Depression

1. Nerve cell (neuron): basic fundamental unit of nervous system. 3 main parts: dendrites (receive signal from neighboring neurons), axon (responsible for transmission of the nerve impulse), nerve terminal (bouton or foot; transmits signals to other neurons). Also is a soma/cell body, nucleus, myelin sheath around the neuron. Electrical signal drives the release of NT (due to influx of Ca2+ in case of glu) in presyn neuron, into synaptic cleft, bind to recpetors on the postsynaptic neuron. 1 family iGluR’s: nonselective cation channel. (2 family of NT transporters to get NT out of synaptic cleft and back into presyn cell: glutamate and LeuTA4 (gly, GABA, biogenic amines). Electric signal restored once ion channels open on post synaptic neurons. The opening of the channels leads to depolarization of the plasma membrane and the generation of electric current that goes to the dendrites to axon to the next neuron- driven by the co-transport of Na+. NMDA: in resting state, blocked by Mg, which is relieved as cell depolarizes, so voltage-dependent and ligand-gated channel. Ligand gated ion channels: moves ions down conc gradient (vs. pumps that move against conc gradient and need E (ATP) or coupling to flow of other ions). This polarizes the membrane (to its Nernst potential)- this is the origin of the resting membrane potential. Termination of iGluR response can be mediated by: deactivation (loss of bound agonist) or inactivation/desensitiz (conversion to an unresponsive state; happens by many mechanisms and differs between subunits)Nerve cell (neuron): basic fundamental unit of nervous system. 3 main parts: dendrites (receive signal from neighboring neurons), axon (responsible for transmission of the nerve impulse), nerve terminal (bouton or foot; transmits signals to other neurons). Also is a soma/cell body, nucleus, myelin sheath around the neuron. Electrical signal drives the release of NT (due to influx of Ca2+ in case of glu) in presyn neuron, into synaptic cleft, bind to recpetors on the postsynaptic neuron. 1 family iGluR’s: nonselective cation channel. (2 family of NT transporters to get NT out of synaptic cleft and back into presyn cell: glutamate and LeuTA4 (gly, GABA, biogenic amines). Electric signal restored once ion channels open on post synaptic neurons. The opening of the channels leads to depolarization of the plasma membrane and the generation of electric current that goes to the dendrites to axon to the next neuron- driven by the co-transport of Na+. NMDA: in resting state, blocked by Mg, which is relieved as cell depolarizes, so voltage-dependent and ligand-gated channel. Ligand gated ion channels: moves ions down conc gradient (vs. pumps that move against conc gradient and need E (ATP) or coupling to flow of other ions). This polarizes the membrane (to its Nernst potential)- this is the origin of the resting membrane potential. Termination of iGluR response can be mediated by: deactivation (loss of bound agonist) or inactivation/desensitiz (conversion to an unresponsive state; happens by many mechanisms and differs between subunits)

2. Nerve cell (neuron): basic fundamental unit of nervous system. 3 main parts: dendrites (receive signal from neighboring neurons), axon (responsible for transmission of the nerve impulse), nerve terminal (bouton or foot; transmits signals to other neurons). Also is a soma/cell body, nucleus, myelin sheath around the neuron. Electrical signal drives the release of NT (due to influx of Ca2+ in case of glu) in presyn neuron, into synaptic cleft, bind to recpetors on the postsynaptic neuron. 1 family iGluR’s: nonselective cation channel. (2 family of NT transporters to get NT out of synaptic cleft and back into presyn cell: glutamate and LeuTA4 (gly, GABA, biogenic amines). Electric signal restored once ion channels open on post synaptic neurons. The opening of the channels leads to depolarization of the plasma membrane and the generation of electric current that goes to the dendrites to axon to the next neuron- driven by the co-transport of Na+. NMDA: in resting state, blocked by Mg, which is relieved as cell depolarizes, so voltage-dependent and ligand-gated channel. Ligand gated ion channels: moves ions down conc gradient (vs. pumps that move against conc gradient and need E (ATP) or coupling to flow of other ions). This polarizes the membrane (to its Nernst potential)- this is the origin of the resting membrane potential. Termination of iGluR response can be mediated by: deactivation (loss of bound agonist) or inactivation/desensitiz (conversion to an unresponsive state; happens by many mechanisms and differs between subunits)Nerve cell (neuron): basic fundamental unit of nervous system. 3 main parts: dendrites (receive signal from neighboring neurons), axon (responsible for transmission of the nerve impulse), nerve terminal (bouton or foot; transmits signals to other neurons). Also is a soma/cell body, nucleus, myelin sheath around the neuron. Electrical signal drives the release of NT (due to influx of Ca2+ in case of glu) in presyn neuron, into synaptic cleft, bind to recpetors on the postsynaptic neuron. 1 family iGluR’s: nonselective cation channel. (2 family of NT transporters to get NT out of synaptic cleft and back into presyn cell: glutamate and LeuTA4 (gly, GABA, biogenic amines). Electric signal restored once ion channels open on post synaptic neurons. The opening of the channels leads to depolarization of the plasma membrane and the generation of electric current that goes to the dendrites to axon to the next neuron- driven by the co-transport of Na+. NMDA: in resting state, blocked by Mg, which is relieved as cell depolarizes, so voltage-dependent and ligand-gated channel. Ligand gated ion channels: moves ions down conc gradient (vs. pumps that move against conc gradient and need E (ATP) or coupling to flow of other ions). This polarizes the membrane (to its Nernst potential)- this is the origin of the resting membrane potential. Termination of iGluR response can be mediated by: deactivation (loss of bound agonist) or inactivation/desensitiz (conversion to an unresponsive state; happens by many mechanisms and differs between subunits)

3. Nerve cell (neuron): basic fundamental unit of nervous system. 3 main parts: dendrites (receive signal from neighboring neurons), axon (responsible for transmission of the nerve impulse), nerve terminal (bouton or foot; transmits signals to other neurons). Also is a soma/cell body, nucleus, myelin sheath around the neuron. Electrical signal drives the release of NT (due to influx of Ca2+ in case of glu) in presyn neuron, into synaptic cleft, bind to recpetors on the postsynaptic neuron. 1 family iGluR’s: nonselective cation channel. (2 family of NT transporters to get NT out of synaptic cleft and back into presyn cell: glutamate and LeuTA4 (gly, GABA, biogenic amines). Electric signal restored once ion channels open on post synaptic neurons. The opening of the channels leads to depolarization of the plasma membrane and the generation of electric current that goes to the dendrites to axon to the next neuron- driven by the co-transport of Na+. NMDA: in resting state, blocked by Mg, which is relieved as cell depolarizes, so voltage-dependent and ligand-gated channel. Ligand gated ion channels: moves ions down conc gradient (vs. pumps that move against conc gradient and need E (ATP) or coupling to flow of other ions). This polarizes the membrane (to its Nernst potential)- this is the origin of the resting membrane potential. Termination of iGluR response can be mediated by: deactivation (loss of bound agonist) or inactivation/desensitiz (conversion to an unresponsive state; happens by many mechanisms and differs between subunits)Nerve cell (neuron): basic fundamental unit of nervous system. 3 main parts: dendrites (receive signal from neighboring neurons), axon (responsible for transmission of the nerve impulse), nerve terminal (bouton or foot; transmits signals to other neurons). Also is a soma/cell body, nucleus, myelin sheath around the neuron. Electrical signal drives the release of NT (due to influx of Ca2+ in case of glu) in presyn neuron, into synaptic cleft, bind to recpetors on the postsynaptic neuron. 1 family iGluR’s: nonselective cation channel. (2 family of NT transporters to get NT out of synaptic cleft and back into presyn cell: glutamate and LeuTA4 (gly, GABA, biogenic amines). Electric signal restored once ion channels open on post synaptic neurons. The opening of the channels leads to depolarization of the plasma membrane and the generation of electric current that goes to the dendrites to axon to the next neuron- driven by the co-transport of Na+. NMDA: in resting state, blocked by Mg, which is relieved as cell depolarizes, so voltage-dependent and ligand-gated channel. Ligand gated ion channels: moves ions down conc gradient (vs. pumps that move against conc gradient and need E (ATP) or coupling to flow of other ions). This polarizes the membrane (to its Nernst potential)- this is the origin of the resting membrane potential. Termination of iGluR response can be mediated by: deactivation (loss of bound agonist) or inactivation/desensitiz (conversion to an unresponsive state; happens by many mechanisms and differs between subunits)

4. Nerve cell (neuron): basic fundamental unit of nervous system. 3 main parts: dendrites (receive signal from neighboring neurons), axon (responsible for transmission of the nerve impulse), nerve terminal (bouton or foot; transmits signals to other neurons). Also is a soma/cell body, nucleus, myelin sheath around the neuron. Electrical signal drives the release of NT (due to influx of Ca2+ in case of glu) in presyn neuron, into synaptic cleft, bind to recpetors on the postsynaptic neuron. 1 family iGluR’s: nonselective cation channel. (2 family of NT transporters to get NT out of synaptic cleft and back into presyn cell: glutamate and LeuTA4 (gly, GABA, biogenic amines). Electric signal restored once ion channels open on post synaptic neurons. The opening of the channels leads to depolarization of the plasma membrane and the generation of electric current that goes to the dendrites to axon to the next neuron- driven by the co-transport of Na+. NMDA: in resting state, blocked by Mg, which is relieved as cell depolarizes, so voltage-dependent and ligand-gated channel. Ligand gated ion channels: moves ions down conc gradient (vs. pumps that move against conc gradient and need E (ATP) or coupling to flow of other ions). This polarizes the membrane (to its Nernst potential)- this is the origin of the resting membrane potential. Termination of iGluR response can be mediated by: deactivation (loss of bound agonist) or inactivation/desensitiz (conversion to an unresponsive state; happens by many mechanisms and differs between subunits)Nerve cell (neuron): basic fundamental unit of nervous system. 3 main parts: dendrites (receive signal from neighboring neurons), axon (responsible for transmission of the nerve impulse), nerve terminal (bouton or foot; transmits signals to other neurons). Also is a soma/cell body, nucleus, myelin sheath around the neuron. Electrical signal drives the release of NT (due to influx of Ca2+ in case of glu) in presyn neuron, into synaptic cleft, bind to recpetors on the postsynaptic neuron. 1 family iGluR’s: nonselective cation channel. (2 family of NT transporters to get NT out of synaptic cleft and back into presyn cell: glutamate and LeuTA4 (gly, GABA, biogenic amines). Electric signal restored once ion channels open on post synaptic neurons. The opening of the channels leads to depolarization of the plasma membrane and the generation of electric current that goes to the dendrites to axon to the next neuron- driven by the co-transport of Na+. NMDA: in resting state, blocked by Mg, which is relieved as cell depolarizes, so voltage-dependent and ligand-gated channel. Ligand gated ion channels: moves ions down conc gradient (vs. pumps that move against conc gradient and need E (ATP) or coupling to flow of other ions). This polarizes the membrane (to its Nernst potential)- this is the origin of the resting membrane potential. Termination of iGluR response can be mediated by: deactivation (loss of bound agonist) or inactivation/desensitiz (conversion to an unresponsive state; happens by many mechanisms and differs between subunits)

5. Nerve cell (neuron): basic fundamental unit of nervous system. 3 main parts: dendrites (receive signal from neighboring neurons), axon (responsible for transmission of the nerve impulse), nerve terminal (bouton or foot; transmits signals to other neurons). Also is a soma/cell body, nucleus, myelin sheath around the neuron. Electrical signal drives the release of NT (due to influx of Ca2+ in case of glu) in presyn neuron, into synaptic cleft, bind to recpetors on the postsynaptic neuron. 1 family iGluR’s: nonselective cation channel. (2 family of NT transporters to get NT out of synaptic cleft and back into presyn cell: glutamate and LeuTA4 (gly, GABA, biogenic amines). Electric signal restored once ion channels open on post synaptic neurons. The opening of the channels leads to depolarization of the plasma membrane and the generation of electric current that goes to the dendrites to axon to the next neuron- driven by the co-transport of Na+. NMDA: in resting state, blocked by Mg, which is relieved as cell depolarizes, so voltage-dependent and ligand-gated channel. Ligand gated ion channels: moves ions down conc gradient (vs. pumps that move against conc gradient and need E (ATP) or coupling to flow of other ions). This polarizes the membrane (to its Nernst potential)- this is the origin of the resting membrane potential. Termination of iGluR response can be mediated by: deactivation (loss of bound agonist) or inactivation/desensitiz (conversion to an unresponsive state; happens by many mechanisms and differs between subunits)Nerve cell (neuron): basic fundamental unit of nervous system. 3 main parts: dendrites (receive signal from neighboring neurons), axon (responsible for transmission of the nerve impulse), nerve terminal (bouton or foot; transmits signals to other neurons). Also is a soma/cell body, nucleus, myelin sheath around the neuron. Electrical signal drives the release of NT (due to influx of Ca2+ in case of glu) in presyn neuron, into synaptic cleft, bind to recpetors on the postsynaptic neuron. 1 family iGluR’s: nonselective cation channel. (2 family of NT transporters to get NT out of synaptic cleft and back into presyn cell: glutamate and LeuTA4 (gly, GABA, biogenic amines). Electric signal restored once ion channels open on post synaptic neurons. The opening of the channels leads to depolarization of the plasma membrane and the generation of electric current that goes to the dendrites to axon to the next neuron- driven by the co-transport of Na+. NMDA: in resting state, blocked by Mg, which is relieved as cell depolarizes, so voltage-dependent and ligand-gated channel. Ligand gated ion channels: moves ions down conc gradient (vs. pumps that move against conc gradient and need E (ATP) or coupling to flow of other ions). This polarizes the membrane (to its Nernst potential)- this is the origin of the resting membrane potential. Termination of iGluR response can be mediated by: deactivation (loss of bound agonist) or inactivation/desensitiz (conversion to an unresponsive state; happens by many mechanisms and differs between subunits)

6. hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI). hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI).

12. hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI). hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI).

13. hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI). hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI).

14. hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI). hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI).

15. hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI). hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI).

16. hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI). hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI).

17. hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI). hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI).

18. hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI). hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI).

19. hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI). hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI).

20. hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI). hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI).

21. hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI). hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI).

22. hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI). hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI).

23. hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI). hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI).

24. hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI). hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI).

25. hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI). hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI).

26. hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI). hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI).

27. hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI). hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI).

28. hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI). hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI).

29. hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI). hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI).

30. hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI). hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI).

31. hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI). hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI).

32. hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI). hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI).

33. hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI). hypothesis that the pathophysiology of depression is caused solely by a decrease in the synaptic availability of monoaminergic neurotransmitters (especially serotonin, norepinephrine, and dopamine) has been questioned. Based on accumulating data, it seems more plausible that a cross-talk exists between neurotransmitter systems in the central nervous system, including the glutamatergic system. Classes: (TCAs), selective serotonin reuptake inhibitors (SSRI), and selective noradrenaline reuptake inhibitors (SNRI).