Neural Function

Carroll, E.W. and Curtis, R.L., Organization and control of neural function, in Pathophysiology, Concepts of Altered Health States, 5th ed., Porth, C.M., Ed., Lippincott-Raven Publishers, Philadelphia, 1998, chap. 37. 

Primary active cation transporters energize many of the most basic neural functions 73... 

ATP-dependent Ca2+ pumps and Na+,Ca2+ antiporters act in concert to maintain a low concentration of free cytosolic Ca2+ 79 The uniquely high resolution structural data available for the SERCAla Ca2+ pump illuminates the structure of all P-type transporters 81 P-type copper transporters are important for neural function 82... 

P-type copper transporters are important for neural function. Wilson s and Menke s diseases have major neurological components (Ch. 45). The Wilson s disease gene codes for a transporter, expressed chiefly in liver, that probably functions in Cu2+ excretion. The Menke s disease gene codes for a closely related transporter that regulates intestinal Cu2+ absorption [32],... 

Neurons and glia exhibit a remarkable diversity of shapes. These different morphologies are so characteristic and distinctive that they have been used since the time of Cajal to define functional neural functions. For example, Purkinje cells in the cerebellum have such distinctive morphologies... 

F. A Welsh (eds), Cerebral Metabolism and Neural Function. Baltimore Williams Wilkins, 1980, pp. 243-254. 

Figure 17.4. Epigenetics in the nervous system. Regulation occurs in response to synaptic inputs and/or other psychosocial-environmental stimuli. The external stimuli result in changes in the transcriptional profile of the neuron and eventually affects neural function(s). Many disorders of human cognition might involve dysfunction of epigenetic tagging. (See color insert.)...

Mactutus CF, Tilson HA. 1985. Evaluation of long-term consequences in behavioral and/or neural function following neonatal chlordecone exposure. Teratology 31(2) 177-186. 

Arise in ammonia concentration would push this equation to the left so that the concentrations of both oxoglutarate and NADH would decrease the former change conld decrease the flux through the Krebs cycle, and the latter change could decrease the rate of electron transfer. Either wonld lead to a decrease in the ATP/ADP concentration which could impair neural function. 

In addition to leukopenia and manifestations of neurotoxicity (tremor, ataxia), monkeys treated with vincristine had degenerative changes in the liver and kidney. Vindesine at doses in the range of 0.1-0.3 mg/kg weekly produced leukopenia and reduced spermatogenesis in rats but apparently did not alter neural function 42). The acute intravenous LD50 for vindesine in mice is 6.3 mg/kg, and that for the congener in which two vindesine units are linked by a disulfide bridge is 6.9 mg/kg 32). 

Metabolites that are less reactive than suicide inhibitors may impact more distant enzymes, within the same cell, adjacent cells, or even in other tissues and organs, far removed from the original site of primary metabolism. For example, organopho-sphates (OPs), an ingredient in many pesticides, are metabolized by hepatic CYPs to intermediates, which, when transported to the nervous system, inhibit esterases that are critical for neural function. Acetylcholinesterase (AChE) catalyzes the hydrolysis of the ester bond in the neurotransmitter, acetylcholine, allowing choline to be recycled by the presynaptic neurons. If AChE is not effectively hydrolyzed by AChE in this manner, it builds up in the synapse and causes hyperexcitation of the postsynaptic receptors. The metabolites of certain insecticides, such as the phos-phorothionates (e.g., parathion and malathion) inhibit AChE-mediated hydrolysis. Phosphorothionates contain a sulfur atom that is double-bonded to the central phosphorus. However, in a CYP-catalyzed desulfuration reaction, the S atom is... 

TAs one might predict, mutations in the genes for the subunits of the PDH complex, or a dietaiy thiamine deficiency, can have severe consequences. Thiamine-deficient animals are unable to oxidize pyruvate normally. This is of particular importance to the brain, which usually obtains all its energy from the aerobic oxidation of glucose in a pathway that necessarily includes the oxidation of pyruvate. Beriberi, a disease that results from thiamine deficiency, is characterized by loss of neural function. This disease occurs primarily in populations that rely on a diet consisting mainly of white (polished) rice, which lacks the hulls in which most of the thiamine of rice is found. People who habitually consume large amounts of alcohol can also develop thiamine deficiency, because much of their dietaiy intake consists of the vitamin-free empty calories of distilled spirits. An elevated level of pyruvate in the blood is often an indicator of defects in pyruvate oxidation due to one of these causes. ... 

Thus the BBBs together have a dual function, they firstly provide the especially stable fluid environment that is necessary for complex neural function, and secondly, they protect the CNS from chemical insult and damage. 

Endocannabinoids have now been implicated in a variety of brain functions. For example, EC levels increase with exposure to stressful stimuli, and may play a role in neuroadaptations to stress and well as in neural function and behaviors related to anxiety and affective states (Bortolato et al. 2006 Connell et al. 2006 Gobbi et al. 2005 Hohmann et al. 2005). 

Plant-derived neurotoxic psychodysleptics affect peripheral neural functions and motor coordination, sometimes accompanied by delirium, stupor, trance states, and vomiting. Prominent among these toxins are the pyrollizidines from peyote. Also included are erythrionones from the coral tree and quinolizidines from the mescal bean (see Figure 19.2). 

The most welcome technical achievements in life science are the ones that enhance well-being or restore impaired or lost biological functions. Rehabilitation engineering is a research field that has devoted its full spectrum of efforts to compensate for malfunctions and disorders in human biological systems. This includes the development of devices for the rehabilitation of neural disorders which are termed neural prostheses. Neural prostheses directly interface with the central and peripheral nervous system. The most commonly known neural prosthesis is the cardiac pacemaker, which has existed for more than 30 years. A variety of other lesser known devices have been developed to partially restore neural functions in disabled people. 

Duncan, J. (2001). An adaptive coding model of neural function in prefrontal cortex. Nat. Rev. Neurosci. 2, 820-829. 

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