Clitoria ternatea (Linn) root extract treatment during growth spurt period enhances learning and memory in rats.

Neonatal rat pups (7 days old) were intubated with either 50 mg/kg body weight or 100 mg/kg body weight of aqueous root extract of Clitoria ternatea (CTR) for 30 days. These rats were then subjected to open field, two compartment passive avoidance and spatial learning (T-Maze) tests (i) immediately after the treatment and (ii) 30 days after the treatment, along with age matched normal and saline control rats. Results showed no change in open field behaviour, but showed improved retention and spatial learning performance at both time points of behavioural tests, indicating the memory enhancing property of CTR which implicates a permanent change in the brain of CTR treated rats.

Effects of p-chlorophenylalanine-induced depletion of brain serotonin on retrieval of appetitive and aversive memories.

This study examined whether depletion of central serotonin produces an improved retrieval of aversive memories in the same way as pre-exposure to inescapable footshocks, in rats. Animals conditioned in a T-maze with appetitive (10% sucrose) and aversive (2.0 mA footshock) events were given i.c.v. 24 hr later a single dose of p-chlorophenylalanine (p-CPA). (100, 200, 400 micrograms/rat) or drug vehicle. The retention performance and activity were assessed 48 hr after treatment with this depletor. While lower doses of p-CPA selectively reduced serotonin levels in striatum and anterior cortex, higher doses reduced both serotonin and norepinephrine levels in hippocampus in a dose-dependent fashion. The depletor however, failed to produce a differential improvement of aversive memory retrieval. On the contrary, p-CPA reduced the latency to enter both, previously shocked and appetitively reinforced, goalboxes. The enhanced traversing behaviour in T-maze, together with an increased central entry in the open field that observed in depleted groups, might suggest an anxiolytic activity of p-CPA.

A study of antitrypsin and macroglobulin levels in serum and saliva of patients with gingivitis.

Periodontal diseases are associated with chronic inflammation. The destruction of connective tissue matrix is responsible for the pathogenesis of chronic inflammatory states. The degradation of matrix is initiated extra and pericellularly by proteinases produced locally at the inflammatory site. The regulation of these proteinases are by inhibitors present in serum and extravascular tissues, and it is the proteinase/proteinase inhibitor balance that determines the progression of chronic inflammatory state. Few contradicting studies are available on changes in the levels of proteinase inhibitors in serum in periodontal disease. The occurrence of these inhibitors in saliva has not been studied in detail. The present study was aimed at measuring the Proteinase inhibitors in serum and saliva of patients with periodontal disease.

Effects of DSP-4-induced depletion of brain norepinephrine on appetitive and aversive memory retrieval.

This study examined whether depletion of central norepinephrine produces an improved retrieval of aversive memories in the same way as pre-exposure to inescapable footshocks, in rats. Animals conditioned in a T-maze with appetitive (10% sucrose) and aversive (2.0 mA footshock) events were given a single dose of DSP-4 (100, 200 or 400 micrograms/rat) or drug vehicle ICV 24 hr later. The retention performance and activity were assessed 48 hr after the treatment with this neurotoxin. DSP-4 had no effect on open field activities but enhanced latencies to enter both, previously shocked and appetitively reinforced, goalboxes. The data thus, suggest that central administration of DSP-4 does not result in selective enhanced aversive memories. On the contrary, post-trial NE depletion with this neurotoxin might interfere with the retrieval of previously learned association with appetitive stimuli. DSP-4 significantly reduced monoamines, depending upon the brain regions assayed and the doses studied. However, only decreased NE in striatum coincided with the memory changes suggesting that NE innervation to striatum may participate in the retrieval process.