By Z. Steve. Tougaloo College. 2017.
Abbreviations CC Crus cerebri PoCom Posterior commissure CilGang Ciliary ganglion PrTecNu Pretectal nucleus EWNu Edinger-Westphal nucleus PulNu Pulvinar nuclear complex ILCC Intermediolateral cell column RetF Reticular formation LGNu Lateral geniculate nucleus RNu Red nucleus MGNu Medial geniculate nucleus SC Superior colliculus ML Medial lemniscus SC order 5mg emsam,Br Superior colliculus, brachium OcNr Oculomotor nerve SCerGang Superior cervical ganglion OpCh Optic chiasm SN Substantia nigra OpNr Optic nerve WRCom White ramus communicans OpTr Optic tract Review of Blood Supply to OpTr, MGB, LGB, SC, and Midbrain Tegementum, Including PrTecNu STRUCTURES ARTERIES OpTr anterior choroidal (see Figure 5–38) MGNu, LGNu thalamogeniculate branches of posterior cerebral (see Figure 5–38) SC and PrTecNu long circumferential branches (quadrigeminal) of posterior cerebral, posterior choroidal, and some from superior cerebellar (to SC) (see Figures 5–27 and 5–38) Midbrain paramedian branches of basilar bifurcation, medial branches Tegmentum of posterior cerebral and posterior communicating, short circumferential branches of posterior cerebral (see Figure 5–27) Optic, Auditory, and Vestibular Systems 221 Pupillary Pathways Dilator muscles of iris Sphincter mus. Optic radiations (in retrolenticular Cuneus limb of internal capsule) Lingual gyrus CalSul 7–26 The origin, course, and distribution of the visual pathway are Neurotransmitters: Cholecystokinin ( ) is present in some shown. Uncrossed retinogeniculate ﬁbers terminate in laminae 2, 3, geniculocalcarine ﬁbers. N-acetylaspartylglutamate is found in some and 5, while crossed ﬁbers end in laminae 1, 4, and 6. Geniculocal- retinogeniculate ﬁbers, and in some lateral geniculate and visual cor- carine ﬁbers arise from laminae 3 through 6. Upper-case let- ters identify the binocular visual ﬁelds (A, B, C, D), the macula (M), and the monocular visual ﬁelds (A , B , C , D ). This illustration is provided for self-evaluation of visual pathway understanding, for the instructor to expand on aspects of the visual pathways not covered in the atlas, or both. Optic, Auditory, and Vestibular Systems 225 226 Synopsis of Functional Components, Tracts, Pathways, and Systems Auditory Pathways 7–29 The origin, course, and distribution of the ﬁbers collectively hearing loss and conduction hearing loss, and to lateralize the deﬁcit. Central to the cochlear nerve and the Weber test, a tuning fork (512 Hz) is applied to the midline of the fore- dorsal and ventral cochlear nuclei this system is, in a general sense, bi- head or apex of the skull. In the normal patient, the sound (conducted lateral and multisynaptic, as input is relayed through brainstem nuclei through the bones of the skull) is heard the same in each year. Synapse and crossing (or re-crossing) of nerve deafness (lesions of the cochlea or cochlear nerve), the sound is best of information can occur at several levels in the neuraxis. Conse- heard in the normal ear, while in conductive deafness, the sound is best heard quently, central lesions rarely result in a total unilateral hearing loss. In the Rinne test, a tuning fork (512 Hz) is placed The medial geniculate body is the thalamic station for the relay of au- against the mastoid process.
The Indicator Dilution Method Measures Plasma water is determined by using Evans blue dye discount emsam 5 mg visa, Fluid Compartment Size which avidly binds serum albumin or radioiodinated serum The indicator dilution method can be used to determine albumin (RISA), and by collecting and analyzing a blood the size of body fluid compartments (see Chapter 14). In effect, the plasma volume is measured known amount of a substance (the indicator), which should from the distribution volume of serum albumin. The as- be confined to the compartment of interest, is adminis- sumption is that serum albumin is completely confined to tered. After allowing sufficient time for uniform distribu- the vascular compartment, but this is not entirely true. In- tion of the indicator throughout the compartment, a plasma deed, serum albumin is slowly (3 to 4% per hour) lost from sample is collected. The concentration of the indicator in the blood by diffusive and convective transport through the plasma at equilibrium is measured, and the distribution capillary walls. To correct for this loss, repeated blood sam- volume is calculated from this formula ples can be collected at timed intervals, and the concentra- tion of albumin at time zero (the time at which no loss Volume Amount of indicator/ would have occurred) can be determined by extrapolation. Concentration of indicator (1) Alternatively, the plasma concentration of indicator 10 If there was loss of indicator from the fluid compart- minutes after injection can be used; this value is usually ment, the amount lost is subtracted from the amount ad- close to the extrapolated value. For example, suppose we want to measure total tween ECF and plasma volumes. We inject 30 mL of deu- terium oxide (D2O) as an isotonic saline solution into an arm vein. After a 2-hr equilibration period, a blood sample Body Fluids Differ in Electrolyte Composition is withdrawn, and the plasma is separated and analyzed for Body fluids contain many uncharged molecules (e. Suppose during the equilibration period, urinary, (ionized substances) contribute most to the total solute respiratory, and cutaneous losses of D2O are 0. Osmolality is stituting these values into the indicator dilution equation, of prime importance in determining the distribution of wa- we get ter between intracellular and ECF compartments. Unfortunately, there is no such ideal indicator, so the exact volume of the If the plasma [Na ] is 140 mmol/L, blood glucose is 100 ECF cannot be measured. The equation indicates that Na and its accompany- termined from the volume of distribution of these ions: ra- ing anions (mainly Cl and HCO3 ) normally account for dioactive Na , radioactive Cl , radioactive sulfate, thio- more than 95% of the plasma osmolality.
It perhaps goes without saying that the proposed transmitter must be shown to be present in the CNS and preferably in the area and at the synapses where it is thought to act proven emsam 5 mg. Stimulation of the appropriate nerves should evoke a measurable release of NT. The proposed NT must produce effects postsynaptically which are identical physiologically (appropriate membrane potential changes) and pharmacologically (sensitivity to antagonists) to that produced by neuronal stimulation and the relased endogenous NT. As guidelines they provide a reasonable scientific framework of the type of investigations that must be undertaken to establish the synaptic role of a substance. As rigid rules they could preclude the discovery of more than one type of neurotransmitter or one form of neurotransmission. Nevertheless, the criteria have been widely employed and often expanded to include other features which will be considered as subdivisions of the main criteria. PRESENCE Distribution and concentration It is generally felt that a substance is more likely to be a NT if it is unevenly distributed in the CNS although if it is widely used it will be widely distributed. Certainly the high concentration (5±10 mmol/g) of dopamine, compared with that of any other monoamine in the striatum or with dopamine in other brain areas, was indicative of its subsequently established role as a NT in that part of the CNS. This does not mean it cannot have an important function in other areas such as the mesolimbic system and parts of the cerebral cortex where it is present in much lower concentrations. In fact the concentra- tion of the monoamines outside the striatum is very much lower than that of the amino acids but since the amino acids may have important biochemical functions that necessitate their widespread distribution, the NT component of any given level of amino acid is difficult to establish. Nevertheless, useful information can be deduced from patterns of distribution. Glycine is concentrated more in the cord than cortex and in ventral rather than dorsal grey or white matter. This alone would be indicative of a NT role for glycine in the ventral horn, where it is now believed to be the inhibitory transmitter at motoneurons. GABA, on the other hand, is more concentrated in the brain than in the cord and in the latter it is predominantly in the dorsal grey so that although it is an inhibitory transmitter like glycine it must have a different pattern of activity. Section of dorsal roots and degeneration of afferent fibres produces a reduction in glutamate and substance P which can then be associated with sensory inputs.
In contrast emsam 5 mg free shipping, it is easier to augment DA than NA by giving the precursor dopa because of its rapid conversion to DA and the limit imposed on its further synthesis to NA by the restriction of dopamine b-hydroxylase to the vesicles of NA terminals. The activity of the rate-limiting enzyme tyrosine hydroxylase is controlled by the cytoplasmic concentration of DA (normal end-product inhibition), presynaptic dopamine autoreceptors (in addition to their effect on release) and impulse flow, which appears to increase the affinity of tyrosine hydroxylase for its tetrahydropteridine co-factor (see below). METABOLISM Just as the synthesis of DA and NA is similar so is their metabolism. They are both substrates for monoamine oxidase (MAO) and catechol-O-methyl transferase (COMT). In the brain MAO is found in, or attached to, the membrane of the intraneuronal mitochondria. Thus it is only able to deaminate DA which has been taken up into nerve endings and blockade of DA uptake leads to a marked reduction in the level of its deaminated metabolites and in particular DOPAC. The final metabolite, homovanillic 142 NEUROTRANSMITTERS, DRUGS AND BRAIN FUNCTION acid (HVA), is one that has been both deaminated and O-methylated so it must be assumed that most of any released amine is initially taken back up into the nerve where it is deaminated and then subsequently O-methylated (Fig. Certainly the brain contains much more DOPAC (the deaminated metabolite of DA) than the corresponding O-methylated derivative (3-methoxytyramine). It is possible, however, that the high levels of DOPAC, as found particularly in rat brain, partly reflect intraneuronal metabolism of unreleased DA and it is by no means certain that the metabolism of DA to HVA is always initially to DOPAC. Thus released DA that is not taken up into neurons is probably O-methylated initially by COMT. O-methylation It is generally accepted that COMT is an extracellular enzyme in the CNS that catalyses the transfer of methyl groups from S-adenylmethionine to the meta-hydroxy group of the catechol nucleus. Until recently the only inhibitors of this enzyme were pyragallol and catechol which were too toxic for clinical use.