Biomedical subjects

E N Hernandez

Publications and source records attributed to E N Hernandez.

4 recordsLinked to original sources

PubMed1990

Modulation of memory retention by neuropeptide K.

Neuropeptide K (NPK) is one of the structures in beta-preprotachykinin which also includes substance P. NPK, a 36 amino acid peptide, contains the sequence of neurokinin A as amino acids 27-36 of its C-terminus. Neurokinin A is also contained separately in the gamma-preprotachykinin precursor. Both NPK (2.5-10 micrograms) and neurokinin A administered intracerebroventricularly after footshock avoidance training in the T-maze enhanced memory retention in CD-1 male mice. Local microinjections of NPK enhanced memory retention when injected into the rostral and caudal portions of the hippocampus (0.25 and 0.50 microgram) and the amygdala (1.0 microgram), but were without effect when injected into the septum and the caudate. The differential effects of NPK on memory retention across brain regions differed from those previously reported for substance P and neuropeptide Y. These studies suggest that NPK, acting through discrete anatomical areas, modulates memory processing. The functional significance of co-localization of neuropeptides with classical neurotransmitters and other transmitter peptides in the same neurons is not well understood, but recent studies have indicated that the neuropeptides modulate the release of the primary transmitter. Since NPK occurs in the same precursor molecule as substance P, NPK may be co-released with the putative neurotransmitter substance P and act with it, in a synergistic manner, to enhance memory processing. These studies provide further evidence that the hippocampus is an anatomical structure involved in memory processing that occurs shortly after training.

Amino Acid Sequence↗

PubMed1989

Modulation of memory processing by neuropeptide Y varies with brain injection site.

Neuropeptide Y (NPY) is a 36 amino acid peptide which was shown to enhance memory retention, recall and prevent amnesia induced by either scopolamine or anisomycin. In this study, we examined the effects of NPY administration into 6 areas of the mouse brain on memory retention for footshock avoidance training in a T-maze. NPY was injected into the rostral and caudal hippocampus, amygdala, caudate, septum and thalamus shortly after training. NPY improved retention when injected into the rostral portion of the hippocampus and septum, impaired retention in the caudal portion of the hippocampus and amygdala and had no effect in the thalamus and caudate. NPY was ineffective at either improving or impairing retention when injected 24 h after training, thus demonstrating that the effects of NPY on retention were time-dependent and not due to proactive effects on retention test performance per se. In addition, NPY had no effect on retention when injected into overlying cortical areas. NPY antibody impaired retention when administered into the rostral hippocampus and septum; it improved retention in the caudal hippocampus and amygdala. Thus NPY antibody had the opposite effect to that of NPY on memory retention suggesting that NPY has a physiological role as a modulator of memory processing within specific anatomical areas of the central nervous system.

Animals↗

PubMed1987

Modulation of memory processing by neuropeptide Y.

Neuropeptide Y (NPY) is a 36 amino acid peptide which occurs in high concentrations in the amygdala and the hippocampus. The studies reported here demonstrate that administration of porcine NPY into the third ventricle of the brain enhanced memory retention for T-maze footshock avoidance and step-down passive avoidance training in mice. Human NPY at 5 micrograms enhanced retention but the inactive free acid form for NPY did not. NPY at 5 micrograms administered subcutaneously did not enhance retention. Post-training administration of NPY produced a dose-dependent, inverted U-shaped dose-response curve for retention of both passive and active avoidance conditioning. NPY enhanced retention in a time-dependent manner. NPY was also found to alleviate the amnesia caused by anisomycin, a protein synthesis inhibitor, and scopolamine, an anticholinergic. Pre-test administration of NPY improved recall but did not affect acquisition. These data support the concept that NPY is a modulator of memory processes.

Amnesia↗

PubMed1987

Neuropeptide Y increases food intake in mice.

Neuropeptide Y (NPY) stimulates eating in a number of species. In the studies reported here, intracerebroventricular administration of porcine NPY increased eating in mice. In the presence of food, NPY caused enhancement of water intake, whereas in the absence of food, NPY suppressed water intake. Behavioral analysis showed that NPY decreased the latency to eat, increased the time spent eating, and decreased grooming. Human NPY also increased food intake, whereas the free acid of NPY was inactive. Although some minor discrepancies in response were noted overall, NPY was as effective at stimulating food intake in genetically obese (ob/ob) mice compared with their lean littermates (ob/-), in genetically diabetic mice (db/db) and their nondiabetic heterozygote control (db/m), in streptozocin-induced diabetic mice and their controls, and in adult (8 mo old) compared with old (25 mo old) mice.

Aging↗