PSY 511.001 Spr 2026
}
“Generates EPSP”
“Generates IPSP”
“Cycloplegia caused by Cyclopentolate 1% instilled in both eyes. By Ilovebaddies (talk) - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=112232286”
“Fig. 1: Map of the cholinergic basal forebrain. The region of interest depicts the cholinergic basal forebrain, based on a cytoarchitectonic map of cholinergic nuclei, overlaid on a human brain template in Montreal Neurological Institute space. The BFCN mask is based on combined histology and postmortem MRI [63], containing several cholinergic subdivisions within the basal forebrain, including the medial septal nucleus, diagonal band of Broca, nucleus subputaminalis, the basal magnocellular complex, and nucleus basalis of Meynert (57, 72)”
“Cholinergic circuitry of the human nucleus basalis. ACh, acetylcholine; DA, dopamine; EAA, excitatory amino acids; NE, norepinephrine; 5HT, serotonin. Question marks indicate that the connection has not been confirmed in the human brain.”
“The cholinergic system and its functions. The cholinergic system originates in the basal forebrain and sends projections to many cortical and subcortical regions. As a result, it has been implicated in a variety of functions including memory, attention, and uncertainty computations. Activity of the basal forebrain is thought to be regulated by prefrontal cortices, as well as other neuromodulatory brain regions.”
“Figure 9.6. Dopamine is synthesized in a two-step process. Tyrosine is converted into DOPA by tyrosine hydroxylase, the rate-limiting step in the pathway. Then dopamine is synthesized from DOPA by DOPA decarboxylase. Dopamine is then packaged into vesicles by vesicular monoamine transporter. ‘Dopamine Synthesis’ by Casey Henley is licensed under a Creative Commons Attribution Non-Commercial Share-Alike (CC BY-NC-SA) 4.0 International License.”
“Overview of distributions for dopamine, norepinephrine and serotonin receptors. Brodmann area map is presented in bottom left corner. A, caudate-putamen; B, globus pallidus; C, diencephalon; D, amygdala; E, CA1 region of hippocampus; F, CA2/3 region of hippocampus; G, dentate gyrus. Figure adapted from Palomero et al. (2015) with permission from Elsevier Journals.”
“The pathway of dopamine synthesis proceeds from tyrosine via tyrosine hydroxylase (TH) catalysis to levodopa (L-DOPA), and subsequent decarboxylation by dopa decarboxylase (DDC) to dopamine. Dopamine is metabolized by intraneuronal monoamine oxidase A (MAOA), and by glial and astrocyte MAOA and MAOB1,11. Selective inhibitors of MAOA (for example, moclobemide) and MAOB (selegiline, rasagiline and safinamide) do not alter the steady-state striatal dopamine levels, although chronic treatment with these drugs does enhance dopamine release, possibly due to the elevation of endogenous brain amines or receptor modulation93,194. However, non-selective MAOA/B inhibitors (such as ladostigil and those shown in Table 2) do induce highly significant increases in the levels of dopamine in the striatum and other regions93,194. Although dopamine does not pass the blood–brain barrier (BBB), L-DOPA can, and DDC inhibitors that do not pass the BBB, such as benzerazide (benserazide) and carbidopa, increase its availability to the brain. Inhibitors of catechol-O-methyltransferase (COMT), such as entacapone, also enhance L-DOPA availability and prevent the inactivation of dopamine by COMT. 3-OMD, 3-O-methyl dopa; D1, D2, dopamine receptors.”
“Depiction of location of adrenal glands in human body; zoom to detail of adrenal gland; zoom to cross section of adrenal gland; cross section shows cortex, including connective tissue capsule, zona glomerulosa, zona fasciculata, and zona reticularis; also shows medulla. By Antinksčio sandara.png Author: EdgarasLe - https://commons.wikimedia.org/wiki/File:Antinks%C4%8Dio_sandara_esp.png, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=127157804”
“The neural connections between the ENS and CNS, and neural connections between gastrointestinal organs, are quite different from those depicted in textbooks. The digestive system contains full reflex circuits of the ENS (motor neurons and interneurons in blue, sensory neurons in purple). Pathways from the gastrointestinal tract project outwards, via intestinofugal neurons (red), to the CNS (neurons in yellow), sympathetic ganglia, gallbladder and pancreas. Neurons in sympathetic prevertebral ganglia (green) receive both CNS and ENS inputs. Sensory information goes both to the ENS, via intrinsic primary afferent (sensory) neurons (purple) and to the CNS via extrinsic primary afferent neurons (also purple) that follow spinal and vagal afferent routes. Pathways from the CNS reach the ENS and gastrointestinal effector tissues through vagal, sympathetic and pelvic pathways. Abbreviations: CNS, central nervous system; ENS, enteric nervous system.”
“In this drawing of the brain, the serotonergic system is red and the mesolimbic dopamine pathway is blue. There is one collection of serotonergic neurons in the upper brainstem that sends axons upwards to the whole cerebrum, and one collection next to the cerebellum that sends axons downward to the spinal cord. Slightly forward the upper serotonergic neurons is the ventral tegmental area (VTA), which contains dopaminergic neurons. These neurons’ axons then connect to the nucleus accumbens, hippocampus, and the frontal cortex. Over the VTA is another collection of dopaminergic cells, the substansia nigra, which send axons to the striatum.”
“In this drawing of the brain, the serotonergic system is red and the mesolimbic dopamine pathway is blue. There is one collection of serotonergic neurons in the upper brainstem that sends axons upwards to the whole cerebrum, and one collection next to the cerebellum that sends axons downward to the spinal cord. Slightly forward the upper serotonergic neurons is the ventral tegmental area (VTA), which contains dopaminergic neurons. These neurons’ axons then connect to the nucleus accumbens, hippocampus, and the frontal cortex. Over the VTA is another collection of dopaminergic cells, the substansia nigra, which send axons to the striatum. By NIH - http://www.drugabuse.gov/pubs/teaching/largegifs/slide-2.gif, Public Domain, https://commons.wikimedia.org/w/index.php?curid=37682508.”
“About 64,000 histamine-producing neurons, located in the tuberomamillary nucleus119 of the human brain, innervate all of the major parts of the cerebrum, cerebellum, posterior piuitary and the spinal cord.”
“About 64,000 histamine-producing neurons, located in the tuberomamillary nucleus119 of the human brain, innervate all of the major parts of the cerebrum, cerebellum, posterior piuitary and the spinal cord.”
Plus control over ANS
“By OpenStax College - Anatomy & Physiology, Connexions Web site. http://cnx.org/contents/IgqATiKA@3/The-Pituitary-Gland-and-Hypoth, Jun 19, 2013., CC BY 3.0, https://commons.wikimedia.org/w/index.php?curid=30148144”
“Figure 1: General scheme of brain acute-stress regulatory pathways. Stressors activate brainstem and/or forebrain limbic structures. The brainstem can generate rapid hypothalamic-pituitary-adrenal (HPA) axis and autonomic nervous system (ANS) responses through direct projections to hypophysiotrophic neurons in the paraventricular nucleus of the hypothalamus (PVN) or to preganglionic autonomic neurons (stress response triggers). By contrast, forebrain limbic regions have no direct connections with the HPA axis or the ANS and thus require intervening synapses before they can access autonomic or neuroendocrine neurons (top-down regulation). A high proportion of these intervening neurons are located in hypothalamic nuclei that are also responsive to homeostatic status, providing a mechanism by which the descending limbic information can be modulated according to the physiological status of the animal (‘middle management’). BST, bed nucleus of the stria terminalis; CVO, circumventricular organ; SAM, sympathoadrenomedullary system.”
“FIGURE 1. Effector systems of the stress response. A stressor elicits rapid activation of the autonomic nervous system with its sympathoneuronal (SN) and sympatho-adrenomedullary (SAM) limbs releasing their main effectors, noradrenaline and adrenaline, respectively. Activation of the hypothalamic-pituitary-adrenocortical (HPA) axis results in synthesis and release of its main effector, cortisol or corticosterone, in rodents. ACTH, adrenocorticotropic hormone; CRF, corticotropin-releasing factor.”
“Figure 3: The brain circuitry that regulates HPA axis stress responses. Stress-induced activation of the dorsal part of the medial parvocellular paraventricular nucleus of the hypothalamus (PVNmpd) originates in several brain regions (excitatory inputs are coloured blue with solid lines and inhibitory (GABA (γ-aminobutyric acid)-ergic) inputs are coloured red with dashed lines). The paraventricular nucleus of the hypothalamus (PVN) receives direct noradrenergic, adrenergic and peptidergic innervation from the nucleus of the solitary tract (NTS). The dorsomedial components of the dorsomedial hypothalamus (dmDMH) and the arcuate nucleus (Arc) provide intrahypothalamic stress excitation. The anterior part of the bed nucleus of the stria terminalis (BST), particularly the anteroventral nucleus of the BST (avBST), activates hypothalamic-pituitary-adrenocortical (HPA) axis stress responses. The PVN also receives a stress-excitatory drive from the dorsal raphe, the tuberomammillary nucleus, the supramammillary nucleus and the spinal cord, among others (omitted in the interest of space). Activation of the PVNmpd is inhibited by numerous hypothalamic circuits, including the medial preoptic area (mPOA), the ventrolateral component of the dorsomedial hypothalamus (vlDMH) and local neurons in the peri-PVN region (pPVN), encompassing the PVN surround and the subparaventricular zone. The posterior subregions of the bed nucleus of the stria terminalis (pBST) provide a prominent forebrain inhibition of HPA axis responses; most of these inputs are GABAergic. Brain sections are modified, with permission, from Ref. 154 © (1998) Academic Press.”
“FIGURE 4. Distribution of mRNA expression of corticotropin-releasing factor (CRF)-related peptides in the rodent brain. Three-dimensional expression patterns of CRF-related peptide were collapsed onto a single sagittal brain section. Depicted are well-documented sites of high to moderate expression. Sites of expression are indicated by colored dots: CRF (orange), urocortin (UCN) 1 (green), UCN2 (light blue), UCN3 (purple). 7, Facial nerve; 12, hypoglossal nerve; Amb, ambiguous nucleus; AP, area postrema; arc, arcuate nucleus; Bar, Barrington’s nucleus; BLA, basolateral amygdala; BNST, bed nucleus of the stria terminalis (d, dorsal aspect; v, ventral aspect); CA1, cornu ammonis subfield 1; CA3, cornu ammonis subfield 3; CC, corpus callosum; CeA, central amygdala; Cereb, cerebellum; CingCx, cingulate cortex; CPu, caudate putamen; DeepN, deep nucleus of cerebellum; DG, dentate gyrus; EW, Edinger Westphal nucleus; FrCx, frontal cortex; GPe, external globus pallidus; Hip, hippocampus; IC, inferior colliculus; IO, inferior olive; IPN, interpeduncular nucleus; LC, locus coeruleus; LH, lateral hypothalamus; LS, lateral septum; LSO, lateral superior olive; LTDg, laterodorsal tegmental nucleus; MeA, medial amygdala; MePO, median preoptic area; MGN, medial geniculate nucleus; MS, medial septum; MVN, medial vestibular nucleus; NAc, nucleus accumbens; NTS, nucleus of the solitary tract; OB, olfactory bulb; OccCx, occipital cortex; OT, olfactory tubercle; PAG, periaqueductal gray; ParCx, parietal cortex; PB, parabrachial nucleus; PFA, perifornical area; PG, pontine gray; Pir, piriform cortex; Pit, pituitary (p, lobe, anterior lobe, intermediate, posterior lobe); PM, premammillary nucleus; PPTg, pedunculopontine tegmental nucleus; PVN, paraventricular nucleus of the hypothalamus; R, red nucleus; RN, raphe nuclei; RTB, reticular thalamic nucleus; SC, superior colliculus; SN, substantia nigra; Sp5n, spinal trigeminal nucleus; SPO, superior paraolivary nucleus; VMH, ventromedial hypothalamus, VTA, ventral tegmental area.”
“Mean plasma levels of ingested (A) and endogenous (B) melatonin. (A) Pharmacokinetics of prolonged‐release (PRM) versus immediate‐release (IR) melatonin 2 mg formulations. Results are mean plasma melatonin levels following drug intake and expressed as % of the AUC (adapted from Zisapel, 2010). (B) Mean endogenous plasma melatonin levels (adapted from Zhdanova et al., 1998).”
“Diagrammatic representation of the control of production and the functions of melatonin, regarding seasonal and circadian timing mechanisms. Abbreviations: SCN: suprachiasmatic nucleus, PVN: paraventricular nucleus, SCG: superior cervical ganglion, NA: norepinephrine (noradrenalin), RHT: retino-hypothalamic-tract, CCG: clock-controlled genes. Based on an original diagram by Dr Elisabeth Maywood, MRC Laboratory of Molecular Biology, Neurobiology Division, Hills Road Cambridge, CB2 2QH, UK.”
“Relationship of plasma melatonin to other major circadian rhythms driven by the internal clock. Abbreviations: VAS: visual analogue scale. Reproduced from Rajaratnam SMW and Arendt J. Lancet 358:999-1005, 2001 by permission.”
“Seven blind men and an elephant parable at a Jain temple. By romana klee from usa - sammati tarka prakarana, CC BY-SA 2.0, https://commons.wikimedia.org/w/index.php?curid=59461928”
In PNS
+ ACh in CNS
