Abstract
People exposed to prolonged periods of bed rest are susceptible to cardiovascular deconditioning (CVD), which is associated with orthostatic intolerance and autonomic imbalance. Hindlimb unloading (HU) in rats induces CVD analogous to that seen in bedridden individuals. The effects of HU are likely related to plasticity within the neuronal network processing cardiovascular afferent information. The nucleus tractus solitarii (nTS) is the first integrative central region for autonomic modulation. GABA and Glutamate are the major inhibitory and excitatory neurotransmitters within this nucleus. This study investigated the mechanisms by which HU affects GABA synaptic processing within the nTS. We hypothesized that HU increases GABA synaptic activity in the nTS and alters the regulation of cross-talk between GABA and glutamate at this region. Stainless wire rings were placed in the tail of male Sprague-Dawley rats (3 weeks old). After one week of recovery the rings were connected to a suspension apparatus and rats were suspended at an angle of 30–35° for two weeks with free access to food and water. Control animals were maintained in normal postural conditions. After the HU protocol, coronal brainstem slices were generated and whole-cell patch clamp was performed to evaluate synaptic neurotransmission and electrophysiological properties of nTS neurons. Compared to control rats, HU had no significant effects on spontaneous inhibitory postsynaptic currents (sIPSCs) but increased the amplitude of IPSCs evoked by nTS stimulation (nTS-IPSC). GABAA receptor antagonists (Gabazine 20µM and Bicuculline 20µM) depolarized membrane potential in HU but not in controls. Moreover, Gabazine increased spontaneous excitatory postsynaptic currents (sEPSC) in control, indicating an increase in network activity, but had no effect in HU. The results indicate that HU increases GABAergic signaling and alters the cross-talk regulation between GABA and Glutamate neurotransmission in the nTS, which may contribute to impaired autonomic and cardiovascular control.
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