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doi: 10.1002/cne.20751pmid: 16255004
The midbrain periaqueductal gray (PAG) and ventromedial medulla (VMM) are generally viewed as the core of an endogenous descending modulatory system. However, available data demonstrate that PAG and VMM do not specifically target nociceptive transmission and that activation of either structure affects numerous homeostatic physiological processes. Pseudorabies virus (PRV) is a useful tracer that is retrogradely and transynaptically transported. PRV injections into homeostatic effector organs invariably label VMM neurons, both serotonergic and nonserotonergic. Studies in anesthetized rats have implicated two types of nonserotonergic VMM neurons in nociceptive modulation: ON cells are thought to facilitate nociception and OFF cells to inhibit nociception. Yet, in the unanesthetized animal, the discharge of VMM neurons changes in response to innocuous stimuli and during situations unrelated to nociception. In particular, VMM cells appear to modulate the timing of micturition, with ON cells promoting the initiation of voiding and OFF cells promoting urine storage. VMM cells also modulate sensory transmission. During both micturition and sleep, OFF cells discharge and sensory responsiveness is depressed. In sum, the VMM is hypothesized to modulate spinal sensory, autonomic, and motor circuits in order to maintain homeostasis. J. Comp. Neurol. 493:2–8, 2005. © 2005 Wiley‐Liss, Inc.
Burstein, Rami; Jakubowski, Moshe
doi: 10.1002/cne.20688pmid: 16258903
Migraine headache is triggered by and associated with a variety of hormonal, emotional, nutritional, and physiological changes. The perception of migraine headache is formed when nociceptive signals originating in the meninges are conveyed to the somatosensory cortex through the trigeminal ganglion, medullary dorsal horn, and thalamus. Is there a common descending pathway accounting for the activation of meningeal nociceptors by different migraine triggers? We propose that different migraine triggers activate a wide variety of brain areas that impinge on parasympathetic neurons innervating the meninges. According to this hypothesis, migraine triggers such as perfume, stress, or awakening activate multiple hypothalamic, limbic, and cortical areas, all of which contain neurons that project to the preganglionic parasympathetic neurons in the superior salivatory nucleus (SSN). The SSN, in turn, activates postganglionic parasympathetic neurons in the sphenopalatine ganglion, resulting in vasodilation and local release of inflammatory molecules that activate meningeal nociceptors. Are there ascending pathways through which the trigeminovascular system can induce the wide variety of migraine symptoms? We propose that trigeminovascular projections from the medullary dorsal horn to selective areas in the midbrain, hypothalamus, amygdala, and basal forebrain are functionally positioned to produce migraine symptoms such as irritability, loss of appetite, fatigue, depression, or the quest for solitude. Bidirectional trafficking by which the trigeminovascular system can activate the same brain areas that have triggered its own activity in the first place provides an attractive network of perpetual feedback that drives a migraine attack for many hours and even days. J. Comp. Neurol. 493:9–14, 2005. © 2005 Wiley‐Liss, Inc.
doi: 10.1002/cne.20785pmid: 16254993
There is a close connection between micturition and emotion. Several species use micturition to signal important messages as territorial demarcation and sexual attraction. For this reason, micturition is coordinated not in the spinal cord but in the brainstem, where it is closely connected with the limbic system. In cat, bladder afferents terminate in a cell group in the lateral dorsal horn and lateral part of the intermediate zone. Neurons in this cell group project to supraspinal levels, not to the thalamus but to the central periaqueductal gray (PAG). Neurons in the lateral PAG, not receiving direct sacral cord afferents, project to the pontine micturition center (PMC). The PMC projects directly to the parasympathetic bladder motoneurons and to sacral GABA‐ergic and glycinergic premotor interneurons that inhibit motoneurons in Onuf's nucleus innervating the external striated bladder sphincter. Thus, PMC stimulation causes bladder contraction and bladder sphincter relaxation, i.e., complete micturition. Other than the PAG, only the preoptic area and a cell group in the caudal hypothalamus project directly to the PMC. The ventromedial upper medullary tegmentum also sends projections to the PMC, but they are diffuse and also involve structures that adjoin the PMC. Neuroimaging studies in humans suggest that the systems controlling micturition in cat and human are very similar. It seems that the many structures in the brain that are known to influence micturition use the PAG as relay to the PMC. This basic organization has to be kept in mind in the fight against overactive bladder (OAB) and urge‐incontinence. J. Comp. Neurol. 493:15–20, 2005. © 2005 Wiley‐Liss, Inc.
doi: 10.1002/cne.20719pmid: 16255005
Barrington's nucleus is a central component of the micturition circuit. This nucleus projects axons to the sacral parasympathetic nucleus, where preganglionic neurons innervating the urinary bladder are located. To clarify the functional role of this nucleus, the firing properties of Barrington's neurons that project axons to the spinal cord were examined. Based on these studies, a model begins to emerge that places Barrington's nucleus in the micturition pathway that is involved in increasing bladder pressure rapidly and strongly, while also maintaining high bladder pressure. In addition, Barrington's neurons are suggested to have another role, that is, increasing the probability of micturition contraction by activating a spinal excitatory pathway or disinhibiting a spinal inhibitory mechanism. In contrast to the excitatory role of Barrington's nucleus, this nucleus does not seem to trigger bladder relaxation. J. Comp. Neurol. 493:21–26, 2005. © 2005 Wiley‐Liss, Inc.
Kavia, Rajesh Bharat Chhaganlal; Dasgupta, Ranan; Fowler, Clare Juliet
doi: 10.1002/cne.20753pmid: 16255006
The central control of the bladder is a complex, multilevel process. Recent advances in functional brain imaging have allowed research into this control in humans. This article reviews the functional imaging studies published to date and discusses the regions of the brain that have been implicated in the central control of continence. Brain regions that have been implicated include the pons (pontine micturition center, PMC), periaqueductal gray (PAG), thalamus, insula, anterior cingulate gyrus, and prefrontal cortices. The PMC and the PAG are thought to be key in the supraspinal control of continence and micturition. Higher centers such as the insula, anterior cingulate gyrus, and prefrontal regions are probably involved in the modulation of this control and cognition of bladder sensations, and in the case of the insula and anterior cingulate, modulation of autonomic function. Further work should aim to examine how the regions interact to achieve urinary continence. J. Comp. Neurol. 493:27–32, 2005. © 2005 Wiley‐Liss, Inc.
Georgiadis, Janniko R.; Holstege, Gert
doi: 10.1002/cne.20735pmid: 16255007
Penile sensory information is essential for reproduction, but almost nothing is known about how sexually salient inputs from the penis are processed in the brain. We used positron emission tomography to measure regional cerebral blood flow (rCBF) during various stages of male sexual performance. Compared to a passive resting condition (without penile erection), sexual stimulation of the penis increased rCBF in an area of the right hemisphere encompassing the posterior insula and adjacent posterior part of the secondary somatosensory cortex (SII) and decreased rCBF in the right amygdala. No activation was observed in either the thalamus, genital part of primary somatosensory cortex (SI), or hypothalamus. Based on these results we put forward the concept that during sexual performance the salience of the stimulus, represented by activation of the insula and SII, is of greater significance than the exact location of the stimulus, encoded in SI. The absence of activation in the hypothalamus indicates that this region is more important for the onset of sexual arousal than for the resulting sexual performance. Deactivation of the amygdala during sexual stimulation of the penis corresponds with a decrease of vigilance during sexual performance. J. Comp. Neurol. 493:33–38, 2005. © 2005 Wiley‐Liss, Inc.
doi: 10.1002/cne.20784pmid: 16255008
Ejaculation is the most reinforcing component of sexual behavior. However, the neural substrates mediating ejaculation and processing ejaculation‐related signals remain poorly understood. We review the current understanding of central control of ejaculation. Specifically, the recent identification of a candidate spinothalamic pathway involved in relay of ejaculation‐specific signals is discussed. In addition, the discovery of a neural population of lumbar interneurons playing an pivotal role in expression of ejaculation is reviewed. J. Comp. Neurol. 493:39–45, 2005. © 2005 Wiley‐Liss, Inc.
doi: 10.1002/cne.20718pmid: 16255000
The Diagnostic and Statistical Manual (DSM)‐IV definition of premature ejaculation is not based on evidence‐based studies. In particular, the absence of a well‐defined quantitative measure of the intravaginal ejaculation latency time (IELT) makes the DSM definition inadequate. Therefore, the DSM‐IV definition should be replaced by a medical definition that incorporates both quantitative as qualitative parameters of premature ejaculation. An evidence‐based medical definition should include a cutoff point of the IELT at the 0.5 and 2.5 percentiles of the IELT distribution in the general male population. Such a definition has recently been proposed on the basis of a stopwatch study of the IELT in 491 men from five different countries. Similarly, a cutoff point of ejaculation frequency in laboratory rats enhances the probability to distinguish genuine rapid‐ejaculator rats. Only by the strict application of these cutoff points is the probability enhanced that human and animal neurobiological research can prove whether these sexual endophenotypes differ in brain activation, have particular genetic genotypes (polymorphisms), are strictly under genetic control, or are dependent on environmental conditions and/or genotypic/environmental interactions. J. Comp. Neurol. 493:46–50, 2005. © 2005 Wiley‐Liss, Inc.
Young, Larry J.; Murphy Young, Anne Z.; Hammock, Elizabeth A.D.
doi: 10.1002/cne.20771pmid: 16255009
Studies in monogamous rodents have begun to elucidate the neural circuitry underlying the formation and maintenance of selective pair bonds between mates. This research suggests that at least three distinct, yet interconnected, neural pathways interact in the establishment of the pair bond. These include circuits involved in conveying somatosensory information from the genitalia to the brain during sexual activity, the mesolimbic dopamine circuits of reward and reinforcement, and neuropeptidergic circuits involved specifically in the processing of socially salient cues. Here we present an integrated description of the interaction of these circuits in a model of pair bond formation in rodents with a discussion of the implications of these findings for evolution, individual variation, and human bonding. J. Comp. Neurol. 493:51–57, 2005. © 2005 Wiley‐Liss, Inc.
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