With key elements of the circuitry

With key elements of the circuitry identified, researchers have turned to ques-tions about the cellular and molecular basis of fear conditioning.

CellsinLAareresponsivetonociceptivestimulation,andsomeofthesamecells respond to auditory inputs as well (Romanski et al., 1993). Thus, the substrate for conditioning (convergence of CS and US information) exists in LA. Indeed, during fear conditioning the firing properties of cells in LA are modified (Collins and Pare, 2000; Maren, 2000; Quirk et al., 1995, 1997; Repa et al., 2001). Conditioned plasticity also occurs in the auditory cortex (Quirk et al., 1997; Weinberger, 1995, 1998). How-ever, the response latencies in LA within trials (

ผลลัพธ์ (อังกฤษ) 1:

With key elements of the circuitry identified, researchers have turned to ques-tions about the cellular and molecular basis of fear conditioning.CellsinLAareresponsivetonociceptivestimulation,andsomeofthesamecells respond to auditory inputs as well (Romanski et al., 1993). Thus, the substrate for conditioning (convergence of CS and US information) exists in LA. Indeed, during fear conditioning the firing properties of cells in LA are modified (Collins and Pare, 2000; Maren, 2000; Quirk et al., 1995, 1997; Repa et al., 2001). Conditioned plasticity also occurs in the auditory cortex (Quirk et al., 1997; Weinberger, 1995, 1998). How-ever, the response latencies in LA within trials (<20 ms) and the rate of acquisition (1–3 trials) is best explained in terms of direct auditory thalamo-amygdala transmis-sion, rather than cortico-amygdala transmission, since conditioned responses in the auditory cortex occur later both within trials and across trials (Quirk et al., 1997). Plasticity in the auditory thalamus (Weinberger, 1995, 1998) could contribute to LA plasticity. Plasticity has also been observed in B (Maren et al., 1991; Uwano et al., 1995)andCE(PascoeandKapp,1985)duringaversiveconditioning,buttheacoustic responses latencies both before and after conditioning are longer than in LA. LA thus seems to be both the initial point of sensory processing and the initial site of plasticity in the amygdala.Plasticity in the amygdala has also been studied using long-term potentiation (LTP), a physiological procedure pioneered in studies of the hippocampus (Bliss and Lomo, 1973). LTP is believed to engage the cellular mechanisms similar to those that underlie natural learning (e.g., Bliss and Collingridge, 1993; Lynch, 1986; Malenka and Nicol1 1999; Martin et al., 2000; Nicoll and Malenka, 1995). However, it has been difficult to specifically relate LTP to memory in the hippocampus (see Barnes, 1995; Eichenbaum, 1997; Martin et al., 2000; Stevens, 1998).Considerable success has been achieved in the attempt to relate LTP memory in studiesoftheamygdala.Thisisduetothefactthatspecificsynapses(thosethattrans-mittheCStotheLA)havebeenimplicatedinaspecificformofmemoryinvolvingthe amygdala, namely fear conditioning. Studies using extracellular recordings in vivo of field potentials in LA have shown that LTP occurs in fear processing pathways, that the processing of natural stimuli similar to those used as a CS in conditioning studies is facilitated following LTP induction, and that fear conditioning and LTP induction produce similar changes in the processing of a CS (Clugnet and LeDoux, 1990; Rogan and LeDoux, 1995; Rogan et al., 1997). While exploration of mecha-nisms are difficult in these in vivo studies, they nevertheless provide some of the strongest evidence to date in any brain system of a relation between natural learning and LTP (Barnes, 1995; Eichenbaum, 1995; Stevens, 1998). LTP has also been found in vivo in the hippocampal-amygdala pathway, which is believed to be involved in context conditioning (Maren and Fanselow, 1995).
The most extensively studied form of LTP occurs in the CA1 region of the hippocampus and involves the interaction between presynaptic glutamate and two classesofpostsynapticreceptors(NicollandMalenka,1995).First,glutamatebindsto AMPA receptors and depolarizes the postsynaptic cell. The depolarization removes the magnesium block on the NMDA class of receptors. Calcium then flows into the cell through the NMDA channel and voltage-gated calcium channels (see Cavus and Teyler, 1996; Magee and Johnston, 1997; Tang et al., 1999) and and triggers a host of intracellular events that ultimately result in gene induction and synthesis of new proteins (see Dudai, 1989; Huang et al., 1996; Shaywitz and Greenberg, 1999; Silva et al., 1998). These then help stablize the changes over long periods of time.

There have been a number of in vitro studies of LTP in the amygdala, mostly involving pathways carrying information from the thalamus or cortex to LA and B (Bauer et al., 2002; Chapman et al., 1990; Chapman and Bellavance, 1992; Gean et al., 1993; Huang et al., 1996; Huang and Kandel, 1998; Weisskopf et al., 1999). Recent studies indicate that as in the CA1 region of hippocampus LTP in the thalamo-amygdala pathway requires an elevation of postsynaptic calcium, and that the cal-cium can enter through either NMDA receptors or voltage-gated calcium channels (VGCCs), depending on the manner in which LTP is induced (Bauer et al., 2002; Weisskopf et al., 1999).

Behavioral studies have shown that blockade of NMDA receptors in the LA/B region prevents fear conditioning (Fendt, 2001; Gewirtz and Davis, 1997; Lee and Kim, 1998; Maren and Fanselow, 1996; Miserendino et al., 1990; Rodrigues et al., 2002). Recently, it has also been shown that disruption of VGCCs in LA/B dis-rupts fear conditioning. These studies suggest that during fear conditioning, both the NMDA- and VGCC-dependent forms of LTP occur in the amygdala

ผลลัพธ์ (อังกฤษ) 2:

Key Elements of the circuitry with Identi fi ED, researchers have turned to ques-tions About Cellular and molecular basis of the Fear conditioning. CellsinLAareresponsivetonociceptivestimulation, Andsomeofthesamecells respond to auditory inputs as well (Romanski et al., the 1,993th). Thus, the substrate for conditioning (convergence of CS and US information) exists in LA. Indeed, during fear conditioning the fi ring properties of cells in LA are modi fi ed (Collins and Pare, 2000; Maren, 2000; Quirk et al., 1995, 1997; Repa et al., 2001). Conditioned plasticity also occurs in the auditory cortex (Quirk et al., 1997; Weinberger, 1995, 1998). How-ever, the response latencies in LA within trials (<20 ms) and the rate of acquisition (1-3 trials) is best explained in terms of direct auditory thalamo-amygdala transmis-sion, rather than cortico-amygdala transmission, since. conditioned responses in the auditory cortex occur later both within trials and across trials (Quirk et al., 1997). Plasticity in the auditory thalamus (Weinberger, 1995, 1998) could contribute to LA plasticity. Plasticity has also been observed in B (Maren et al., 1991; Uwano et al., 1995) andCE (PascoeandKapp, 1985) duringaversiveconditioning, buttheacoustic responses latencies both before and after conditioning are longer than in LA. LA thus seems to be both the Initial Point of sensory Processing and the Initial Site of plasticity in the amygdala. Plasticity in the amygdala has also been studied using long-term potentiation (LTP), a physiological procedure pioneered in Studies of the hippocampus (Bliss. and Lomo, 1973). LTP is believed to engage the cellular mechanisms similar to those that underlie natural learning (eg, Bliss and Collingridge, 1993; Lynch, 1986; Malenka and Nicol1 1999; Martin et al., 2000; Nicoll and Malenka, 1995). However, it has been dif fi Cult to speci fi cally Relate LTP to memory in the hippocampus (See Barnes, the 1995th; Eichenbaum, 1,997th; Martin et al., In 2000; Stevens, 1,998). considerable Success has been achieved in the attempt to Relate LTP memory in. amygdala, namely fear conditioning. Studies using extracellular recordings in vivo of fi eld potentials in LA have shown that LTP occurs in fear processing pathways, that the processing of natural stimuli similar to those used as a CS in conditioning studies is facilitated following LTP induction, and that fear conditioning and LTP induction. produce similar changes in the processing of a CS (Clugnet and LeDoux, 1990; Rogan and LeDoux, 1995; Rogan et al., 1997). While exploration of mecha-nisms are dif fi cult in these in vivo studies, they nevertheless provide some of the strongest evidence to date in any brain system of a relation between natural learning and LTP (Barnes, 1995; Eichenbaum, 1995; Stevens, 1998). LTP has also been Found in vivo in the hippocampal-amygdala Pathway, which is believed to be involved in context conditioning (Maren and Fanselow, 1995th). The Most extensively studied form of LTP occurs in the CA1 Region of the hippocampus and Involves the Interaction. between presynaptic glutamate and two classesofpostsynapticreceptors (NicollandMalenka, 1995) .First, glutamatebindsto AMPA receptors and depolarizes the postsynaptic cell. The depolarization removes the magnesium block on the NMDA class of receptors. Calcium then fl ows into the cell through the NMDA channel and voltage-gated calcium channels (see Cavus and Teyler, 1996; Magee and Johnston, 1997; Tang et al., 1999) and and triggers a host of intracellular events that ultimately result in gene. induction and synthesis of new proteins (see Dudai, 1989; Huang et al., 1996; Shaywitz and Greenberg, 1999; Silva et al., 1998). These then Help stablize the changes over long periods of time. There have been a Number of in vitro Studies of LTP in the amygdala, Mostly involving pathways carrying information from the thalamus or Cortex to LA and B (Bauer et al., 2,002th; Chapman. et al., 1990; Chapman and Bellavance, 1992; Gean et al., 1993; Huang et al., 1996; Huang and Kandel, 1998; Weisskopf et al., 1999). Recent studies indicate that as in the CA1 region of hippocampus LTP in the thalamo-amygdala pathway requires an elevation of postsynaptic calcium, and that the cal-cium can enter through either NMDA receptors or voltage-gated calcium channels (VGCCs), depending on the. Manner in which LTP is induced (Bauer et al., 2002nd; Weisskopf et al., 1,999). Behavioral Studies have shown that blockade of NMDA receptors in the LA / B Region prevents Fear conditioning (Fendt, 2,001; Gewirtz and Davis, in 1997. ; Lee and Kim, 1998; Maren and Fanselow, 1996; Miserendino et al., 1990; Rodrigues et al., 2002). Recently, it has also been shown that disruption of VGCCs in LA / B dis-rupts fear conditioning. These studies suggest that during fear conditioning, both the NMDA- and VGCC-dependent forms of LTP occur in the amygdala.