No idea on this one. That's what your doctor is for in how this will help you get back to full recovery.
The role of orphanin FQ/nociceptin in neuroplasticity: relationship to stress, anxiety and neuroinflammation
The neuropeptide, orphanin FQ/nociceptin (OFQ/N or simply, nociceptin),
is expressed in both neuronal and non-neuronal tissue, including the
immune system. In the brain, OFQ/N has been investigated in relation to
stress, anxiety, learning and memory, and addiction. More recently, it
has also been found that OFQ/N influences glial cell functions,
including oligodendrocytes, astrocytes, and microglial cells. However,
this latter research is relatively small, but potentially important,
when observations regarding the relationship of OFQ/N to stress and
emotional functions is taken into consideration and integrated with the
growing evidence for its involvement in cells that mediate inflammatory
events. This review will first provide an overview and understanding of
how OFQ/N has been implicated in the HPA axis response to stress,
followed by an understanding of its influence on natural and learned
anxiety-like behavior.
What emerges from an examination of the
literature is a neuropeptide that appears to counteract anxiogenic
influences, but paradoxically, without attenuating HPA axis responses
generated in response to stress. Studies utilized both central
administration of OFQ/N, which was shown to activate the HPA axis, as
well as antagonism of NOP-R, the OFQ/N receptor. In contrast, antagonist
or transgenic OFQ/N or NOP-R knockout studies, showed augmentation of
HPA axis responses to stress, suggesting that OFQ/N may be needed to
control the magnitude of the HPA axis response to stress. Investigations
of behavior in standard exploratory tests of anxiogenic behavior (eg.,
elevated plus maze) or learned fear responses have suggested that OFQ/N
is needed to attenuate fear or anxiety-like behavior. However, some
discrepant observations, in particular, those that involve appetitive
behaviors, suggest a failure of NOP-R deletion to increase anxiety.
However, it is also suggested that OFQ/N may operate in an anxiolytic
manner when initial anxiogenic triggers (eg., the neuropeptide CRH) are
initiated.
Finally, the regulatory functions of OFQ/N in relation to
emotion-related behaviors may serve to counteract potential
neuroinflammatory events in the brain. This appears to be evident within
the glial cell environment of the brain, since OFQ/N has been shown to
reduce the production of proinflammatory cellular and cytokine events.
Given that both OFQ/N and glial cells are activated in response to
stress, it is possible that there is a possible convergence of these two
systems that has important repercussions for behavior and
neuroplasticity.
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