Search PubMed⌕ Search

Biomedical subjects

N H Neff

Publications and source records attributed to N H Neff.

At least 145 records · Page 8Linked to original sources
PubMed1980

Regional distribution of cholinergic muscarinic receptors in spinal cord.

Quinuclidinylbenzilate ([3H]QNB) binding sites are present in the rat spinal cord. The binding site are muscarinic in character based on displacement of [3H]QNB by cholinoceptive drugs. They are distributed rather uniformly along the cord, although the receptor density is greater in gray matters than in white matter. Binding to white matter may be associated with glial cells. Within the gray matter, the receptor density is higher in the ventral horn than in the dorsal horn. In the thoracic region receptor density is about equal in the intermediate zone and ventral horn. Mid-thoracic transection of the cord does not change the receptor density or the dissociation constant of [3H]QNB in the lumbar cord. In contrast, treatment with the neurotoxin, 6-aminonicotinamide, which produces lesions of the cord, loss of motor control and paralysis, reduces the receptor density and affinity of [3H]QNB for lumbar gray matter but not white matter. The presence of [3H]QNB binding sites thrughout the spinal cord as well as the documented presence of acetylcholine-containing neurons, suggest that muscarinic receptors play a role in all phases of spinal cord physiology.

6-Aminonicotinamide↗
PubMed1979

Muscarinic receptor binding in the rat adrenal medulla.

Muscarinic receptor binding sites are present in rat adrenal gland andare associated primarily with the medulla. A Scatchard analysis using the ligand [3H]-quinuclidinyl benzylate (eH-QNB) revealed a KD of 0.064 nM and a Bmax of 66 fmol/mg prot. Denervation of the adrenal gland had no significant effect on 3H-QNG binding. The presence of muscarinic receptor binding sites in the adrenal medulla is consistent with reports that muscarinic receptors play a role in the release of adrenal catecholamines and modulation of cycle 3',5'-guanosine monophosphate.

Adrenal Medulla↗
PubMed1979

Central mediation of the antihypertensive effect of pargyline in spontaneously hypertensive rats.

The monoamine oxidase (MAO) inhibitor pargyline induced a moderate (about 20 mm Hg) but persistent (48 h) decrease of systolic blood pressure in unanesthetized adult spontaneously hypertensive rats (SHR) but not in normotensive rats. The fall of blood pressure correlated with the blockade of norepinephrine (NE) deamination by brain homogenates. After an intracerebroventricular (icv) injection of 6-hydroxydopamine, which lowered brain NE content by about 70%, pargyline was unable to diminish arterial pressure. Blockade of central alpha-adrenoceptors by treatment with phentolamine (100 microgram icv) could either prevent or reverse the fall of blood pressure in SHR induced by pargylline. Moreover, a low dose of pargyline injected directly into the brain lowered arterial pressure. We conclude that the hypotensive action of pargylline in SHR appears to be the consequence of NE accumulating at an inhibitory alpha-adrenoceptor in brain.

Animals↗
PubMed1979

Activation of rat sympathetic ganglia SIF cell dopamine metabolism by muscarinic agonists.

The biochemical responsiveness of the dopamine-containing small intensely fluorescent (SIF) cells to cholinoceptive drugs was evaluated in rat superior cervical ganglion (SCG), middle-inferior cervical ganglion and celiac ganglion. Amines and metabolites were analyzed by mass fragmentography. The major metabolite of dopamine (DA) in all ganglia was 3,4-dihydroxyphenylacetic acid (DOPAC). Stimulation of muscarinic receptors with carbachol induced a 3-10 fold increase of DOPAC concentration in the ganglia, the celiac ganglion being the most responsive and the SCG being the least. Pretreatment with atropine blocked the rise of DOPAC. The rise of DOPAC after activation of muscarinic receptors was not the consequence of blocking the removal of this acid from the ganglion. We concluded that DA metabolism in SIF cells is enhanced by stimulation of muscarinic receptors and that the magnitude of the DOPAC increase in a ganglion may reflect the importance of DA in ganglionic transmission.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1978

Light stimulates tyrosine hydroxylase activity and dopamine synthesis in retinal amacrine neurons.

Retinal dopamine-containing amacrine neurons are rapidly activated by light, as shown by an increase in the rate of dopamine formation in vivo and a concomitant increase in the activity of tyrosine hydroxylase, measured in vitro with a subsaturating concentration of pteridine cofactor. Activation of tyrosine hydroxylase also occurs when isolated eyes from rats killed in the dark are exposed to a strobe light. Studies of amacrine neurons should provide basic data about the biochemical processing of visual information, as well as the physiological presynaptic regulatory mechanisms of dopamine-containing neurons.

Animals↗
PubMed1978

Increased adenylate cyclase activity and rapid weight loss following intraseptal injection of cholera toxin.

Cholera toxin, stereotaxically injected into the medial septal nucleus of the rat, leads within 24 h to a dramatic decrease in body weight and an increase in septal adenylate cyclase activity. Toxin-treated rats drink one-third the water of vehicle-treated animals while excreting two-and-one half times the urine. Food intake over the 24-h period is depressed to 13% of control but feces production was normal. The dramatic increase of urinary output suggests that cholera toxin activates a septal adenylate cyclase system which supressess the release of antidiuretic hormone. Cholera toxin injection into the septum may be a unique alternative to electrical stimulation for investigating septal involvement in the regulation of neuronal and metabolic processes.

Adenylyl Cyclases↗