PubMed · 14147458
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
M V BENNETT. 1964. NERVOUS FUNCTION AT THE CELLULAR LEVEL.. https://doi.org/10.1146/annurev.ph.26.030164.001445
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
The cholinergic division of the avian nucleus isthmi, the homolog of the mammalian nucleus parabigeminalis, is composed of the pars parvocellularis (Ipc) and pars semilunaris (SLu). Ipc and SLu were studied with in vivo and in vitro tracing and intracellular filling methods. 1) Both nuclei have reciprocal homotopic connections with the ipsilateral optic tectum. The SLu connection is more diffuse than that of Ipc. 2) Tectal inputs to Ipc and SLu are Brn3a-immunoreactive neurons in the inner sublayer of layer 10. Tectal neurons projecting on Ipc possess "shepherd's crook" axons and radial dendritic fields in layers 2-13. 3) Neurons in the mid-portion of Ipc possess a columnar spiny dendritic field. SLu neurons have a large, nonoriented spiny dendritic field. 4) Ipc terminals form a cylindrical brush-like arborization (35-50 microm wide) in layers 2-10, with extremely dense boutons in layers 3-6, and a diffuse arborization in layers 11-13. SLu neurons terminate in a wider column (120-180 microm wide) lacking the dust-like boutonal features of Ipc and extend in layers 4c-13 with dense arborizations in layers 4c, 6, and 9-13. 5) Ipc and SLu contain specialized fast potassium ion channels. We propose that dense arborizations of Ipc axons may be directed to the distal dendritic bottlebrushes of motion detecting tectal ganglion cells (TGCs). They may provide synchronous activation of a group of adjacent bottlebrushes of different TGCs of the same type via their intralaminar processes, and cross channel activation of different types of TGCs within the same column of visual space.
Leptin produces effects in central nervous system and peripheral tissues via its specific receptors. Leptin also stimulates nitric oxide release in a concentration-dependent manner. In this study, our aim was to test the hypothesis that whether leptin has a modulatory role on endothelium or smooth muscle function in streptozotocin (STZ)-induced diabetic rats. Wistar-Albino rats were divided into four groups: 1 -- Control, 2 -- Diabetic, 3 -- Control + leptin and 4 -- Diabetic + leptin. Experimental diabetes was produced by intraperitoneal injection of a single dose of STZ (55 mg/kg). Diabetes was determined by increased fasting blood glucose level on the 7th day of the experiment. Leptin (0.1 mg/kg/day) was administered intraperitoneally for 5 days. At the end of the 5th day, thoracic aortas were isolated and phenylephrine (Phe)-induced contractions and acetylcholine (ACh)-induced relaxations of each group were estimated. In diabetic rats, Phe-induced contractility was increased (p < 0.05). Leptin pre-treatment increased the Phe-induced contractility significantly in aortic rings obtained from diabetic rats (p < 0.05). In normal rats, leptin administration produced only a slight and non-significant increase in Phe-induced contractions. Although the relaxant responses were decreased in diabetic rats, leptin administration enhanced the ACh-induced relaxation in both normal and diabetic animals significantly. As a conclusion; chronic leptin pre-treatment caused a significant increase both in Phe-induced contractions and ACh-induced Endothelial-Derived Relaxing Factor (EDRF)/Nitric oxide-mediated relaxations in the aortic rings isolated from streptozotocin-induced diabetic rats. This peptide hormone caused a significant increase in the relaxations obtained by ACh while not inducing a significant alteration in the contractile effect of Phe in control rats.
Mild cognitive impairment (MCI) is a condition with an increased risk of developing Alzheimer's disease. Chief complaint and diagnostic criterion in subjects with mild cognitive impairment is memory failure. We hypothesized that cholinergic malfunction may underlie memory impairment in these subjects and applied a low dosage of an acetylcholinesterase inhibitor and modulator of nicotinic acetylcholine receptors, galantamine (4 mg bid), for 7 days. We used neuropsychological tests to investigate attention, cognitive flexibility, verbal and visual short-term and working memory, susceptibility to interference and episodic memory and functional magnetic resonance imaging to assess spatial navigation both prior to and after treatment. Late episodic learning and delayed recall improved on treatment as did recruitment of the hippocampal region during spatial navigation. Performance in all other neuropsychological measures remained unchanged. We show that an increase of cholinergic neurotransmission in subjects with MCI specifically improves hippocampal function and thus that a cholinergic deficit is functionally relevant in subjects with MCI. Malfunction of the cholinergic system may be tackled pharmacologically via the inhibition of acetylcholinesterase even when the impairment is slight.