Parvocellular Cell

Handbook of Stress and the Brain

Allison J. Fulford , Michael S. Harbuz , in Techniques in the Behavioral and Neural Sciences, 2005

The parvocellular paraventricular nucleus is the apex of the HPA axis

The peptides, CRF and AVP are synthesised in the tuberoinfundibular parvocellular cells of the paravenlricular nucleus (PVN) that evoke release of ACTH via their synergistic deportment on pituitary corticotrophs. The axon terminals of the parvocellular neurons terminate in the external zone of the median eminence adjacent to the capillaries of the hypophysial portal blood supply where they secrete their contents into the portal blood. Parvocellular AVP, in contrast to magnocellular AVP, is involved with regulation of pituitary ACTH release and does not contribute to osmotic balance regulation.

CRF is the primary ACTH secretagogue, whereas AVP colocalises with CRF in approximately 50% of the CRF-containing neurones of resting animals and humans (Whitnall, 1993). The two peptides human action synergistically on ACTH secretion in vitro (Gillies et al., 1982) and in vivo (Rivier and Vale, 1983); however, AVP alone has piddling ACTH secretagogue activity. In addition to evoking release of ACTH, CRF induces transcription of pro-opiomelanocortin (POMC) mRNA, the ACTH precursor poly peptide (Lightman and Young, 1988). CRF is thought to be the only hypothalamic-releasing factor that can induce POMC cistron expression. Thus, stressinduced HPA centrality activation is highly reliant on neuroendocrine CRF. A population of parvocellular CRF-containing neurones project to extrahypothalamic sites including limbic nuclei and the brainstem (Sawchenko, 1987a). Therefore, in add-on to coordinating the pituitary-adrenal system, CRF is directly involved in the orchestration of robust autonomic and behavioural responses to stress.

During activation of the HPA centrality, the synthesis and secretion of both secretagogues is increased leading to a direct increase in ACTH and glucocorticoid secretion. Thus, expression of CRF mRNA and AVP mRNA in the PVN is increased and POMC mRNA expression is increased in the adenohypophysis (Antoni, 1986; Harbuz and Lightman, 1992). The importance of dual peptide control of ACTH release by the pituitary corticotroph is not fully understood. Although CRF is the principal and nearly potent ACTH secretagogue, AVP appears to be involved in the regulation of stress-induced ACTH release (Scott and Dinan, 1998). Show suggests that during chronic stress, the CRF:AVP ratio may increase, maybe due to differential sensitivity of the secretagogues to negative-feedback regulation (Scott and Dinan, 1998). In improver to AVP, various neuropeptides are colocalised inside the parvocellular CRF neurones including enkephalin, neurotensin, cholecystokinin, vasoactive intestinal peptide and galanin (Palkovits, 1988). In some cases CRF-containing neurones limited the inhibitory amino acrid neurotransmitter, γ,-aminobutyric acid (GABA), instead of AVP (Meister et al., 1988). The coexistence of these peptides or transmitters with CRF provides a mechanism for subtle regulation of ACTH release.

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Parental Beliefs

K. Numan , in Encyclopedia of Behavioral Neuroscience, 2010

Oxytocin (OT) and Maternal Behavior

Other than DA, about of the research on the neurochemical control of maternal behavior has focused on OT, which exerts powerful modulatory influences at critical nodes within some of the neural circuits nosotros have described. The parvocellular cells of the paraventricular hypothalamic nucleus (PVN) are one site of OT production, and some of these neurons terminate within the brain which allows OT to act locally as a neurotransmitter or neuromodulator.

The hormonal events associated with late pregnancy and the vaginal and cervical stimulation at birth influence both the synthesis and release of OT into the brain. The current view is that OT release into various neural sites is of import for the initiation of maternal responsiveness at birth, but once maternal behavior has become established, OT no longer plays an essential role in the maintenance of the behavior. For example, PVN lesions performed during pregnancy disrupt the onset of maternal behavior at parturition in rats, but such lesions are not disruptive if produced after maternal behavior has go established. Similar results are obtained with more selective methods: intracerebral injections of OT receptor (OTR) antagonists during parturition disrupt the onset of maternal behavior, but like injections postpartum are ineffective. Although OT is not essential for the continuance of maternal beliefs, it may exert subtle modulatory influences on the degree of maternal grooming of infants and on the particular nursing postures the mother shows.

The hormonal and other events of tardily pregnancy, particularly rising estradiol levels, also increase the synthesis and expression of OTRs – which would allow critical brain nuclei to respond to OT. In rats, OTR expression increases in the MPOA and VTA at parturition and bear witness shows that microinjection of an OTR adversary directly into either the MPOA or VTA disrupts the onset of maternal beliefs at parturition. There is also some piece of work on prairie voles which suggests a part for OT action on the NA in maternal behavior control. Therefore, at the time of parturition, OT may human action at critical nodes along the circuitry regulating proactive maternal responses and such action may allow these circuits to piece of work at optimal efficiency ( Figure 4 ).

Effigy 4. The coordinating function of oxytocinergic neural pathways in the regulation of the onset of maternal behavior. The parvocellular neurons of the paraventricular hypothalamic nucleus (PVNp) release oxytocin (OT) into diverse neural sites. The hormones of tardily pregnancy and the vaginocervical stimulation (VCS) which occurs during parturition promote the synthesis and release of OT. Pregnancy hormones also stimulate the synthesis of OT receptors (OTR) in the medial preoptic area (MPOA) and ventral tegmental area (VTA). At parturition, OT action on the MPOA, VTA, and, perchance, nucleus accumbens (NA) promotes the efficient operation of the MPOA–VTA–NA circuit which is essential for proactive maternal responses. DA   =   dopamine.

In addition to OT's influence on appetitive maternal responding, OT – in conjunction with MPOA effects – may downregulate activity in fright and feet-related neural circuitry, and this influence may continue into the postpartum period. Nosotros return to this issue in our word on postpartum maternal aggression and feet reduction.

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Morphology of the human being hypothalamus

Bertalan Dudás Grand.D., Ph.D. , in Atlas of the Homo Hypothalamus, 2021

Paraventricular and supraoptic nuclei

According to this compartmentalized view, paraventricular nucleus occupies primarily the preoptic region extending into the tuberal zone where it tapers off (Figs. 12 and 13 ). The superior edge of the nucleus is the hypothalamic sulcus that too marks the edge betwixt the thalamus and the hypothalamus. Mediolaterally the paraventricular nucleus is located in the medial hypothalamic surface area and the periventricular zone. In human, the old region is filled by and large by darkly stained magnocellular neurons that are easily detectable with Nissl staining, while the latter expanse is populated primarily with smaller, less intensely stained parvocellular cells. Magnocellular neurosecretory system is responsible for the production of oxytocin and vasopressin; the axons of these neurons form the hypothalamo-hypophyseal tract running through the hypophyseal stalk and projecting to the neurohypophysis where oxytocin and vasopressin are eventually stored in nerve terminals (Herring bodies). The neurons that secrete oxytocin and vasopressin inhabit different zones in the magnocellular system; vasopressin-secreting perikarya form a dumbo cluster populating the ventrolateral zone of the paraventricular nucleus, while oxytocin-producing cells tend to avoid this zone and instead they are more than scattered throughout the nucleus ( Saper, 2004).

Neurons composing the supraoptic nucleus have like morphology to the cells populating the magnocellular part of the paraventricular nucleus; they accept large, intensely stained perikarya populating the corner of lateral hypothalamus betwixt the basal surface and the optic tract (Figs. 11–13). Magnocellular neurons also grade additional cell clusters scattered along an biconvex line between the supraoptic and paraventricular nuclei as well every bit forth the medial edge of the optic tract. Like to the rest of the magnocellular cells, these perikarya are oxytocin- or vasopressin-immunoreactive and projection to the neurohypophysis. Both supraoptic and paraventricular nuclei are densely vascularized, and magnocellular neurons are ofttimes associated with claret vessels.

Figure ten. Coronal department of the anterior part of the hypothalamus illustrating the most appreciable structures with Nissl staining. Abbreviations: DBB, diagonal band of Broca; Inf, infundibulum; LC, lamina terminalis cinerea; MPO, medial preoptic surface area; NDB, nucleus of diagonal ring of Broca; OCh, optic chiasm; SC, suprachiasmatic nucleus.

Figure 11. Coronal department of the preoptic part of the hypothalamus illustrating the most observable structures with Nissl staining. Abbreviations: DBB, diagonal band of Broca; Inf, infundibulum; MPO, medial preoptic area; NBM, nucleus Basalis of Meynert; OCh, optic chiasm; SC, suprachiasmatic nucleus; SON, supraoptic nucleus.

Effigy 12. Coronal section of the anterior infundibular region of the hypothalamus illustrating the most appreciable structures with Nissl staining. Abbreviations: Air-conditioning, anterior commissure; Inf, infundibulum; Fx, fornix; LHA, lateral hypothalamic area; MPO, medial preoptic area; OT, optic tract; PVNd, paraventricular nucleus, dorsal part; PVNm, paraventricular nucleus, magnocellular office; SI, substantia innominata; SON, supraoptic nucleus.

Figure thirteen. Coronal section through the infundibular recess of the hypothalamus illustrating the most appreciable structures with Nissl staining. Abbreviations: Am, accessory magnocellular neurons; AN, arcuate nucleus; DM, dorsomedial nucleus; Fx, fornix; LHA, lateral hypothalamic area; LT, lateral tuberal nucleus; OT, optic tract; PVNd, paraventricular nucleus, dorsal part; PVNm, paraventricular nucleus, magnocellular function; SON, supraoptic nucleus; VMd, ventromedial nucleus, dorsomedial subdivision; VMv, ventromedial nucleus, ventrolateral subdivision.

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Vision 2

B. Krekelberg , in The Senses: A Comprehensive Reference, 2008

two.09.4.three.1 Input from the lateral geniculate nucleus

In cats and primates, few retinal or lateral geniculate nucleus (LGN) cells are management selective, but many cells in primary visual cortex are (Hubel, D. H. and Wiesel, T. North., 1959; 1962). Hence, much of the research guided past the motion free energy model has been devoted to determining whether a linear summation of the output of appropriate LGN cells tin lead to a direction-selective response in the cortex.

Cai D. et al. (1997) probed cat LGN RFs with single flashes. They showed that the space–time RFs were typically not slanted. The space–time response maps resembled the outputs at stage Three (A, B) shown in Figure 5. Note, however, that even though these LGN space–time response maps were not slanted, they were are too not separable. That is, their space–time response map could not be written as the product of a spatial impulse response function and a temporal impulse response role. For the discussion of motion detection, all the same, I volition ignore this and approximate them by separable functions. Qualitatively this is a practiced approximation.

Stage 4 of the motion free energy model requires inputs that are delayed with respect to each other. In the LGN of the cat, the lagged and nonlagged cell classes seem to fulfill this prediction quite well (Mastronarde, D. N., 1987a; 1987b; Saul, A. B. and Humphrey, A. L., 1990; Cai, D. et al., 1997 ). Primate LGN as well has classes of cells that are delayed with respect to each other; the magnocellular cells typically requite fast, transient responses, while parvocellular cells answer with a later sustained firing rate ( Marrocco, R. T., 1976; Schiller, P. H. and Malpeli, J. G., 1978).

In the spatial domain, the inputs to the motility detector also need to be shifted; either in phase, or in space. A shift in stage, combining an odd and an fifty-fifty symmetric cell whose spatial RFs are in so-called quadrature, would be optimal (Figure eight(b)). Near cells in the LGN, however, have even symmetric spatial RFs; hence it will be hard to construct an optimal motion detector from combining LGN cells. The movement energy detector, however, can also function with two RFs that are shifted spatially. Because LGN cells have RFs roofing the whole visual field and because neighboring LGN cells are organized in a retinotopic fashion, collecting input from two LGN cells with slightly shifted spatial inputs should exist relatively straightforward.

Given that appropriate input neurons exist in both true cat and primate LGN, what is the evidence that these really provide the input to the direction-selective cells of main visual cortex? Certainly, both lagged and nonlagged cells project to the cortex, and unproblematic cells – specially those in layer 4B – contain subregions of the RF in which response properties mimic those of LGN lagged cells and other subregions that match properties of nonlagged cells (Saul, A. B. and Humphrey, A. 50., 1992). Moreover, some direction-selective (DS) simple cells have been shown to receive monosynaptic inputs from lagged LGN cells (Alonso, J. M. et al., 2001). However, this does not necessarily hateful that all DS cells must receive their input direct from the LGN. The alternative hypothesis is that the LGN projects to non-DS simple cells and these provide the input to DS unproblematic cells.

There is evidence that at least some DS cells follow this indirect route. Peterson M. R. et al. (2004) recorded from pairs of monosynaptically connected elementary cells; one was DS, the other was non. For each cell in such a pair, they adamant the infinite–time response map and so subtracted the RF of the not-DS cell from the RF of the DS jail cell. Given the linearity assumptions of the movement energy model, this should upshot in the RF of the missing second-input neuron. Peterson M. R. et al. show examples of DS unproblematic cells in which the not-DS simple cell provides the late-input component. Because such a DS unproblematic prison cell receives its delayed input from another simple jail cell, it does not have to rely on a lagged LGN cell. This shows that a direct input from lagged LGN cells is not necessary for DS.

Using these aforementioned methods, Peterson Thousand. R. et al. besides showed that in that location is a range of time delays between the two inputs of DS cells, and most are much smaller than predicted by the original move energy model. In the original model, the inputs were in temporal quadrature (Effigy eight(c)). While this relationship produces an optimal detector (Watson, A. B. and Ahumada, A. J., 1985), information technology is not necessary to create moderate DS. Taken together the bear witness from the cat suggests that DS simple cells receive both directly lagged and nonlagged LGN input also as input from other (non-DS) elementary cells. The temporal delay between these inputs varies considerably across cells.

In monkey V1, De Valois and colleagues (De Valois, R. L. and Cottaris, Northward. P., 1998; De Valois, R. L. et al., 2000) investigated the source of the input signals of DS simple cells past determining the temporal contour of the response in V1 simple cells. Co-ordinate to the motion energy model, this temporal profile should consist of the sum of 2 components; i delayed with respect to the other (Figure 8(c)). To extract these components, De Valois R. L. et al. used primary components analysis. Outset, they looked at non-DS cells. These cells typically had only a unmarried significant component and in that location were two clearly distinct subsets. 1 set of cells had a contour with a short latency and a biphasic temporal profile; the other fix had a longer latency and a monophasic contour. And then, they determined the response profiles of direction-selective cells. These cells had two pregnant input components, i matched the early on biphasic contour, and the other matched the late monophasic contour of the non-DS cells. This strongly suggests that DS cells get direction selective by linear summation of the output of cells from the two singled-out classes of non-DS unproblematic cells (or their LGN inputs). Interestingly, the delay between the ii temporal profiles corresponds closely to temporal quadrature, which suggests that these motility detectors are better optimized than those in the cat (Peterson, M. R. et al., 2004). In the spatial domain, the relationship betwixt the inputs was more than varied and the optimal spatial quadrature relationship between the two inputs is expected to exist rare.

The two temporal profiles observed in V1 simple cells represent quite closely to the response backdrop of two anatomically identifiable subclasses of LGN cells. Magnocellular cells have brusk latencies and transient biphasic responses. Parvocellular cells have longer latencies and typically a monophasic sustained response. Hence, the view that arises from this piece of work is that magnocellular and parvocellular LGN cells each have their ain non-DS simple cell targets in V1. Other elementary cells then sum the input from these not-DS simple cells to generate DS in the linear manner envisaged by the motion energy model.

This is controversial because anatomical, lesion, and psychophysical studies have all been used to argue that motility is processed past the magnocellular stream. Anatomical evidence shows that layer IVcα of V1 – where many DS cells are found – mainly receives magnocellular input (Blasdel, Grand. G. and Fitzpatrick, D., 1984). The counter argument is that there is also evidence showing strong vertical interactions inside a column; hence even if the parvocellular properties cannot reach DS cells subsequently crossing one synapse, they can after two. Second, lesion studies have been interpreted as showing a selective involvement of the magnocellular pathway in motion perception (Merigan, W. H. and Maunsell, J. H., 1993), but in that location are counter examples. Ii studies have recorded from V1 cells while reversibly inactivating magnocellular and/or parvocellular layers in the LGN (Malpeli, J. G. et al., 1981; Nealey, T. A. and Maunsell, J. H., 1994). These studies showed that many DS uncomplicated cells receive input from both classes of LGN neurons and that DS is oft but abolished when both magnocellular and parvocellular inputs take been silenced. While this shows that a contribution of parvocellular cells to movement detection is certainly likely, it remains unlikely that the roles of the magnocellular and parvocellular cells in motion detection are as symmetric as in the de Valois model. For example, lesions of the magnocellular layers of the LGN have a greater influence on the responses of management-selective cells in the middle temporal area (Maunsell, J. H. et al., 1990).

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Vision

Juan Angueyra , Wei Li , in The Senses: A Comprehensive Reference (Second Edition), 2020

i.31.four.three The Parvocellular Pathway: A Channel for High-Resolution Exploited for Cone-Opponency

The parvocellular layers of LGN receive input from on- and off-midget retinal ganglion cells (Leventhal et al., 1981; Perry et al., 1984), which constitute more than ∼80% of primate RGCs (Polyak, 1941). Midget RGCs receive input from midget bipolar cells, which have very small-scale dendritic fields that contact merely i–3 cones (Cold-shoulder and Wässle, 1991; Kolb et al., 1992). Midget BCs too have unique connectivity patterns: on-midget BCs grade synapses with Grand- and L-cones but non with S-cones, while off-midget BCs can form synapses with all cone types (Herr et al., 2003; Klug et al., 2003; Patterson et al., 2019b; Wool et al., 2019) (Fig. 3B). In the fovea, midget BCs contact a unmarried cone and a single midget RGC, creating a circuit with the smallest receptive field possible (Kolb et al., 1992; Polyak, 1941). In the far periphery, midget RGCs contact iii–iv midget BCs, which in turn typically contact 3 cones (Kolb and Marshak, 2003). Much like the evolution of a fovea, such midget circuitry is novel and unique to primates, and lacks a direct correlate in rodents (Peng et al., 2019).

Functionally, the midget organization and their minor receptive fields are uniquely poised to support loftier-resolution vision and its appearance predates the development of trichromacy (Nathans, 1999), and in marmosets (where only some females are trichromatic), responses in the parvocellular layers of LGN are indistinguishable between di- and trichromatic individuals (Yeh et al., 1995; Martin et al., 2011 ). In trichromatic primates, parvocellular cells are very well modulated past stimuli that differentially actuate M- or Fifty-cones ( De Valois et al., 1958; Jacobs and De Valois, 1965; De Valois et al., 1966; Hubel and Wiesel, 1966; Gouras, 1968; Derrington et al., 1984; Yeh et al., 1995), a property that is likely inherited from midget RGCs (Field et al., 2010; Lee et al., 2012; Wool et al., 2018). Because midget BCs in the fundamental retina contact a single cone, they acquit signals with the spectral sensitivity of that cone in the center of their receptive field. Additionally, the lateral inhibition provided past horizontal cells combines signals with spectral sensitivities inherited from the surrounding cones that they contact (Verweij et al., 2003); for example, if an on-midget BC contacts a single Fifty-cone and is primarily surrounded by 1000-cones, this midget BC will be activated past stimuli that activate Fifty-cones (L+) and inhibited past stimuli that activate Yard-cones (M-), thus making it L+/M- opponent. This kind of cone-opponency can arise with even small biases in the spectral composition of surrounding cones—a mutual occurrence given the clumpy distributions of One thousand- and 50-cones in primate retina (Paulus and Kröger-Paulus, 1983; Field et al., 2010; Buzás et al., 2013; Wool et al., 2018).

Electron microscopy has revealed that on-midget BCs contact M- and 50-cones exclusively, but off-midget BCs in macaque brand contacts with Southward-cones (Herr et al., 2003; Klug et al., 2003), although corresponding functional data has been thin in parvocellular LGN. Careful characterization of the receptive field of peripheral RGCs at very high resolution has shown that on-midget RGCs do not receive functional input from Southward-cones — though off-midget RGCs can — however, most of their input still derives from the more numerous Yard- and L-cones (Field et al., 2010). More recent studies in fundamental retina were, for the starting time time, able to record straight from off-midget RGCs that receive input from a unmarried S-cone, showing that their receptive field follows the same middle-environment organisation and carries a (L+Thou)+/S- chromatic signature (Patterson et al., 2019a; Wool et al., 2019). It is interesting to notation that marmosets may lack this type of off-midget RGC (Lee et al., 2005).

In summary, the midget/parvocellular pathway is unique to primates, carries high-resolution information, and sets limits for discriminability in the unabridged visual system (Rossi and Roorda, 2010). In trichromatic primates, without the need for any modification (Mancuso et al., 2009; Martin et al., 2011), the aforementioned receptive fields acquire a new dimension, enabling them to encode chromatic differences between centre and environment, creating the Yard+/L- and Fifty+/M- cone-opponent axis of LGN cells. A minority of parvocellular cells must likewise behave opponent information between Due south-cones and L/M-cones, but such data is limited by the sparse distribution of Due south-cones and the rarity of off-midget BCs that contact a unmarried S-cone.

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Social Vision

Daniel N. Albohn , Reginald B. AdamsJr., in Neuroimaging Personality, Social Cognition, and Character, 2016

3.ane Neuroanatomy of Basic Vision

If social vision is a complicated animate being, then the sense of vision is its perplexing brute of a parent. It is not surprising, so, to see that introductory biological psychology and homo biology textbooks devote whole chapters to this one sense, all the while leaving the other iv senses lumped into a carve up singular chapter. Consider for a moment the intricate process of merely watching the classroom door for a professor to enter. First, light has to enter the pupil and be focused by the lens and cornea so that it can pass through the clear vitreous humor between the lens and the retina. Side by side, the retina needs to interpret this low-cal through a series of dedicated cells. Lite activates specialized receptor cells (i.e., rods and cones), which in turn activate bipolar cells that send signals to ganglion cells.

In the primate encephalon, ganglion cells come in 3 flavors, each with a specific purpose: parvocellular, magnocellular, and koniocellular. The first type of jail cell, parvocellular, has small receptive fields and is adept at detecting visual particular, then it may pick up on the pattern that the professor is wearing, or the fine color particular of his or her briefcase. In dissimilarity, magnocellular ganglion cells take large receptive fields and are colorblind; they answer largely to movement and therefore might be attuned to the gait of the entering professor or the sudden motionlessness of the class equally he or she enters. Lastly, koniocellular ganglion cells appear to take several functions and be throughout the retina. Of the iii specialized types of cells, koniocellular are the least studied, and their exact purpose is simply now becoming elucidated (run into Hendry and Reid 138 for further review).

Advancing past the retina, the ganglion jail cell axons bundle together to form the optic nerve, which exits at the dorsum of the eye. As the optic nerve travels out of the eye farther into the brain, half of the axons from the nasal side of each eye cross at the optic chiasm and keep to the contralateral side of the brain. The other half of the axon bundle (i.e., the temporal side) travel to the ipsilateral side of the encephalon. Virtually of the ganglion bundle goes to the lateral geniculate nucleus, and from at that place, other axons are sent to the thalamus and the occipital cortex, known as the primary vision center of the brain. From the occipital cortex, visual information may be sent to a number of places, such as the prefrontal cortex, to be further systematically analyzed, or the fusiform face area for specialized processing. Other visual information skips some of the downstream visual cortices entirely and proceeds on a more direct route to the amygdala for quicker survival-related processing and action. Perhaps most fascinating is that this whole process takes identify continually while nosotros navigate our social world and occurs effectively at speeds within hundreds of milliseconds of viewing a stimulus.

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Cardiovascular Neuroendocrinology

Gina L.C. Yosten , Willis Thou. Samson , in Handbook of Neuroendocrinology, 2012

The PVN and Autonomic Nervous Arrangement Function

Using retrograde tracing techniques, Sawchenko and Swanson 57 demonstrated that neurons in the locus coeruleus, the dorsal vagal complex (A2 catecholamine neurons) and the ventrolateral medulla (A1 catecholamine neurons) projection directly to the PVN and the locus coeruleus. They farther identified singled-out stereotypic innervation of the PVN past these brainstem nuclei, using an autoradiographic tracing approach. The locus coeruleus appeared to project primarily to the parvocellular cells adjacent to the 3rd ventricle (neuroendocrine neurons). Cells in the A2 region of the dorsal vagal complex (including the NTS) projected mainly to parvocellular elements of the PVN next to the tertiary ventricle and in the dorsomedial PVN, merely not the magnocellular neurons. On the other hand, the A1 catecholamine neurons in ventrolateral medulla appeared to innervate not only parvocellular elements, similar to the A2 projections, just likewise, uniquely, the magnocellular elements of the PVN. These classic studies further identified reciprocal innervation of the A1 and A2 cell groups, which is significant if just because the A2 cells in NTS are those receiving information for the baroreceptors via cranial fretfulness IX and 10. Thus the anatomic framework was established for a circuitry which linked incoming cardiovascular data with the PVN and its return of commands to the autonomic centers in medulla and spinal cord.

Efferent projections from parvocellular preautonomic cells of the PVN class the basis of the hypothalamic command of cardiovascular function. 6,57–59 Those efferents innervate not only the intermediolateral prison cell column (preganglionic sympathetic neurons) just as well the NTS and the dorsal motor nucleus of the vagus, thus influencing the activity of both the parasympathetic and sympathetic branches of the autonomic nervous arrangement. 58 Some of those preautonomic projection neurons surprisingly contain oxytocin and vasopressin (in add-on to other neuropeptides such every bit somatostatin, and the enkephalins), establishing their presence in not only magnocellular simply as well parvocellular neurons of the PVN. 58 More recently, retrograde tracing techniques utilizing tagged microspheres accept revealed that some of the descending fibers from parvocellular PVN innervate both the pressor region of the rostral ventrolateral medulla (RVLM) and the intermediolateral prison cell cavalcade of the spinal cord. 6 In this style, control neurons in the parvocellular PVN tin can affect cardiovascular role through a balance of sympathetic (contractile actions in the vasculature and positive chronotropic/inotropic effects in center) and parasympathetic (negative chronotropic actions in middle) actions, and via renal sympathetic afferents controlling sodium excretion. sixty The importance of the connectivity of neurons in the paraventricular nucleus of the hypothalamus with autonomic centers in medulla and spinal cord to the integrated command of blood pressure has recently been extensively reviewed elsewhere. 61

The PVN responds not only to osmotic stimuli via the CVOs and afferent input from high (aortic and carotid) and low (atrial) pressure baroreceptors via the IXth and Xth cranial nerves via relays in the NTS and RVLM, 62 but likewise to vasoactive hormones present in the circulation and produced locally inside the hypothalamus. Whether the product and/or release of these hormones centrally is coordinated to circulating levels is unknown; nevertheless, peptides from both sources exert stiff actions on the hypothalamic control of thirst, salt appetite, autonomic part and vasopressin release. 63–67

BOX 13.ane

HOW DO WE KNOW THAT THE HYPOTHALAMIC PARAVENTRICULAR NUCLEUS LINKS TO BRAINSTEM AND SPINAL CORD NEURONS Decision-making CARDIOVASCULAR Function?

The importance of preautonomic, parvocellular neurons of the hypothalamic paraventricular nucleus in the command of cardiovascular homeostasis is based upon numerous evidences. However, a critical step in establishing that importance was the identification of a direct innervation by those neurons of medullary cardiovascular control centers and the intermediolateral cell column of the spinal cord. Employing anterograde (Phaseolus vulgaris leucoagglutinin, PHA-L) and retrograde (cholera toxin subunit b, CTb) labeling methods, Hosoya and Matsushita 1 established directly innervation of spinal preganglionic neurons in the upper thoracic spinal cord. Injection of PHA-L into the paraventricular nucleus resulted in transport of the marker to terminal fields in the intermediolateralis pars principalis and pars funicularis of the of the upper thoracic spinal cord, in close apposition to the diffuse dendritic fields of the resident, sympathetic preganglionic neurons. Those sympathetic preganglionic sympathetic neurons were identified past the presence within the cells of the retrograde mark (CTb) that had been injected into the superior cervical ganglion.

These preautonomic, parvocellular paraventricular neurons were later demonstrated to project to both sympathetic pregangionic neurons in the spinal string, and, via axon collaterals, to neurons located in the rostral ventrolateral medulla (RVLM), an important brain stalk cardiovascular center. This was accomplished over again with the use of neuronal track tracing techniques. Shafton and colleagues 2 injected fluorescein-labeled microspheres into the intermediolateral cell column of the rat spinal cord and, in the same animals, rhodamine-labeled microspheres into the RVLM. The microspheres were taken up by the axon terminals and transported in a retrograde fashion to the cell bodies of the project neurons in PVN. The light-green- and scarlet-labeled microspheres were detected histologically in parvocellular PVN neurons 7 days later, indicating those neurons projecting to one or both injection sites. A pregnant population of the dark-green, fluorescein-labeled cells that projected to spinal cord too contained red, rhodamine-labeled microspheres. Thus, preautonomic neurons of the hypothalamic PVN are capable of influencing cardiovascular function via both medullary and spinal cord autonomic centers.

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Stress and Encephalon Health: Across the Life Class

Angela Clow , Nina Smyth , in International Review of Neurobiology, 2020

two What is cortisol?

Cortisol is an important and pervasive steroid hormone performing a wide range of "housekeeping" duties to ensure healthy functioning. As virtually bodily cells have cortisol receptors information technology affects multiple and various systems, ranging from regulation of the metabolic, immune, cardiovascular and cognitive systems (McEwan, 2000 ). All of these functions make cortisol a crucial hormone to protect overall health and well-existence. Information technology is the product of a neuroendocrine cascade, meaning information technology is coordinated from the brain via a signaling organisation known as the hypothalamic-pituitary-adrenal axis (HPA axis). The HPA centrality is a key conduit past which the brain can exert control over physiological activity, which it does in normal everyday activity and likewise in response to stress. The neural control center for the centrality is in the hypothalamus, a region of the brain located below the thalamus within the evolutionary old limbic arrangement, our emotional encephalon. The paraventricular nucleus (PVN) lies deep inside the hypothalamus and is the "trigger point" receiving neuronal input from various modalities including the cognitive and emotional brain (i.e., sensitivity to stressors) as well every bit the hypothalamic suprachiasmatic nucleus, transmitting environmental information denoting dark-light transitions that informs the circadian blueprint of secretion. In response to activation the parvocellular cells of the PVN secrete the neuropeptide, corticotropin releasing gene (CRF) which in turn stimulates the release of adrenocorticotrophic hormone (ACTH) from corticotrophs in the inductive pituitary, an endocrine gland that sits merely beneath the hypothalamus. Adrenocorticotrophic hormone (ACTH) once released into the general circulation stimulates steroidogenic activity and cortisol release from the zona fasciculate of the adrenal cortex. Cortisol (corticosterone in rodents) in common with all of the adrenal hormones is derived from the steroid precursor pregnenolone (itself derived from cholesterol).

In summary, the HPA centrality is a signaling cascade from the brain to the adrenal cortex, resulting in cortisol secretion into the general circulation. As cortisol is lipid-soluble once in the claret stream it is able to pass freely through cellular plasma membranes, giving information technology access to all cells, including the brain. Inside the brain cortisol's effects are widespread, dependent upon two types of receptor which differ in their distribution and properties: the glucocorticoid receptor (GR) and the mineralocorticoid receptor (MR). Cortisol exerts effects on the brain through both genomic (directly binding to Deoxyribonucleic acid) and not-genomic mechanisms, affecting neurotransmitters, neurotrophic factors, sex hormones and other stress mediators to shape nowadays and time to come responses to stress (Grey, Kogan, Marrocco, & McEwen, 2017). The MRs are localized in the limbic arrangement and prefrontal cortex, binding cortisol with loftier affinity, whereas GRs, which are more widely distributed throughout the brain, and bind cortisol with approximately one-tenth of the affinity (de Kloet, Meijer, de Nicola, de Rijk, & Joëls, 2018). MR activation is related to the onset of the stress response whereas GR are associated with facilitation of recovery. The distinct departure in receptor type, distribution and sensitivity allows cortisol to regulate brain office in dissimilar ways depending on ambient concentrations: information technology is the balance between receptor occupancy that determines outcomes (de Kloet, Joëls, & Holsboer, 2005). As reviewed in these volumes the stress response and its feedback is complex, having many and diverse effects on encephalon structure and function. Salivary cortisol concentrations represent the net effect of these brain processes, underpinning its validity in the study of stress and brain health.

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Neuroendocrinology of Affective Disorders

D.A. Gutman , C.B. Nemeroff , in Encyclopedia of Neuroscience, 2009

Arginine–Vasopressin

Biology

Arginine–vasopressin (AVP), too known as antidiuretic hormone, is a nonapeptide synthesized in the lateral magnocellular neurons of the paraventricular and supraoptic nuclei of the hypothalamus, and it is released directly into the bloodstream from axon terminals in the posterior pituitary. These AVP-containing neurons terminate in the neurohypophysis of the pituitary and secrete AVP into the systemic apportionment, although they likewise project nervus terminals to the hypothalamo-hypophyseal portal organisation. Another grouping of AVP-containing neurons project from the medial parvocellular subdivision of the PVN to the median eminence. Inside the median eminence, the parvocellular-derived AVP is released from axon terminals, secreted into the hypothalamo-hypophyseal portal circulation, and transported to the inductive lobe of the pituitary gland. Extrahypothalamic AVP-containing neurons lie within limbic structures such every bit the septum and amygdala, also as in the brain stem and spinal cord. AVP and the other major posterior pituitary hormone, the nonapeptide oxytocin, are believed to play a function in modulating neural activeness in hypothalamic, limbic, and autonomic circuits.

AVP has prominent roles in controlling fluid balance via its furnishings on the kidney, in regulating blood pressure by its vasoconstrictive effects on blood vessels, and information technology can direct promote thirst. AVP can too act synergistically with CRF to promote the release of ACTH in humans and laboratory animals post-obit stressful stimuli. Chronic stress or adrenalectomy increases the activity of the parvocellular AVP system. CRF and AVP are co-localized in the parvocellular cells of the human being hypothalamus and may exist secreted together into the human hypothalamic-hypophyseal portal apportionment. The amount of AVP and CRF released into the hypothalamic-hypophyseal portal circulation varies in different species and in response to dissimilar stressors.

AVP in Anxiety and Depression

CSF AVP concentrations in patients with major depression, particularly those with singular depression, were reported to exist reduced in comparing to those of control subjects. CSF AVP is likely largely extrahypothalamic and not reflective of PVN AVP circuits. Basal plasma concentrations of AVP (secreted from the magnocellular neurons of the PVN later on osmotic and/or baroreceptor stimulation) in depressed patients are also reportedly decreased in comparison to those of historic period-matched controls, although others have found no such difference. In one study, reduced plasma AVP concentrations, as well as a blunted GH and AVP response to both clonidine and apomorphine, were reported in depressed patients; no differences in basal or stimulated oxytocin concentrations were observed.

Combined infusion of lysine–vasopressin and human CRF produced nonsuppression of cortisol following the DST in healthy controls; in these same patients, neither agent infused separately produced DST nonsuppression. This suggests that both CRF and AVP contribute to the HPA axis hyperactivity characteristic of low. AVP serum concentrations following the DST take also been reported to be elevated in both patients with chronic major depressive disorder and patients with symptomatic and remitted bipolar disorder.

A mildly blunted ACTH response to exogenous AVP administration has been reported in depression, but this finding was not replicated in 2 other studies. In a postmortem tissue study, an increase in the number of PVN AVP neurons, as well equally those that co-localize AVP and CRF neurons, was reported in depressed patients compared to controls. Increased AVP mRNA expression has been reported in the PVN and supraoptic nucleus (SON) of 9 depressed patients compared to eight control subjects. This is of interest in view of the ability of AVP to potentiate the actions of CRF at corticotrophs.

Interestingly, elevations in CSF and plasma AVP concentrations have been reported in manic patients in comparison to patients with unipolar depression and controls. Clearly, hypothalamic and extrahypothalamic AVP circuits are regulated independently. Additional work is warranted, peculiarly in view of the emerging evidence of antidepressant action of AVP receptor antagonists in a variety of animal models. Whether the perturbations of AVP secretion in patients with neuropsychiatric disorders are country or trait dependent has notwithstanding to be elucidated.

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Audition

Donata Oertel , Xiao-Jie Cao , in The Senses: A Comprehensive Reference (Second Edition), 2020

2.27.2 Innervation by the Auditory Nerve

Transduction of audio to electric signals in the cochlea is tonotopically organized. The mechanics of the cochlea acts as an acoustic prism that spreads out vibrations, in near mammals as a roughly logarithmic office of frequency along the length of the cochlea. Sounds of low frequencies activate hair cells at the apical end and sounds of high frequencies activate hair cells at the basal cease of the cochlea.

Blazon I and Type II spiral ganglion cells are singled-out (Spoendlin, 1969; Perkins and Morest, 1975; Kiang et al., 1982). Audio-visual information is carried to the brain mainly, and mayhap exclusively, by blazon I spiral ganglion cells.

Type II spiral ganglion cells comprise simply about seven% of afferent fibers in mice (Ehret, 1979). These pocket-size unmyelinated cells receive input from outer hair cells. These neurons respond only weakly to depolarization of outer hair cells (Weisz et al., 2009, 2014). Similar type I fibers, they bifurcate in the nerve root to form ascending and descending branches. They contact targets through en passant swellings and terminal boutons. Sometimes these fibers co-operative near the nervus root (Merchan et al., 1988 ). Nigh 2-thirds of swellings are in parvocellular cell regions that environment the VCN ( Brown et al., 1988a; Ryugo et al., 1991; Berglund and Brownish, 1994; Morgan et al., 1994, Muniak et al., 2016). The descending branches of some fibers brim the octopus cell area and go along into the fusiform cell layer of the dorsal cochlear nucleus (DCN). Type II fibers resemble pain fibers and may report cochlear damage (Liu et al., 2015; Wu et al., 2018).

The axons of type I spiral ganglion cells, ∼93% of auditory nervus fibers, convey acoustic information from inner hair cells to the cochlear nuclei. On average one inner hair cell contacts about ten blazon I spiral ganglion cells and blazon I screw ganglion cells more often than not receive input from only a unmarried inner hair cell. Type I screw ganglion cells thus contain a tonotopic assortment of fibers, each fiber reporting the presence of acoustic energy over the narrow range of frequencies to which information technology is tuned. The cochlear nuclear circuitous comprises 2 nuclei, an unlayered VCN and a layered DCN. Each auditory nerve fiber bifurcates in the nerve root, sending its ascending branch anteriorly to the anteroventral cochlear nucleus (aVCN). The descending branch passes through the multipolar cell surface area and and then through the octopus cell surface area of the posteroventral cochlear nucleus (pVCN) before turning into the deep layer of the DCN.

The orderly, topographic project of auditory nerve fibers from the cochlea to the cochlear nuclei imposes the tonotopic organisation that is generated in the cochlea onto both ventral and dorsal cochlear nuclei, as shown schematically in Fig. 1. That tonotopic organization is forwarded to downstream targets of the main cells of the cochlear nuclei, most encephalon stalk nuclei, the junior colliculus, the medial geniculate body of the thalamus, and to principal and secondary auditory cortex (Kandler et al., 2009). The tonotopic organization of the cochlear nuclei is established very early in development; spiral ganglion cells projection topographically earlier target cells in the cochlear nuclei cease dividing (Koundakjian et al., 2007; Ghimire and Deans, 2019; Fritzsch et al., 2010), indicating that they are guided past molecular cues that are only first to exist understood (Macova et al., 2019; Lu et al., 2014; Koundakjian et al., 2007; Schmidt and Fritzsch, 2019). Even in strains of mice that never hear, the topographic system of the cochlear nuclei is not detectably abnormal (Cao et al., 2008; Wright et al., 2014). Spontaneous activity that is initiated past random events in the cochlea before the onset of hearing likely helps to sharpen connections (Tritsch et al., 2007; Tritsch and Bergles, 2010; Babola et al., 2018).

Effigy 1. Acoustic information enters the brain through the auditory or Viii cranial nerve (VIII N). Sound is transduced tonotopically in the cochlea, with low frequency sounds transduced past hair cells at the apex and loftier frequency sounds past hair cells at the base. Hair cells convey electric signals synaptically to spiral ganglion cells (SG) which in turn finish in the cochlear nuclear complex. The cochlear nuclear complex comprises two distinct nuclei, the layered dorsal cochlear nucleus (DCN) and the unlayered ventral cochlear nucleus (VCN) that are separated by a lamina of granule cells and associated interneurons (nighttime greyness). The small cell cap (ssc) lies merely beneath the granule cell lamina. The nerve root divides the VCN into the anteroventral cochlear nucleus (aVCN) and the posteroventral cochlear nucleus (pVCN). The orderly topographic projection of auditory nerve fibers imposes a tonotopic organization on the VCN and DCN. Auditory nerve fibers innervate several arrays of excitatory (dark green) and inhibitory (orange) target neurons whose names are shown in Fig. ii.

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