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Chapter 7 Serotonin Involvement in Plasticity of the Visual Cortex Qiang Gu Department of Neurobiology and Anatomy, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157, USA 7.1 Introduction Serotonin (5-hydroxytryptamine, 5-HT) is widely distributed in the nervous system, and has been implicated in many aspects of behavioral and physiological regulation, including the control of blood pressure, body temperature, sleep, pain perception, sensory processing, anxiety, impulsivity, aggression, depression, sex and feeding behaviors, learning, and memory (Curzon, 1988; Wilkinson and Dourish, 1991; Lucki, 1992; Westenberg et al., 1996). A number of studies over the past decades provided evidence that serotonin also is involved in structural and functional remod- eling of cortical circuits. Neurons in cortical areas that process sensory information such as vision, audition, and somatic sensation can modify their response properties following prolonged alterations in input activity, especially during early postnatal life. For instance, visual experience plays a pivotal role in shaping visual cortex structure and function during postnatal development. In addition, it has been also shown that nonvisual inputs to the visual cortex are important regulators for visual cortex plasticity (Gu, 2002, 2003). Neurotransmission of serotonin in the visual cortex is considered one of the nonvisual inputs that may serve as the neurochemical basis of attention, arousal, and motivation. In the following sections, serotonin- induced neuronal responses in the visual cortex will be briefly described. The contri- bution of serotonin to ocular dominance plasticity in the visual cortex and possible underlying mechanisms will then be discussed. 7.2 Serotonergic Actions in the Visual Cortex One function of serotonergic transmission in the visual cortex appears to modify neuronal responsiveness to visual input. Visual cortex excitability was modulated by 114 Gu electrical stimulation of the raphe nucleus (Moyanova and Dimov, 1986; Gasanov et al., 1989), the origin of serotonergic projection to the cortex (Lidov et al., 1980). Similar to the electrical stimulation of raphe nucleus, which caused release of sero- tonin from its axon terminals, direct application of 5-HT to visual cortical neurons in vivo showed either facilitation or suppression of neuronal activity (Krnjevic and Phillis, 1963; Reader, 1978; Waterhouse et al., 1990). Because many 5-HT receptor subtypes are present in the neocortex, these diverse 5-HT effects are presumably dependent on postsynaptic composition of 5-HT subtype receptors as well as interac- tions of the serotonergic system and other transmitter systems. Among the various 5- HT subtype receptors, activation of 5-HT1 receptors results in increased conductance of potassium ions across the cell membrane and a subsequent decrease in neuronal excitability (McCormick et al., 1993). In contrast, 5-HT2 and 5-HT4 receptors in- crease cell excitability and firing rate by decreasing resting conductance of potas- sium ions and hence depolarizing the cell membrane (Andrade and Chaput, 1991; Panicker et al., 1991; Bockaert et al., 1992). The function of 5-HT3 receptors is to mediate fast synaptic transmission (Roerig et al., 1997; Ferezou et al., 2002). Activa- tion of the 5-HT3 receptor decreases the amplitude and lateral extent of excitation in the visual cortex of the ferret (Roerig and Katz, 1997), probably resulting from an increase in GABAergic synaptic activity (Xiang and Prince, 2003). The expression of 5-HT3 receptors in subpopulations of GABAergic interneurons in the cortex pro- vided anatomical evidence that serotonergic terminals can directly interact with GABAergic neurons (Tecott et al., 1993; Morales and Bloom, 1997; Paspalas and Papadopoulos, 2001; Ferezou et al., 2002). The serotonergic actions on visual infor- mation processing may be related behaviorally to arousal and attention. 7.3 Serotonergic Contributions to Ocular Dominance Plasticity The primary visual cortex is the earliest stage of the visual pathway at which inputs of both eyes are mixed together. Visual cortical neurons have response specifications that are more complex than retinal ganglion cells and relay neurons in the lateral geniculate nucleus (LGN), including selective responses based on binocularity, ori- entation and direction of the visual stimulus (Hubel and Wiesel, 1962, 1963). Wiesel and Hubel were the first to demonstrate that the proper development of the visual cortex is dependent on visual experience. In a series of experiments (Wiesel and Hubel, 1963a, b, 1965), they showed that depriving kittens of vision in one eye by suturing eyelids early in their lives had three major consequences. First, the animals displayed little or no visual capacities through the deprived eye after the eyelids were re-opened. Second, cells in the LGN layer connected to the deprived eye were smaller than those cells receiving input from the normal eye. Third, cortical cells lost functional connections with the deprived eye, and the vast majority of cortical cells encountered were activated only by the stimulation of the nondeprived eye. These findings have been widely replicated, and similar effects of monocular deprivation have been observed in other species, such as monkey (Baker et al., 1974; Crawford et al., 1975; Hubel et al., 1977), rat (Maffei et al., 1992; Fagiolini et al., 1994), mouse (Gordon and Stryker, 1996), and ferret (Issa et al., 1999). In monocularly deprived animals, the strong input from the normal eye competes with the weak one Serotonin Involvement in Plasticity of the Visual Cortex 115 from the deprived eye at the cortical level, so that input connections to the normal eye are retained and input connections to the deprived eye are decayed. Because the responsiveness of cortical neurons to visual stimulation can be easily manipulated by visual experience, ocular dominance plasticity has become an in vivo model for studying experience-dependent modifications of neural circuits (Hubel and Wiesel, 1970; Movshon and van Sluyters, 1981; Sherman and Spear, 1982; Frégnac and Imbert, 1984; Rauschecker, 1991; Daw, 1994, 1995; Singer, 1995; Katz and Shatz, 1996). A contribution of 5-HT to ocular dominance plasticity was implicated when sero- tonin axons in kitten primary visual cortex were destroyed by chronic infusion of 5,7-dihydroxytryptamine (5,7-DHT) (Gu and Singer, 1995). In normal kittens, most visual cortical neurons respond to visual stimulation of either eye. Intracortical infu- sion of 5,7-DHT disrupted ocular dominance plasticity in the visual cortex. Despite monocular eyelid suture, neurons in the visual cortex remained binocular, while most neurons in the control (saline-treated) hemispheres displayed a normal shift of ocular dominance toward the nondeprived eye (Fig. 7.1). Figure 7.1 Ocular dominance (OD) histograms compiled from the primary visual cortex in three kittens after an intracortical infusion of saline (A) or of 5,7-DHT (B) coincident with 7 days of monocular deprivation. “n” refers to the number of recorded cells. Neurons assigned to OD categories 1 and 5 were monocular and activated by only the right eye (●) or the left (○) eye, respectively. Neurons in OD category 3 were activated equally by stimulation of either eye. Cells in OD categories 2 and 4 were binocular, but their responses were clearly domi- nated by either the right or the left eye, respectively. The category labeled U contains those cells that could not be activated with the visual stimuli used. The OD distributions in the control and the 5,7-DHT-treated hemispheres differed significantly (p < 0.005, χ2-test) (Gu and Singer, 1995). In a different set of experiments, two broad serotonergic receptor antagonists, ketanserin and methysergide (Bradley et al., 1986), were infused either alone or together into the visual cortex of kittens. This combined intracortical infusion re- duced ocular dominance plasticity and significantly blocked the expected shift in ocular dominance, but each of them infused alone had no effect (Gu and Singer, 1995). In addition, effects of intracortical infusion of mesulergine, a specific sero- 116 Gu tonin 5-HT2c receptor antagonist, on ocular dominance plasticity were examined in kittens. Similarly, mesulergine reduced ocular dominance shifts in visual cortex of monocularly deprived kittens (Fig. 7.2). These results suggest that serotonin contrib- utes to ocular dominance plasticity, and that the 5-HT2c receptor subtype plays a key role in experience-dependent synaptic modifications in kitten visual cortex. Figure 7.2 Ocular dominance (OD) histograms compiled from 1,060 cells recorded in the primary visual cortex of 19 kittens that had received an intracortical infusion of mesulergine (A) or vehicle (B) coincident with 7 days of monocular deprivation. “n” refers to the number of recorded cells. Cells of group 1 were activated by the deprived eye (●); for cells of group 2, there was marked dominance of the deprived eye; for group 3, slight dominance. For cells in group 4, there was no obvious difference between the two eyes. In group 5, the nondeprived eye dominated slightly and in group 6, markedly. Cells in group 7 were activated only by the nondeprived eye (○). The difference between the OD distributions in the control and mesuler- gine-treated hemispheres was statistically significant (p < 0.001, χ2-test) (Wang et al., 1997). 7.4 Serotonergic Effects on Plasticity in Visual Cortex Slices In parallel to in vivo electrophysiological examinations of cortical plasticity, visual cortex slices have been utilized in studies of long-term potentiation (LTP) and long- term depression (LTD), which are measures of long-lasting changes in synaptic efficacy (Artola and Singer, 1987; Komatsu et al., 1988; Perkins and Teyler, 1988; Kirkwood and Bear, 1994; Kojic et al., 1997). While in vitro studies of synaptic plasticity have demonstrated certain similarities to in vivo studies, such as age- dependent decline of plasticity in the visual cortex, they also have distinct character- istics. For instance, the outcome of slice preparations depends on more variables, such as the stimulation-–recording path and the composition of the slice incubation medium. A number of studies were carried out using visual cortex slices to deter- mine a potential role of serotonin in visual cortex plasticity. The results were more diverse than those of in vivo studies. In slices from the visual cortex of 40- to 80-day-old kittens, application of sero- tonin in the incubation medium markedly facilitated the induction of both LTP and LTD in layer 4, with underlying white matter stimulations (Kojic et al., 1997). The effect of serotonin was completely blocked by mesulergine (Kojic et al., 1997, Serotonin Involvement in Plasticity of the Visual Cortex 117 2001). These in vitro results are consistent with in vivo results, and suggest that serotonin promotes visual cortex plasticity and that the 5-HT2c receptor is a major contributor for mediating serotonergic facilitation. It has been shown that 5-HT2c receptors are not evenly distributed in kitten visual cortex; they are transiently ex- pressed in alternate 5-HT2c receptor-rich and 5-HT2c receptor-poor zones that have a similar dimension as that of ocular dominance columns (Dyck and Cynader, 1993a). Further correlation analyses in kitten visual cortex revealed that serotonin promoted LTP in 5-HT2c receptor-rich zones, whereas serotonin promoted LTD in 5-HT2c re- ceptor-poor zones (Kojic et al., 2000). These results imply a molecular mechanism, by which serotonin may facilitate activity-dependent segregation of ocular domi- nance columns through 5-HT2c receptors (Fig. 7.3). A B Initial innervation of LGN terminals 5HT2c 5HT2c 5HT2c Cortical Layer 4 rich 5HT2c rich 5HT2c rich 5HT2c poor poor poor LGN terminals of one eye LFS + 5-HT C 5HT2c 5HT2c 5HT2c 5HT2c 5HT2c 5HT2c Transient expression rich rich rich poor poor poor of 5HT2c columns LTP LTP LTP LTD LTD LTD D Activity-dependent LTP LTP LTP LTD LTD LTD synaptic modifications E Segregation into ocular dominance columns Figure 7.3 Possible mechanism by which a transient expression pattern of 5-HT2c receptors could leads to segregation of LGN terminals in the visual cortex. (A) Low-frequency stimula- tion (LFS) in the presence of 5-HT-induced LTP within 5-HT2c receptor-rich columns, whereas LTD was induced within 5-HT2c receptor-poor columns (Kojic et al., 2000). LGN terminals initially innervate the entire cortical layer 4 (B). However, because of differentially expressed 5-HT2c receptors within layer 4 during visual cortex development (C), the same input could induce either LTP or LTD depending on postsynaptic 5-HT2c receptor levels (D). LGN terminals with LTP will gain functional strength and stay, while LGN terminals with LTD will loss functional connectivity and withdraw, which lead ultimately to segregation of LGN terminals into ocular dominance columns (E). 118 Gu During visual cortex development, LGN terminals representing the two eyes are initially mixed and evenly distributed in cortical layer 4. They later become sepa- rated into discrete columns that represent either the left or the right eye. Transient expression of 5-HT2c receptors in “rich” and “poor” columns during visual cortex development could provide spatial and temporal instructions that allow axon termi- nals in the 5-HT2c receptor-rich zone to stay (via LTP) and axon terminals in the 5- HT2c receptor-poor zone to withdraw (via LTD). This model, based on the expression of particular transmitter receptors, may help to explain the segregation of input axon terminals and the formation of ocular dominance columns in the visual cortex. How- ever, several issues need to be resolved before this model can be fully established: (i) which eye dominance columns do 5-HT2c receptor-rich columns represent, the left or right eye?; (ii) What would be the complementary transmitter/receptor systems or neurochemical molecules that contribute to the other eye’s dominance columns?; (iii) Is the correlation of these neurochemical markers and eye dominance columns ge- netically determined, or is it dependent on other factors during early visual cortex development? A number of neurochemical markers have already been found to dis- play columnar distribution patterns in the developing visual cortex (Schoen et al., 1990; Dyck and Cynader, 1993a, b; Trepel et al., 1998; Murphy et al., 2001). The challenging tasks for future investigations would be to identify molecular cues that contribute to the formation of ocular dominance columns and to correlate the mo- lecular cues with the respective eye input terminals. Studies of serotonergic effects on synaptic plasticity using visual cortex slices de- rived from rats generated somewhat different results. Recording in layers 2 and 3 with stimulation in layer 4 in 3- to 5-week-old rat visual cortex indicated that either serotonin (Edagawa et al., 1998a), 8-hydroxy-2-(N,N-dipropylamino)tetralin (8-OH- DPAT) (Edagawa et al., 1998b) (a 5-HT1A receptor agonist), or 1-(2,5-dimethyl-4- iodophenyl)-2-aminopropane (DOI) (Edagawa et al., 2000) (a 5-HT2 receptor ago- nist) prevented the induction of LTP, whereas pindolol (a 5-HT1 receptor antagonist) or ritanserin (a 5-HT2/5-HT7 receptor antagonist) could abolish the effect of sero- tonin or 8-OH-DPAT or DOI (Edagawa et al., 1998a, b, 2000). Bath application of methysergide-induced LTP in cortical layers 2 and 3 following white matter stimula- tion in 5-week-old rat visual cortex, which in the absence of methysergide showed no LTP after high-frequency stimulation in the white matter (Edagawa et al., 2001). In addition, depletion of serotonin by 5,7-DHT (Edagawa et al., 2001) or by para- chloroamphetamine (Kim et al., 2006) increased LTP induction in visual cortex slices of 5-week-old rats. These results suggest that serotonin has an inhibitory effect on LTP in rat visual cortex. However, when recorded in layer 5 with stimulation in layer 4 in 15- to 25-day-old rat visual cortex, bath application of ketanserin, a 5-HT2 receptor antagonist, reduced the incidence of LTP (Komatsu, 1996), suggesting that activation of 5-HT2 receptors is required to initiate LTP in this pathway. Together, the available evidence suggests that serotonin facilitates LTP and LTD in kitten visual cortex slices (Kojic et al., 1997, 2000, 2001), while in rat visual cor- tex slices serotonin may inhibit (Edagawa et al., 1998a, b, 2000, 2001; Kim et al., 2006) or facilitate LTP (Komatsu, 1996) depending on the specific protocol used. It remains to be determined whether serotonin has any effect on LTD in rat visual cortex slices, since the plasticity of ocular dominance is correlated with homosynap- tic LTD rather than LTP in the visual cortex (Rittenhouse et al., 1999; Heynen et al., 2003). The apparent discrepancies concerning 5-HT effects on LTP between cat and Serotonin Involvement in Plasticity of the Visual Cortex 119 rat visual cortex slices were attributed to a species difference as well as different synaptic pathways tested (Edagawa et al., 2001). This is conceivable, since seroton- ergic innervation in the visual cortex showed different developmental profiles be- tween cats and rats. For example, the level of serotonin in 4-week-old kitten visual cortex, which is at its highest level of cortical plasticity, is already at the peak (Jons- son and Kasamatsu, 1983), while in rat visual cortex it continuously increases until adulthood (Edagawa et al., 2001). In addition, postnatal expression of serotonin subtype receptors in the visual cortex of rats and cats showed different laminar dis- tribution patterns and development profiles (Marcinkiewicz et al., 1984; Pazos and Palacios, 1985; Gozlan et al., 1990; Dyck and Cynader, 1993a). Since different stimulation and recording protocols have been applied in electrophysiological studies of cats’ and rats’ visual cortex slices, it would be more appropriate to compare re- sults when a unified protocol is employed and the same synaptic pathway (e.g., stimulation in the white matter and recording in layer 4) is examined. 7.5 Mechanisms of Serotonin in the Plasticity of Ocular Dominance Serotonin affects membrane potentials at the cellular level, either directly through ion-gated channel or indirectly through intracellular second messengers, and conse- quently to modulate membrane excitability. Serotonin also interacts with other transmitter systems, such as glutametergic and GABAergic transmission. A mecha- nism associated with NMDA receptor-gated synaptic modifications may be consid- ered to explain the facilitatory action of serotonin in ocular dominance plasticity. In vitro experiments have shown that serotonin enhances depolarizing responses to excitatory amino acids in the neocortex of cats (Nedergaard et al., 1987) and rats (Reynolds et al., 1988). This response could be achieved by reducing potassium ion conductance (Andrade and Chaput, 1991; Panicker et al., 1991; Bockaert et al., 1992), leading to a slow membrane depolarization that in turn enhances the flux of calcium ions from extra- to intracellular compartments through NMDA receptors. Another possibility is that synergistic interactions at the level of second messen- gers enhance the intracellular signals induced by the excitatory visual input. For instance, activation of 5-HT2c receptors stimulate phospholipid turnover (Hoyer and Martin, 1997), which in turn could contribute to enhance intracellular effects via inositol triphosphate through calcium release from intracellular stores and protein kinase C activation via diacyl glycerol. Through the augmentation of intracellular responses following NMDA receptor activation, input activity can then induce activ- ity-dependent modifications of synaptic connections (Choi et al., 2005). Thus, acti- vation of serotonergic receptors could increase the probability that retinal input drives cortical neurons above the threshold that needs to be reached for the weaken- ing of the deprived visual afferents (Frégnac et al., 1988). Evidences also indicate that 5-HT axons can directly connect with GABAergic interneurons (Paspalas and Papadopoulos, 2001) and influence GABAergic inhibi- tion in the visual cortex (Roerig et al., 1997; Xiang et al., 1998; Edagawa et al., 2000). Therefore, another possible mechanism of 5-HT in cortical plasticity is to regulate neuronal inhibition, an important factor for determining the threshold for activity-dependent synaptic modifications (Hensch et al., 1998; Fagiolini and Hensch, 2000). 120 Gu 7.6 Conclusions The available evidence suggests that the role of 5-HT in the cerebral cortex is to modulate the excitability of cortical neurons, in order to gate information processes, to enhance the signal-to-noise ratio, and to determine the threshold for activity- dependent synaptic modifications. The involvement of 5-HT in plasticity of the vis- ual cortex has been investigated in vivo and in vitro; 5-HT appears to facilitate the plasticity of ocular dominance in the developing visual cortex. Among 5-HT receptor subtypes, the 5-HT2c receptor emerges to be a predominant player in ocular domi- nance plasticity. A prerequisite for cortical plasticity is the activation of NMDA receptors in the cortex (Singer et al., 1988; Collingridge and Singer, 1990; Bear, 1996). However, activation of NMDA receptor-dependent processes appears to be only a necessary, but not sufficient, condition to induce activity-dependent modifica- tions. For example, monocular light stimulation alone cannot induce an ocular domi- nance shift in the visual cortex of anaesthetized and paralyzed animals. Therefore, the occurrence of adaptive changes in the visual cortex depends not only on the vis- ual input, but also on the functional state of the visual cortex. The latter is mainly controlled by nonvisual input systems, which can enhance visual input responses to overcome the threshold for activity-dependent physiological and anatomical changes. The nonvisual inputs could be the neuromodulatory inputs from subcortical regions, since these transmitters can influence the state of arousal, attention, and motivation. 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