Serotonin inhibits GABA synaptic transmission in presympathetic paraventricular nucleus neurons

Predifferentiated GABAergic Neural Precursor Transplants for Alleviation of Dysesthetic Central Pain Following Excitotoxic Spinal Cord Injury

“…Two weeks after QUIS lesion, there appeared substantially fewer number of endogenous GABA-IR in the superficial laminae I and II (Figure 2B) as described previously (Lee et al, 2008). Such a loss was specific to spinal level within the QUIS injury, since endogenous GABA-IR in the contralateral side and spinal levels outside the QUIS lesion area were not affected (Figure 2A).…”

“…The lesion caused collapse of the gray matter into a thin dorso-ventral neuropil. Most neurons in the superficial laminae I and II, however, were spared from the injury even 3 weeks after QUIS lesion and a large number of NeuN-immunoreactive (NeuN-IR) cells were observed with a minimal gray matter disruption as previously reported (Lee et al, 2008). In almost all cases, neuronal cell losses were confined only to the dorsal gray matter ipsilateral to lesion.…”

“…QUIS injured rats exhibit nociceptive behaviors for mechanical and cold allodynia and self-injurious overgrooming behaviors (Brewer and Yezierski, 1998; Gorman et al, 2001). Overgrooming behavior is thought to be mediated by dysesthetic sensations originating from the affected at-level dermatomes and/or DRGs ipsilateral to insult (Brewer et al, 2008), and disruption of inhibitory tone maintained by endogenous GABAergic neurons in the superficial dorsal horn (Lee et al, 2008). QUIS injury also up-regulates ERK1/2, TNF-α, and cytokines known to be involved in molecular events leading to development of nociception (Yu and Yezierski, 2005; Brewer and Nolan, 2007).…”

“…Loss of endogenous GABA-IR cells following QUIS or CNS/PNS injuries may play an important function in modulating nociception (Zhang et al, 1994; Lee et al, 2008), yet their role remains elusive (Polgar et al, 2003; Polgar and Todd, 2008). Chronic constriction injury in rats induce increased number of picnotic cells, hyperchromatic “dark neurons” possibly indicative of transsynaptic degeneration in the superficial spinal or medullary dorsal horn, in the superficial dorsal horn by one week post injury (Ibuki et al, 1997), and spared nerve injury decreases primary afferent-induced IPSCs in lamina II neurons, presumably due to the loss of GABA resulting from decreased GAD 65 expression (Moore et al, 2002).…”

In Vivo Discharge Properties of Hypothalamic Paraventricular Nucleus Neurons With Axonal Projections to the Rostral Ventrolateral Medulla

“…They indicate that many are quiescent in anesthetized rats and those with spontaneous activity most often fire slowly (Յ1.5 spike/s) at rest (Bains and Ferguson 1995;Bains et al 1992;Chen and Toney 2003a;Lovick and Coote 1988a,b). In response to local application of various neurotransmitters (Bains and Ferguson 1995;Cato and Toney 2005;Lee et al 2008;Li et al 2004;Lovick and Coote 1988a) and inputs activated by circulating hormones (e.g., angiotensin II, ANP) (Bains and Ferguson 1995;Bains et al 1992;Cato and Toney 2005;Lovick and Coote 1988a), high-frequency discharge can be evoked. There is also evidence that some spontaneously active PVN-IML neurons are targeted by inhibitory inputs from arterial (Bains and Ferguson 1995;Chen and Toney 2003a;Lovick and Coote 1988b) and cardiopulmonary baroreceptors (Lovick and Coote 1988a,b).…”