Brain cortex functions

Stressful stimuli of many types produce marked increases in brain noradrenergic function. Stress produces regional selective increases in NE turnover in the locus coeruleus (LC), limbic regions (hypothalamus, hippocampus, and amygdala), and cerebral cortex. These changes can be elicited with immobilization stress, foot-shock stress, tail-pinch stress, and conditioned fear. Exposure to stressors from which the animal cannot escape results in behavioral deficits termed learned helplessness. The learned helplessness state is associated with depletion of NE, probably reflecting the point where synthesis cannot keep up with demand. These studies have been reviewed elsewhere in detail (Bremner et al. 1996a,b). 

Included among drugs that alter the permeability of the membrane are phosphatidylserine, S-adenosylmethionine, and ganglioside extracts. Phosphatidylserine, produced from purified extracts of bovine brain cortex, alters the permeability and functionality of the neuronal membrane. A study... 

An important criterion for the identification of receptor subtypes is that they are related to distinct functional responses. Based on the functional potencies of thioperamide and of tiotidine, H3A- and H3B-receptors were suggested to be linked to H3-receptor mediated inhibition of histamine release and synthesis, respectively (West et al., 1990b). At present, not much additional evidence for this suggestion has been presented. Histamine H3-receptors inhibiting noradrenaline release in mouse brain cortex slices have been suggested to represent the H3A-receptor subtype (Schlicker et al., 1992 Schlicker et al., 1994). To our knowledge, functional responses in brain tissue related to the g-receptor have never been observed however. 

Fig. 3 Autoreceptor versus heteroreceptor functions of a2-adrenoceptor subtypes, (a and b) Inhibition of electrically evoked [3H]-adrenaline release by the 012-agonist, medetomidine, from mouse brain cortex (a) or heart atria (b). In wild-type tissue specimens, medetomidine inhibited transmitter release by >90%. In tissues from a2AC-deficient mice, the agonist effect was absent (a, cortex) or significantly reduced (b, atria). Reproduced with permission from Trendelenburg et al. 2003b. (c) Overview of auto- and heteroreceptor functions of a2-adrenoceptor subtypes. For references, see text.

In addition to their functions as presynaptic autoreceptors, 0C2AR can also modulate release of other neurotransmitters (Figure 3). In the CNS, 0C2A and 0C2C receptors inhibit dopamine release in basal ganglia (Bucheler et al. 2002) as well as serotonin secretion in mouse hippocampus and brain cortex (Scheibner et al. 2001a). In the enteric nervous system, the release of acetylcholine as determined by [3H] -choline overflow from tissue slices was selectively inhibited by (X2aAR (Scheibner et al. 2002). 

Finally, several studies of brain metabolic functioning reveal that in highly symptomatic OCD patients there is a significant increase in metabolic activity (thus increased activation) in the prefrontal cortex and basal ganglia. Furthermore, this abnormal metabolic activity becomes normalized when patients are treated with SSRI antidepressants. (Baxter et al. 1992 Rapoport 1991). 

Binding to receptors from AR42J cell membranes showed an increase of bound radiopeptide as a function of amount of receptor, reaching 1.6 and 1.1% respectively for Lu-DOTATATE and l-DOTATATE. In the case of receptors obtained from rat brain cortex, a similar response was observed, reaching 8.0 and 7.6%, respectively. 

Benjamin AM, Quastel JH (1975) Metabolism of amino acids and ammonia in rat brain cortex slices in vitro a possible role of ammonia in brain function. J Neurochem 25 197-206. 

Fig. 5. Biologically active ( free ) ACh in a suspension of synaptic vesicles from rat brain cortex as a function of time. ( ) control, before acid boiling, ( ) vesicles treated with phospholipase A, (////) ACh released from control and phospholipase A-treated vesicles by acid boiling.

The following conclusions appear to appropriately describe the present state of information (a) hydroxyl functions at the steroid skeleton do not discriminate between the isoenzymes from human cardiac muscle and brain cortex (see below) (b) the lead structure proper in digitalis compounds is not 5)8,14)8-androstane-3)8,14-diol, but 5)8,14)8-androstane. 

FIGURE 6.22.4 In their concept of brain visual function, Kbrner and Matsumoto (2002) attribute a visual representation of objects to various older structures of the brain (colliculus superior (CS) and lateral geniculate nucleus (LGN)). Higher-level processing in the inferotemporal cortex is limited by persona attributes defined by the amygdala (part of the limbic system). (From Kbrner, E. and Matsumoto, G., IEEE Eng. Med. Biol. Mag., 21, 121, September/October 2002. With permission. 2002 IEEE.)... 

The ability of TMS technique to elicit neuronal response has until recently been limited to brain cortex. The coils used for TMS (such as round or a figure-of-eight coils) induce stimulation in cortical regions mainly just superficially under the windings of the coH. The intensity of the electric field drops dramatically deeper in the brain as a function of the distance from the coil [Maccabee et al., 1990 Tofts, 1990 Tofts et al., 1991 Eaton, 1992]. Therefore, to stimulate deep brain regions, a very high intensity... 

Figure 1 Map of brain cortex, indicating communication and speech functions.

Nunes, A., Bussy, C., Gherardini, L., Menegheth, M., Henero, M.A., Bianco, A., Prato, M., Pizzorusso, T, Al-Jamal, K.T., Kostarelos, K., 2012. In vivo degradation of functionalized carbon nanotubes after stereotactic administration in the brain cortex. Nanomedicine (Lond.) 7, 1485-1494. 

Figure 10.1. Ferrier (1876) mapped the different functions of the macaque brain (a) by direct stimulation of the cortex and transposed the functions to the human cortex (b).

One might have thought that d Arsonval s discovery would be sufficient to generate further studies of brain function by magnetic stimulation, but the technical solutions to this had to wait for the best part of the twentieth century until 1985 when Anthony Barker and colleagues at the University of Sheffield successfully stimulated the motor cortex and pro-... 

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