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Intraperitoneal injection or IP injection is the injection of a substance into the peritoneum (body cavity). It is more often applied to non-human animals than to humans. In general, it is preferred when large amounts of blood replacement fluids are needed or when low blood pressure or other problems prevent the use of a suitable blood vessel for intravenous injection.
The compound crosses the blood-brain-barrier and exerts central TrkB blockade, producing effects as early as 30 minutes (~400 nM) and as long as 6 hours (~10 nM) following intraperitoneal injection in mice. [1] It blocks the neurotrophic actions of BDNF without compromising neuron survival. [1]
In one study, intraperitoneal injection of α-Interferon was done on mice and there was no impact on monoamine levels. Another study conducted a similar experiment using the ICV injection method. This study showed reduced monoamine levels in the frontal cortex, in a dose-dependent manner. [ 6 ]
Routes of administration of injections in laboratory mice are mainly subcutaneous, intraperitoneal and intravenous. Intramuscular administration is not recommended due to small muscle mass. [ 62 ] Intracerebral administration is also possible.
Lixisenatide was equally effective at a lower dose compared to liraglutide in some of the measured parameters after ten weeks of daily intraperitoneal injections with liraglutide (2.5 or 25 nmol/kg) or lixisenatide (1 or 10 nmol/kg) or saline of APP/PS1 mice at an age when amyloid plaques had already formed.
With intraperitoneal injection to mice, deoxygedunin crosses the blood-brain-barrier into the central nervous system and possesses a long duration of action, with onset of action at 2 hours post-administration and peaking between 4–8 hours. [1] Relative to 7,8-DHF, deoxygedunin has weaker binding affinity for TrkB (K d = 1.4 μM).
Oral intake of Lac-Phe does not have anti-obesity effects in mice, though intraperitoneal injection does reduce food intake and weight gain. [6] Activity dependent cell labeling indicates Lac-Phe activated neural populations in the hypothalamus and brainstem. [15]
Cell culture models show that retinal ganglion cells can be prevented from dying by certain pharmacological treatments. Intraperitoneal injection of Epo in DBA/2J mice protected / slowed down the degeneration of Retinal ganglion cell (RGC). [26] Overexpression of Epo and Epo mutants in the eye via, viral vectors is toxic to the retina.