Search bioRxiv⌕ Search

Biology subjects

Zangrossi, H.

Publications and source records attributed to Zangrossi, H..

2 recordsLinked to original sources

Minocycline engages microglia in the midbrain periaqueductal grey to attenuate hypoxia-triggered panic-like behaviour in rats

Panic disorder (PD) is a chronic and highly disabling psychiatric disorder characterised by recurrent and unexpected panic attacks, with underlying neurobiological mechanisms poorly understood. Emerging evidence suggests that inflammatory processes may contribute to the triggering of panic attacks, with a subset of PD patients exhibiting alterations in circulating cytokine levels, while animal studies indicate that an immunoresponsive microglial phenotype may contribute to the disorders pathophysiology. Minocycline, a tetracycline-class antibiotic that crosses the blood-brain barrier, exerts anti-inflammatory effects and has demonstrated therapeutic potential in attenuating panic attacks, supporting its potential as an alternative strategy for reducing PD-related symptoms by modulating microglial activity. In this study, we investigated whether exposure of male Sprague-Dawley rats to a panicogenic stimulus, hypoxia (7% O2), is followed by microglial morphological remodelling in the midbrain periaqueductal grey (PAG), a well-known panic-associated structure, at baseline and after minocycline treatment. The effects of hypoxia on the expression of panic-like jumping behaviour were measured during the respiratory challenge, whereas microglial morphology was assessed at 1, 6, or 24h following the aversive stimulus. In a second experiment, the effects of minocycline (30 mg/kg, i.p., administered once daily for 5 days) on the immediate behavioural responses to hypoxia were compared with those produced by an acute administration of alprazolam (2 mg/kg, i.p.), a benzodiazepine widely used in the clinical management of PD. Minocycline effects on microglial morphology in the PAG were also assessed. Our findings show that hypoxia elicited robust jumping behaviour, without affecting overall locomotion. This panicogenic effect was accompanied by marked and time-dependent microglial morphological changes in the dorsomedial (dmPAG) and ventrolateral (vlPAG) columns of the PAG, consistent with a shift towards an immunoresponsive phenotype. Notably, minocycline, similarly to alprazolam, reduced the number of jumps, indicating a panicolytic effect, while also preventing hypoxia-induced microglial remodelling in the dmPAG. Altogether, these findings suggest a role for microglia in regulating hypoxia-induced panic- like behaviour, indicating that microglial inhibition, as achieved here with minocycline, represents a promising therapeutic strategy for preventing panic attacks.

neuroscience↗

Activation of the TRKB receptor mediates the panicolytic-like effect of NOS inhibitor aminoguanidine

Nitric oxide (NO) triggers escape reactions in the dorsal periaqueductal gray matter (dPAG), a core structure mediating panic-associated responses, and decreases the release of BDNF in vitro. BDNF mediates the panicolytic effect induced by antidepressant drugs and produces these effects per se when injected into the dPAG. Based on these findings, we hypothesize that nitric oxide synthase (NOS) inhibitors would have panicolytic properties associated with increased BDNF signaling in the dPAG. We observed that the repeated (7 days), but not acute (1day), systemic administration of the NOS inhibitor aminoguanidine (AMG; 15 mg/kg/day) increased the latency to escape from the open arm of the elevated T-maze (ETM) and inhibited the number of jumps in hypoxia-induced escape reaction in rats, suggesting a panicolytic-like effect. Repeated, but not acute, AMG administration (15mg/kg) also decreased nitrite levels and increased TRKB phosphorylation at residues Y706/7 in the dPAG. Notwithstanding the lack of AMG effect on total BDNF levels in that structure, the microinjection of the TRK antagonist K252a into the dPAG blocked the anti-escape effect of this drug in the ETM. Taken together our data suggest that the inhibition of NO production by AMG increased the levels of pTRKB, which is required for the panicolytic-like effect observed.

neuroscience↗