes local interneurons as well as propriospinal and ascending tract cells [17]. In terms of pain transmission, neurons located in the DDH (i.e. lamina IV–VI) are important because; (i) functional activity mapping studies suggest that the greatest increase in, and spatial spread of, nociceptor-induced neural activity occurs in deeper regions of the spinal cord [3,14], (ii) the DDH has an abundant population of wide dynamic range neurons [5] which encode many of the physiological components of pain sensation [1,2], and (iii) the DDH con- tains a significant fraction of the ascending tract cells which convey nociceptive information to the brain [17]. We sought to determine whether long-lasting alterations in the synaptic properties of DDH neurons could be induced by bursts of primary afferent activity. These changes would appear as either a maintained increase in synaptic efficacy termed long-term potentiation (LTP) or a maintained reduc- tion in synaptic efficacy termed long-term depression (LTD). While synaptic plasticity and its underlying mech- anisms have been studied in great detail at many central synapses, the observations of LTP and LTD in spinal cord have been identified only recently [7,8,11,13,15]. Typically, glutamate receptor activation initiates the events which lead to long-term synaptic alterations, and both NMDA and AMPA/kainate ionotropic receptors have been implicated in synaptic plasticity of spinal neurons following nocicep- tive stimulation [7,8,15]. The present study uses whole cell recordings to permit a cellular demonstration of synaptic plasticity in DDH neu- rons. Because of the functional heterogeneity of cell popu- lations within the DDH, our goal was not to characterize the cellular mechanisms of plasticity but rather to determine whether the behavior could be induced. Experiments were undertaken in two age groups; 3–6- and 9–16-day-olds. In these experiments, slices were 500–700 mm thick with attached dorsal rootlets, prepared from Sprague–Dawley rats, and the whole-cell ‘blind’ patch recording technique was used [6]. Recording electrodes contained (in mM); K- gluconate 140; EGTA 0.2; HEPES 10; GTP, Tris salt, 1; and ATP, magnesium salt 4 (pH 7.3). In order to observe synap- tic actions in the absence of contamination with Na + spikes, some recording electrodes also included 3 mM QX-314. Only recordings where series resistance and leak conduc- tance values were relatively unaltered (10% change) for the duration of data collection were accepted for analysis (36/75 cells). Identification of cell location was accom- Neuroscience Letters 230 (1997) 61–64 0304-3940/97/$17.00  1997 Elsevier Science Ireland Ltd. All rights reserved PII S0304-3940(97)00475-8 * Corresponding author. Room 420, Basic Medical Sciences Building, Department of Physiology, University of Manitoba, 770 Bannatyne Ave., Winnipeg, MB, Canada R3E 0W3; Tel.: +1 204 7893274; fax: +1 204 7893934; e-mail; shawn@scrc.umanitoba.ca