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GABAB receptors decrease inhibitory synaptic transmission onto sympathetic preganglionic neurones (SPNs) in the rat spinal cord slice preparation.
Author(s) -
Wang LiHua,
Deuchars Jim,
Deuchars Susan A
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a884-b
Subject(s) - inhibitory postsynaptic potential , gabab receptor , postsynaptic potential , neurotransmission , spinal cord , baclofen , chemistry , neuroscience , excitatory postsynaptic potential , receptor , biophysics , gabaa receptor , biology , agonist , biochemistry
Activation of GABA B receptors has a profound effect on sympathetic outflow from the spinal cord (Cheng et al 2005 J. Appl. Physiol. 99 –1667) but little is known about the role of these receptors on synaptic transmission in autonomic regions. We determined how baclofen affects inhibitory synaptic transmission onto SPNs. Wistar rats (11 days old) were anaesthetized with urethane and whole‐cell patch clamp recordings made from SPNs in 300μm transverse slices of thoracic spinal cord. Bath application of baclofen (0.5–5μM) hyperpolarised 21/41 SPNs associated with a decrease in input resistance. These low concentrations hyperpolarised 4/4 interneurones but glial cells were not affected (n = 4). Inhibitory postsynaptic potentials (IPSPs) elicited by stimulating the lateral funiculus (Lf) or the central autonomic area (CAA) were significantly (p<0.05) reduced in amplitude by 1 μM baclofen (Lf 12.4± 1.7 mV (mean ± S.E.M.) to 9.4 ± 1.2 mV, n= 10; CAA 9.6 ± 1.6 mV to 7.0 ± 1.3 mV, n= 13). These decreases were accompanied by an increase in paired pulse ratio of amplitude of IPSPs elicited from both regions. Similar effects on IPSP amplitudes were observed regardless of the postsynaptic response and whether or not potassium channel blockers were included in the patch solution. Thus, these results indicate that presynaptic GABA B receptors can influence sympathetic outflow. Supported by The British Heart Foundation.