GABA signaling tracks anxiety- and depression-like behavior in rodents
Several of these studies converge on GABA as a signal that moves with mood-related behavior, though in different models. In mice exposed to fluoride, anxiety-like behavior in the elevated zero maze and depression-like behavior in the tail suspension test were accompanied by lower GABA levels and reduced expression of the GABA-synthesis proteins GAD65 and GAD67 and the vesicular GABA transporter VGAT; exercise reversed both the behaviors and those GABA-related changes [1]. In rats, melatonin and diazepam altered anxiety- and depression-like behavior in a way the authors interpret as involving central GABA neurotransmission [5]. These are different manipulations, but they point in the same direction: when GABA signaling is disturbed, anxiety- and depression-like behavior tends to shift with it.
The strongest causal evidence in this set comes from a specific group of GABA neurons in the ventral tegmental area (VTA), a midbrain region. One day after a single session of unpredictable footshock, mice showed more anxiety-related behavior and their VTA GABA neurons were more excitable, with increased glutamatergic input and reduced postsynaptic GABA-A and GABA-B receptor signaling [4]. Chemically activating those VTA GABA neurons was enough to raise anxiety-related behavior in unstressed mice, and chemically inhibiting them suppressed anxiety-related behavior in stressed mice [4]. That is a direct demonstration that this GABA population can drive anxiety-like behavior, at least in this stress model.
Dopamine neurons and photoperiod switching are not tested here
The question asks about switching between GABA and dopamine neurons under photoperiod control. None of these studies manipulated day length to flip a neuron population between GABA and dopamine identities, and none measured dopamine neuron activity alongside anxiety- or depression-like behavior. Dopamine appears only as a passing mention: one rat study lists dopamine among neurotransmitters in its abstract without testing a dopaminergic mechanism [5], and the VTA work focuses on GABA neurons without examining dopamine neurons in the same circuits [4]. So the specific photoperiod-driven GABA-to-dopamine switch is not addressed by this evidence.
What the studies do show is that the behavioral effects depend heavily on the model and the manipulation. Mifepristone, a receptor antagonist, produced antidepressant- and anxiolytic-like effects in rodents, but a review of that literature found the results depended on dose, duration, the type and intensity of stress, and the species or strain used, with more reports after acute than chronic administration [3]. That variability is a caution for any simple story that one neurotransmitter population maps cleanly onto one mood behavior.
Other pathways can produce the same behavioral changes
GABA is not the only route to these behaviors in the evidence. In mice subjected to chronic unpredictable mild stress, listening to music at night completely prevented depression- and anxiety-like behavior across several tests, and the authors attribute this to restored corticosterone levels and reduced oxidative stress, inflammation, and neurotrophic factor deficits rather than to a GABA-dopamine switch [2]. That study is a reminder that anxiety- and depression-like behavior in rodents can be shifted by many upstream systems, so a photoperiod-GABA-dopamine mechanism would need to be tested against these alternatives rather than assumed.
For a reader trying to connect photoperiod to mood through neuron switching, the honest state of this evidence is that the pieces exist separately: GABA signaling is linked to anxiety- and depression-like behavior [1][4][5], and photoperiod is mentioned only as a housing condition in one rat study [5], not as a variable that switches neuron identity. Testing the full chain would require studies that manipulate day length, track whether GABA and dopamine neuron populations change, and measure anxiety- and depression-like behavior in the same animals.
Sources used in this answer
Exercise Ameliorates Fluoride-induced Anxiety- and Depression-like Behavior in Mice: Role of GABA
In fluoride-exposed mice, exercise reduced anxiety- and depression-like behavior while restoring GABA levels and the expression of GABA synthesis and transport proteins GAD65, GAD67, and VGAT.
Music prevents stress-induced depression and anxiety-like behavior in mice
In mice under chronic unpredictable mild stress, listening to music at night prevented depression- and anxiety-like behavior, with effects attributed to restored corticosterone and reduced oxidative stress, inflammation, and neurotrophic factor deficits.
Mifepristone’s effects on depression- and anxiety-like behavior in rodents
A review of mifepristone in rodents found antidepressant- and anxiolytic-like effects that depended on dose, duration, stress type and intensity, and species or strain, with more reports after acute than chronic administration.
Stress-induced anxiety-related behavior in mice is driven by enhanced excitability of ventral tegmental area GABA neurons
In mice, a single unpredictable footshock increased anxiety-related behavior and VTA GABA neuron excitability; activating these neurons raised anxiety-related behavior and inhibiting them suppressed it after stress.
Melatonin and diazepam affect anxiety-like and depression-like behavior in Wistar rats: possible interaction with central GABA neurotransmission
In Wistar rats, melatonin and diazepam altered anxiety- and depression-like behavior, with the authors suggesting an interaction with central GABA neurotransmission.