Yes, in mice.
Is your doctor and stroke hospital going to followup on this with researchers to get this tested in humans? If not, incompetence reigns in your stroke hospital, beginning at the top with the stroke president and board of directors. Have them all fired.
Triiodothyronine modulates neuronal plasticity mechanisms to enhance functional outcome after stroke
The
development of new therapeutic approaches for stroke patients requires a
detailed understanding of the mechanisms that enhance recovery of lost
neurological functions. The efficacy to enhance homeostatic mechanisms
during the first weeks after stroke will influence functional outcome.
Thyroid hormones (TH) are essential regulators of neuronal plasticity,
however, their role in recovery related mechanisms of neuronal
plasticity after stroke remains unknown. This study addresses important
findings of 3,5,3′-triiodo-L-thyronine (T3) in the regulation
of homeostatic mechanisms that adjust excitability – inhibition ratio
in the post-ischemic brain. This is valid during the first 2 weeks after
experimental stroke induced by photothrombosis (PT) and in cultured
neurons subjected to an in vitro model of acute cerebral ischemia. In
the human post-stroke brain, we assessed the expression pattern of TH
receptors (TR) protein levels, important for mediating T3 actions.
Our results show that T3 modulates several plasticity mechanisms that may operate on different temporal and spatial scales as compensatory mechanisms to assure appropriate synaptic neurotransmission. We have shown in vivo that long-term administration of T3 after PT significantly (1) enhances lost sensorimotor function; (2) increases levels of synaptotagmin 1&2 and levels of the post-synaptic GluR2 subunit in AMPA receptors in the peri-infarct area; (3) increases dendritic spine density in the peri-infarct and contralateral region and (4) decreases tonic GABAergic signaling in the peri-infarct area by a reduced number of parvalbumin+ / c-fos+ neurons and glutamic acid decarboxylase 65/67 levels. In addition, we have shown that T3 modulates in vitro neuron membrane properties with the balance of inward glutamate ligand-gated channels currents and decreases synaptotagmin levels in conditions of deprived oxygen and glucose. Interestingly, we found increased levels of TRβ1 in the infarct core of post-mortem human stroke patients, which mediate T3 actions. Summarizing, our data identify T3 as a potential key therapeutic agent to enhance recovery of lost neurological functions after ischemic stroke.
Our results show that T3 modulates several plasticity mechanisms that may operate on different temporal and spatial scales as compensatory mechanisms to assure appropriate synaptic neurotransmission. We have shown in vivo that long-term administration of T3 after PT significantly (1) enhances lost sensorimotor function; (2) increases levels of synaptotagmin 1&2 and levels of the post-synaptic GluR2 subunit in AMPA receptors in the peri-infarct area; (3) increases dendritic spine density in the peri-infarct and contralateral region and (4) decreases tonic GABAergic signaling in the peri-infarct area by a reduced number of parvalbumin+ / c-fos+ neurons and glutamic acid decarboxylase 65/67 levels. In addition, we have shown that T3 modulates in vitro neuron membrane properties with the balance of inward glutamate ligand-gated channels currents and decreases synaptotagmin levels in conditions of deprived oxygen and glucose. Interestingly, we found increased levels of TRβ1 in the infarct core of post-mortem human stroke patients, which mediate T3 actions. Summarizing, our data identify T3 as a potential key therapeutic agent to enhance recovery of lost neurological functions after ischemic stroke.
