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Chapter 4. Chemical Neuroanatomy of the Primate Brain

Darlene S. Melchitzky, M.S.; David A. Lewis, M.D.
DOI: 10.1176/appi.books.9781585623860.416623

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Other chapters in this textbook address the questions of how psychotropic medications affect the brain to reduce the severity of the clinical features and symptoms of psychiatric disorders and to produce the side effects that frequently accompany their administration. Appropriately, much attention has been directed toward the neurotransmitter systems that are the targets of these medications. A potential consequence of this emphasis is the idea, in its simplest form, that an excess or deficit in the functional activity of a given neurotransmitter is the pathophysiological basis for the clinical features of interest. Although variants of this view have been very useful in motivating investigations of the molecular underpinnings and biochemical features of neurotransmitter systems and in spurring the development of novel psychopharmacological agents that influence these systems, in the extreme case this perspective tends to consider a given psychiatric disorder as the consequence solely of the postulated disturbance in a neurotransmitter system.

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FIGURE 4–1. Projections of dopamine-, norepinephrine-, serotonin-, and acetylcholine-containing neurons in the human brain.SN = substantia nigra; VTA = ventral tegmental area.Source. Adapted from Heimer 1995.

FIGURE 4–2. Low-power darkfield photomicrograph of a coronal section through macaque monkey brain processed for dopamine transporter (DAT) immunoreactivity.Consistent with its localization to dopaminergic structures, intense DAT immunoreactivity (DAT-IR) is evident in the substantia nigra pars compacta (SNc) and pars reticulata (SNr), as well as in the nigrostriatal projection to the caudate (Cd) and putamen (Pt) nuclei. Also note the marked differences in density of DAT-IR axons across the cortical regions on this section. DAT-IR axons are also present in areas not traditionally thought to contain DA axons, such as the dentate gyrus (DG) and the thalamus (Th). Scale bar = 2.0 mm. CgS = cingulate sulcus; CS = central sulcus; DA = dopamine; LS = lateral sulcus; STS = superior temporal sulcus.Source. Reprinted from Lewis DA, Melchitzky DS, Sesack SR, et al: "Dopamine Transporter Immunoreactivity in Monkey Cerebral Cortex: Regional, Laminar and Ultrastructural Localization." Journal of Comparative Neurology 432:119–138, 2001. Copyright 2001, Wiley. Used with permission.

FIGURE 4–3. Darkfield photomicrographs of (A) tyrosine hydroxylase–, (B) dopamine -hydroxylase–, (C) choline acetyltransferase–, and (D) serotonin-immunoreactive axons in area 9 of macaque monkey prefrontal cortex.Note the differences in relative density and the distinctive laminar distribution of each afferent system. Scale bar = 200 m. WM = white matter.Source. Adapted from Lewis et al. 1992.

FIGURE 4–4. Schematic representation of coronal sections from macaque monkey prefrontal cortex illustrating the relative densities of dopamine, norepinephrine, serotonin, and acetylcholine axons.Numbers refer to the cortical areas described by Walker (1940). CS = cingulate sulcus; LO = lateral orbital sulcus; MO = medial orbital sulcus; PS = principal sulcus; RS = rostral sulcus.Source. Adapted from Lewis 1992.

FIGURE 4–5. Darkfield photomicrographs of adjacent sections through the caudal part of the mediodorsal thalamic nucleus in macaque monkey labeled for (A) dopamine transporter (DAT), (B) tyrosine hydroxylase (TH), and (C) dopamine -hydroxylase (DBH).Note that the DAT- and TH-immunoreactive axons are primarily located in the ventral portion of the mediodorsal thalamic nucleus. In contrast, DBH-immunoreactive axons are present throughout the mediodorsal thalamic nucleus. Scale bar = 700 m. dc = densocellular; pc = parvocellular.Source. Reprinted from Melchitzky DS, Lewis DA: "Dopamine Transporter–Immunoreactive Axons in the Mediodorsal Thalamic Nucleus of the Macaque Monkey." Neuroscience 103:1033–1042, 2001. Copyright 2001, Elsevier. Used with permission.

FIGURE 4–6. Darkfield photomicrographs of (A) dopamine transporter (DAT)–, (B) tyrosine hydroxylase (TH)–, and (C) dopamine -hydroxylase (DBH)–immunoreactive axons in adjacent sections through vermal lobule VIIIB of macaque monkey cerebellum.Note that both the TH- and DAT-immunoreactive axons are primarily restricted to the granule cell layer (GC), with some clusters of axons extending into the Purkinje cell layer. TH-immunoreactive axons are also present in the molecular layer (ML), but no DAT-immunoreactive axons are detectable in this layer. In contrast, DBH-immunoreactive axons are distributed across all layers. In addition, the restricted lobular distribution of DAT-immunoreactive axons is illustrated by the marked paucity of these axons in the GC (asterisks in B) of the folium across the white matter, whereas the density of DBH-immunoreactive axons does not seem to differ across lobules. Scale bar = 150 m.Source. Reprinted from Melchitzky DS, Lewis DA: "Tyrosine Hydroxylase- and Dopamine Transporter–Immunoreactive Axons in the Primate Cerebellum: Evidence for a Lobular- and Laminar-Specific Dopamine Innervation." Neuropsychopharmacology 22:466–472, 2000. Copyright 2000, Elsevier. Used with permission.

FIGURE 4–7. Brightfield photomicrograph of a coronal section through macaque monkey brain illustrating the distribution of cannabinoid CB1 receptor–immunoreactive axons.Association areas such as the cingulate cortex (area 32), insula (Ig, Idg), auditory association cortex (RP), and entorhinal cortex (EI) have an overall higher density of CB1-immunoreactive axons than do primary somatosensory areas (areas 3, 1, 2) and primary motor cortex (area 4). Note the distinct differences in laminar distribution of labeled processes at the boundaries of some cytoarchitectonic regions (arrows). In subcortical structures, the intensity of CB1 immunoreactivity is high in the claustrum (Cl), the basal and lateral nuclei of the amygdala, and both segments of the globus pallidus (GP); intermediate to low in the caudate (Cd) and putamen (Pu) and the central and medial nuclei of the amygdala; and not detectable in the thalamus (Th). Scale bar = 2 mm. ABmc = accessory basal nucleus, magnocellular division; ABpc = accessory basal nucleus, parvicellular division; Bi = basal nucleus, intermediate division; Bmc = basal nucleus, magnocellular division; Bpc = basal nucleus, parvicellular division; CC = corpus callosum; Cd = caudate; Ce = central amygdaloid nucleus; Cgs = cingulate sulcus; Cl = claustrum; COp = posterior cortical nucleus; cs = central sulcus; EI = entorhinal cortex, intermediate field; GPe = globus pallidus, external; GPi = globus pallidus, internal; Idg = insula, dysgranular; Ig = insula, granular; ips = intraparietal sulcus; Ldi = lateral nucleus, dorsal intermediate division; lf = lateral fissure; Lv = lateral nucleus, ventral division; Lvi = lateral nucleus, ventral intermediate division; Me = medial amygdaloid nucleus; PN = paralaminar nucleus; Pu = putamen; R = rostral auditory area (core primary auditory); rf = rhinal fissure; RM = rostromedial auditory belt; RP = rostral auditory parabelt; SII = second somatosensory cortex; sts = superior temporal sulcus; TE = inferotemporal cortex; Th = thalamus; TPO = temporal parieto-occipital associated area in sts.Source. Reprinted from Eggan SM, Lewis DA: "Immunocytochemical Distribution of the Cannabinoid CB1 Receptor in the Primate Neocortex: A Regional and Laminar Analysis." Cerebral Cortex 17:175–191, 2007. Copyright 2007, Oxford. Used with permission.

FIGURE 4–8. (A) Schematic illustration of synaptic contacts between different subpopulations of GABA neurons and a layer 3 pyramidal neuron in monkey prefrontal cortex. (B) Film autoradiograms showing signals for parvalbumin (PV), somatostatin (SST), and calretinin (CR) mRNAs in human prefrontal cortex.(A) The indicated synaptic connections of each subpopulation of GABA neuron are based on previous studies (see text for details).(B) Note the different laminar distribution of these three subclasses of GABA neurons. GABA = -aminobutyric acid; WM = white matter.Source. Adapted from Gonzalez-Burgos G, Hashimoto T, Lewis DA: "Inhibition and Timing in Cortical Neural Circuits" (Images in Neuroscience). American Journal of Psychiatry 164:12, 2007. Copyright 2007, American Psychiatric Association. Used with permission.

FIGURE 4–9. Schematic diagram of basal ganglia circuitry, illustrating the direct and indirect pathways.See text for details. DA = dopamine; DYN = dynorphin; ENK = enkephalin; GABA = -aminobutyric acid; GPe = external globus pallidus; GPi = internal globus pallidus; SNc = substantia nigra pars compacta; SNr = substantia nigra pars reticulata; SP = substance P; STN = subthalamic nucleus.Source. Adapted from Parent A, Sato F, Wu Y, et al: "Organization of the Basal Ganglia: The Importance of Axonal Collateralization." Trends in Neurosciences 23:S20–S27, 2000. Copyright 2000, Elsevier. Used with permission.

FIGURE 4–10. Organization of striatonigralstriatal projections.The organization of functional corticostriatal inputs (red = limbic, green = associative, blue = motor) is illustrated (see text for details). DLPFC = dorsolateral prefrontal cortex; IC = internal capsule; OMPFC = orbital and medial prefrontal cortex; SNc = substantia nigra pars compacta; SNr = substantia nigra pars reticulata. VTA = ventral tegmental area.Source. Adapted from Haber SN, Fudge JH, McFarland NR. "Striatonigrostriatal Pathways in Primates Form an Ascending Spiral From the Shell to the Dorsolateral Striatum." Journal of Neuroscience 20:2369–2382, 2000. Copyright 2000, Society for Neuroscience. Used with permission.

FIGURE 4–11. Projections of orexin-containing neurons in the human brain.SN = substantia nigra; VTA = ventral tegmental area.Source. Adapted from Heimer 1995.

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